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228 Sentences With "metabolizes"

How to use metabolizes in a sentence? Find typical usage patterns (collocations)/phrases/context for "metabolizes" and check conjugation/comparative form for "metabolizes". Mastering all the usages of "metabolizes" from sentence examples published by news publications.

Bacteria. "Any smell you have is a combination of what the human metabolizes and what the bacteria metabolizes," says Dr. Maria Mendes Soares of the Mayo Clinic.
So when the fat gets damaged, your immune system comes and metabolizes them.
Here's what to keep in mind as your bank account metabolizes the difference.
When THC goes through the liver, it metabolizes into another more potent psychoactive molecule.
The body metabolizes these foods into sugar almost immediately, which causes your blood sugar to rise.
But differences in the way your body metabolizes drugs might render you prone to side effects.
A liver, while not a reproductive organ, is included in the system because it metabolizes drugs.
"Alcohol metabolizes out of the milk supply just as it does out of your bloodstream," she continued.
Ask Well Differences in the way your body metabolizes drugs might render you prone to side effects.
Rationing meant he didn't eat in order to keep from having to give insulin that metabolizes food.
When the scientists disabled the gene that metabolizes fructose and repeated the experiment, neither group developed chronic kidney disease.
The effects of the hormone, which is available without a prescription, vary because each human body metabolizes it differently.
It metabolizes quickly, within four to six hours, and, unlike other insomnia drugs, does not usually result in daytime drowsiness.
Once inside the human body, this compound metabolizes into the more familiar GHB, a drug commonly associated with date rape.
For people on the keto diet, this might mean filling a plate with carbohydrates, which the body metabolizes as glucose.
Officials didn't believe her cocaine excuse because coke metabolizes "almost immediately" and would likely not show up if taken that long ago.
Alcoholic fermentation occurs when yeast metabolizes a source of sugar (glucose, sucrose or fructose), turning it into ethanol (alcohol) and carbon dioxide.
Apparently, marijuana edibles feel more intense than smoking because your liver metabolizes the THC differently, converting it into a stronger, more psychedelic form.
Researchers like Shah believe that as the brain metabolizes the ketamine, new neural pathways are created that help restore function obliterated by depression.
One possible reason for this is the way our body metabolizes booze, Adams says, which involves enzymes breaking down the alcohol into toxic byproducts.
The researchers suggested that irregular feedings affect the circadian cycle of the liver and the way it metabolizes food, thus influencing overall energy balance.
As the researchers discovered in a later study, stress can change the way your body metabolizes fats, even reducing the benefits of eating a healthy meal.
Part of the pain of a hangover is caused by acetaldehyde, a byproduct produced as the body metabolizes ethanol, or the type of alcohol people drink.
At a low dose, these risks are diminished, but it's difficult to predict how susceptible you are to them, since everybody metabolizes ketamine differently, Giordano adds.
Men's wear metabolizes change more slowly than its women's counterpart, and men in the world more slowly than their brethren in the ranks of the fashion industry.
"Basically once you put the alcohol into his blood it metabolizes that instead, and gives the antifreeze time to pass in a less toxic form," the vet explained.
Even if there are individual differences — how efficiently a person metabolizes dietary refined carbohydrates or fat — these don't matter if a person isn't eating too much of these.
I think the American public metabolizes conversations about race being led by white people differently than they do when those same conversations are being led by people of color.
It is caused by the build-up of fat-like substances, most notably in the kidneys, due to the deficiency or lack of an enzyme that metabolizes these lipids.
Everyone metabolizes and absorbs CBD at different rates, and they may respond differently to it once they metabolize it, with some experiencing heightened effects, and others lowered effects, Giordano says.
Theoretically, if you only have a drink per hour (which is about how fast the body metabolizes alcohol), you could stay out late and still feel fine the next day.
While the results are temporary, they're still significant — depending on how fast your body metabolizes the fillers, the results can last anywhere from one to three years, according to Dr. Liotta.
No matter the cadence of the economy or stance of policymakers, the market metabolizes it all by breaking the world down into corporate profitability, the cost of money and crowd psychology.
With each drink, an older person's blood alcohol levels will rise higher than a younger drinker's, Dr. Schuckit noted; older people have less muscle mass, and the liver metabolizes alcohol more slowly.
What's more, during Su's first tasting, his face turned scarlet, a reaction known as Asian flush, which affects about a third of all East Asians—myself included—and is caused by a deficiency of the enzyme that metabolizes alcohol.
She notes that women can be more expensive to test than men, as researchers have to control where the woman is in her menstrual cycle (or if she's post-menopausal) because hormones affect how the body metabolizes a drug.
And in order to unpack exactly how pollution or pesticides may lead to autism (or not), researchers also need to understand how a person's genetics determines how well their body metabolizes chemicals, responds to stress, and any number of other potential assaults.
They shut down one pathway — converting energy for our body through the breathing process — and switch to another that metabolizes glucose (the only energy source the brain and red blood cells can use) and avoids the build-up of fructose in tissues, which causes damage.
Produced in collaboration with Anton Carlson, the scientific director of the Research Council on Problems of Alcohol, the educational PSA covers everything from the production of different kinds of "intoxicating beverages" to how the body metabolizes different alcoholic beverages to the psychological and social effects of drinking too much.
"These different metabolic processes ebb and flow at different times of the day, and they play a role in how your body metabolizes food energy, which ultimately affects your weight, cholesterol levels and blood sugar control -- and so it has tremendous implications for what is considered optimal times for eating," Freuman said.
"Michael in the Bathroom" taps so clearly into the traumatized horror of adolescence that it metabolizes the angst into pure energy, the kind of energy that can lift the cast album from a tiny regional musical out of obscurity and to the top of billboard, that can propel a show from New Jersey to an off-Broadway theater.
CYP1A1 also metabolizes polyunsaturated fatty acids into signaling molecules that have physiological as well as pathological activities. CYP1A1 has monoxygenase activity in that it metabolizes arachidonic acid to 19-hydroxyeicosatetraenoic acid (19-HETE) (see 20-Hydroxyeicosatetraenoic acid) but also has epoxygenase activity in that it metabolizes docosahexaenoic acid to epoxides, primarily 19R,20S-epoxyeicosapentaenoic acid and 19S,20R-epoxyeicosapentaenoic acid isomers (termed 19,20-EDP) and similarly metabolizes eicosapentaenoic acid to epoxides, primarily 17R,18S-eicosatetraenic acid and 17S,18R-eicosatetraenic acid isomers (termed 17,18-EEQ). Synthesis of 12(S)-HETE by CYP1A1 has also been demonstrated. 19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule, e.g.
The bacteria metabolizes sugars that the yeast cannot, and the yeast metabolizes byproducts of bacterial fermentation. Commercially produced yeast will not accomplish these processes in rye flour. Rugbrød is almost always very low in fat, comparable to most other varieties of bread. It contains no added oils or fats.
Carnitine metabolizes at rates of about 400 μmol per day, an amount less than 1% of total body stores.
Sphingomonas elodea metabolizes maltodextrin (oligosaccharides of glucose) externally into glucose by the putative exo-acting glucosidase. Sphingomonas elodea utilizes the Entner-Doudoroff pathway for glucose metabolism.
The enzyme also metabolizes some steroids and carcinogens. Most drugs undergo deactivation by CYP3A4, either directly or by facilitated excretion from the body. Also, many substances are bioactivated by CYP3A4 to form their active compounds, and many protoxins being toxicated into their toxic forms (for examples – see table below). CYP3A4 also possesses epoxygenase activity in that it metabolizes arachidonic acid to epoxyeicosatrienoic acids (EETs), i.e. (±)-8,9-, (±)-11,12-, and (±)-14,15-epoxyeicosatrienoic acids.
The murine homolog of human 15(S)-lipoxygenase-2 (ALOX15B), 8(S)-lipoxygenase, while preferring arachidonic acid over linoleic acid, metabolizes linoleic acid predominantly to (9(S)-HpODE, which in tissues and cells is rapidly reduced to 9(S)-HODE.Mol Carcinog. 1999 Feb;24(2):108-17Oncogene. 2005 Feb 10;24(7):1174-87 However, ALOX15B, similar to human 15-lipoxygenase-1 (ALOX15), metabolizes linoleic acid to 13(S)-HODE but not to 9(S)-HODEs.Eur.
CYP2D6 also activates some prodrugs. This enzyme also metabolizes several endogenous substances, such as hydroxytryptamines, neurosteroids, and both m-tyramine and p-tyramine which CYP2D6 metabolizes into dopamine in the brain and liver. Considerable variation exists in the efficiency and amount of CYP2D6 enzyme produced between individuals. Hence, for drugs that are metabolized by CYP2D6 (that is, are CYP2D6 substrates), certain individuals will eliminate these drugs quickly (ultrarapid metabolizers) while others slowly (poor metabolizers).
Gene variation in these enzymes can lead to variation in catalytic efficiency between individuals. The liver is the major organ that metabolizes ethanol due to its high concentration of these enzymes.
A 15-hydroxyicosatetraenoate dehydrogenase metabolizes 15-Hydroxyicosatetraenoic acid (i.e. 15(S)-hydroxy-5Z,8Z,11Z,13E-eicosatetraenoic acid or 15-HETE) to its 15-keto analog, 15-oxo-ETE (see 15-Hydroxyicosatetraenoic acid using NAD+ and NADH rather than NADP+ and NADPH as its co-factors (see 15-hydroxyicosatetraenoate dehydrogenase). 15-oxo-ETE appears to have a somewhat different spectrum of activities than its precursor, 15-HETE (see 15-oxo-ETE section of 15-Hydroxyicosatetraenoic acid). Other eicosanoid oxoreductases that use NAD+ and NADH as co-factors include: 12-hydroxyicosatetraenoate dehydrogenase which metabolizes 12-Hydroxyeicosatetraenoic acid (12-HETE) and LTB4 to their corresponding 12-oxo analogs and 11-hydroxy-TXB2 dehydrogenase, which metabolizes TXB2 to its 11-oxo analog;Prog Lipid Res.
It is not in any way an indicator for the drunkenness of an individual. A mild flushing reaction occurs when the body metabolizes alcohol more quickly into acetaldehyde, a toxic metabolite. A more severe flushing reaction occurs when the body metabolizes the acetaldehyde more slowly, generally due to an inactive aldehyde dehydrogenase enzyme. Both of those conditions—faster conversion of alcohol to acetaldehyde and slower removal of acetaldehyde—reduce the risk for excessive drinking and alcohol dependence.
Levomethamphetamine can register on urine drug screens as either methamphetamine, amphetamine, or both, depending on the subject's metabolism and dosage. L-methamphetamine metabolizes completely into L-amphetamine after a period of time.
The liver receives many lipids from the systemic circulation and metabolizes chylomicron remnants. It also synthesizes cholesterol from acetate and further synthesizes bile salts. The liver is the sole site of bile salts formation.
Oxidation of Disulfoton happens rapidly and metabolizes disulfoton into sulfones and sulfoxides, oxidation to oxygen analogs and/or hydrolysis to produce a corresponding phosphorothionate or phosphate. Microsomal enzymes are being inhibited during the metabolism.
CYP1A2 is a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. CYP1A2 localizes to the endoplasmic reticulum and its expression is induced by some polycyclic aromatic hydrocarbons (PAHs), some of which are found in cigarette smoke. The enzyme's endogenous substrate is unknown; however, it is able to metabolize some PAHs to carcinogenic intermediates. Other xenobiotic substrates for this enzyme include caffeine, aflatoxin B1, and paracetamol (acetaminophen). The transcript from this gene contains four Alu sequences flanked by direct repeats in the 3' untranslated region. CYP1A2 also metabolizes polyunsaturated fatty acids into signaling molecules that have physiological as well as pathological activities. It has monoxygenase activity for certain of these fatty acids in that it metabolizes arachidonic acid to 19-hydroxyeicosatetraenoic acid (19-HETE) (see 20-Hydroxyeicosatetraenoic acid) but also has epoxygenase activity in that it metabolizes docosahexaenoic acid to epoxides, primarily 19R,20S-epoxyeicosapentaenoic acid and 19S,20R-epoxyeicosapentaenoic acid isomers (termed 19,20-EDP) and similarly metabolizes eicosapentaenoic acid to epoxides, primarily 17R,18S-eicosatetraenic acid and 17S,18R-eicosatetraenic acid isomers (termed 17,18-EEQ).
A milliliter of pure GBL metabolizes to the equivalent 1.65g of NaGHB, the common form, so doses are measured in the single milliliter range, either taken all at once or sipped over the course of a night.
The body metabolizes methamphetamine into amphetamine (in addition to less active metabolites). A quarter of methamphetamine will ultimately become amphetamine. After comparing only the common ground between dextroamphetamine and dextromethamphetamine, the latter is said to be the stronger stimulant.
Glucose clamp technique is a method for quantifying insulin secretion and resistance. It is used to measure either how well an individual metabolizes glucose or how sensitive an individual is to insulin.Linda von Wartburg, “What's a Glucose Clamp, Anyway?” Diabetes Health.
Metronidazole (Flagyl), which is used to treat certain parasitic infections as well as pseudomembranous colitis, causes similar effects to disulfiram. Coprine (which is an amino acid found in certain coprinoid mushrooms) metabolizes in vivo to 1-aminocyclopropanol which causes similar effects as well.
These proteins include methionine aminopeptidase 2, an enzyme that occurs in humans and other mammals that does not use the corrin ring of B12, but binds cobalt directly. Another non-corrin cobalt enzyme is nitrile hydratase, an enzyme in bacteria that metabolizes nitriles.
Carboxycyclophosphamide is an inactive metabolite of the cytotoxic antineoplastic drug cyclophosphamide. In the metabolic pathway of cyclophosphamide inactivation it first metabolizes to 4-hydroxycyclophosphamide, then partially tautomerizes into aldophosphamide. Aldophosphamide then, in turn, is oxidized into carboxycyclophosphamide by the enzyme ALDH (aldehyde dehydrogenase).
Methyltransferases are very common in the catecholamine synthesis and deactivation pathways. PNMT is also involved in the biosynthesis of N-methylated trace amines: it metabolizes phenethylamine into N-methylphenethylamine (a positional isomer of amphetamine), p-octopamine into synephrine, and p-tyramine into N-methyltyramine.
Thiopurine methyltransferase methylates thiopurine compounds. The methyl donor is S-adenosyl-L-methionine, which is converted to S-adenosyl-L-homocysteine. This enzyme metabolizes thiopurine drugs via S-adenosyl-L-methionine as the S-methyl donor and S-adenosyl-L-homocysteine as a byproduct.
Primarily, the liver metabolizes it. The main metabolic route in humans is: in cytoplasm, nonspecific NAD-dependent dehydrogenase (polyol dehydrogenase) transforms xylitol to D-xylulose. Specific xylulokinase phosphorylates it to D-xylulose-5-phosphate. This then goes to pentose phosphate pathway for further processing.
2013 Oct;52(4):651-65. . Epub 2013 Sep 19. Review and 15-hydroxyprostaglandin dehydrogenase (NAD+) which metabolizes (5Z,13E)-(15S)-11alpha,15-dihydroxy-9-oxoprost-13-enoate to its 15-oxo analog. Other eicosanoid oxireductatases that use NADP+ and NADPH as cofactors include LTB4 12-hydroxy dehydrogenase which metabolizes LTB4 to is 12-oxo analog,Prog Lipid Res. 2013 Oct;52(4):651-65. . Epub 2013 Sep 19. Review and 15-hydroxyprostaglandin-D dehydrogenase (NADP+), 15-hydroxyprostaglandin-I dehydrogenase (NADP+), and 15-hydroxyprostaglandin dehydrogenase (NADP+) which metabolize PGD2, PGI2, and (13E)-(15S)-11alpha,15-dihydroxy-9-oxoprost-13-enoate, respectively, to their corresponding 15-oxo analogs.
The plant contains diverse phytochemicals, including ursolic acid, tannic acid, gallic acid, some essential oils and resin, hydroquinones (mainly arbutin, up to 17%), tannins (up to 15%), phenolic glycosides and flavonoids. Arctostaphylos uva-ursi leaves contain arbutin, which metabolizes to form hydroquinone, a potential liver toxin.
At low doses it is considered to be acceptable for use during pregnancy. Ritonavir is of the protease inhibitor class. Typically, however, it is used to inhibit the enzyme that metabolizes other protease inhibitors. This inhibition allows lower doses of these latter medication to be used.
Malonomonas is a Gram-negative, non-spore-forming, chemoorganotrophic, anaerobic and motile genus of bacteria with single polar flagellum from the family of Pelobacteraceae with one known species (Malonomonas rubra). Strains of Malonomonas have been isolated from anoxic sediments. the bacteria Malonomonas rubra bacteria metabolizes malonate.
CYP4F12 is expressed in the liver and throughout the gastrointestinal track, is known to metabolize the anti-histamine drugs, ebastine and terfenadine, and therefore is suggested to be positioned for and possibly involved in the processing of these and perhaps other drugs. When expressed in yeast the enzyme is capable of oxidizing arachidonic acid by adding a hydroxyl residue to carbons 18 or 19 to form 18-hydroxyeicosatetraenoic acid (18-HETE) or 19-HETE; however, its physiological function in doing so has not been determined. CYP4F12 also metabolizes prostaglandin H2 (PGH2) and PGH1 to their corresponding 19-hydroxyl analogs in a reaction that might serve to reduce their activities. In addition to these monooxygenase actions, CYP458 possesses epoxygenase activity: it metabolizes the omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid, (EPA) to their corresponding epoxides, the epoxydocosapentaenoic acids (EDPs) and epoxyeicosatetraenoic acids (EEQs), respectively. The enzyme metabolizes DHA primarily to 19R,20S-epoxyeicosapentaenoic acid and 19S,20R-epoxyeicosapentaenoic acid isomers (termed 19,20-EDP) and EPA primarily to 17R,18S-eicosatetraenic acid and 17S,18R-eicosatetraenic acid isomers (termed 17,18-EEQ).
Neutral endopeptidase (NEP) also known as neprilysin is the enzyme that metabolizes natriuretic peptides. Several inhibitors of NEP are currently being developed to treat disorders ranging from hypertension to heart failure. Most of them are dual inhibitors (NEP and ACE). In 2014, PARADIGM-HF study was published in NEJM.
Quinolinic acid (abbreviated QUIN or QA), also known as pyridine-2,3-dicarboxylic acid, is a dicarboxylic acid with a pyridine backbone. It is a colorless solid. It is the biosynthetic precursor to nicotine. Quinolinic acid is a downstream product of the kynurenine pathway, which metabolizes the amino acid tryptophan.
NQ01 metabolizes benzoquinone toward polyphenols (counteracting the effect of MPO). GSH is involved with the formation of phenylmercapturic acid. Genetic polymorphisms in these enzymes may induce loss of function or gain of function. For example, mutations in CYP2E1 increase activity and result in increased generation of toxic metabolites.
In turn, is metabolized from phenethylamine by phenylethanolamine N-methyltransferase, the same enzyme that metabolizes norepinephrine into epinephrine. Like amphetamine, both phenethylamine and regulate monoamine neurotransmission via ; unlike amphetamine, both of these substances are broken down by monoamine oxidase B, and therefore have a shorter half-life than amphetamine.
The METAP2 inhibitor beloranib (ZGN-433) has shown efficacy in reducing weight in severely obese subjects. MetAP2 inhibitors work by re-establishing balance to the ways the body metabolizes fat, leading to substantial loss of body weight. Development of beloranib was halted in 2016 after deaths during clinical trials.
In order to capture an edge in the North American market, Lagunitas released an IPA- inspired refreshment with zero alcohol, zero calories and zero carbohydrates called the Hoppy Refresher in 2019. Using a process called biotransformation, it takes the hops and yeast and metabolizes it into a sparkling beverage.
MAO-A is involved in the metabolism of tyramine; inhibition, in particular irreversible inhibition of MAO-A can result in a dangerous pressor effect when foods high in tyramine are consumed such as cheeses (informally known as the "cheese effect"). MAO-A is involved in the metabolism of serotonin, noradrenaline and dopamine whereas MAO-B metabolises the dopamine neurotransmitter. MAO-B is an enzyme on the outer mitochondrial membrane and catalyzes the oxidation of arylalkylamine neurotransmitters Monoamine oxidase A (MAOA) generally metabolizes tyramine, norepinephrine (NE), serotonin (5-HT), and dopamine (DA) (and other less clinically relevant chemicals). In contrast, monoamine oxidase B (MAOB) mainly metabolizes dopamine (DA) (and other less clinically relevant chemicals).
It metabolizes 1) arachidonic acid to its various epoxides, i.e., the epoxyeicosatrienoic acids (also termed EETs); 2) docosahexaenoic acid to its various epoxides, i.e. the epoxydocosapentaenoic acids (also termed EDPs); and 3) linoleic acid to its various epoxides, i.e. vernolic acid (also termed leukotoxin) and coronaric acid (also termed isoleukotoxin).
Once inside, it metabolizes the carbon dioxide produced by the embryo and provides it with oxygen as a result of photosynthesis. This is an example of symbiosis,Nature Trivia, Spotted Salamander at Henderson State University. Accessed 4 August 2008. and the only known example an intracellular endosymbiont microbe in vertebrates.
Tipiracil is a drug used in the treatment of cancer. It is approved for use in form of the combination drug trifluridine/tipiracil for the treatment of unresectable advanced or recurrent colorectal cancer. Tipiracil helps maintain the blood concentration of trifluridine by inhibiting the enzyme thymidine phosphorylase which metabolizes trifluridine.
Evidence for epigenetic modifications for bipolar disorder is unclear. One study found hypomethylation of a gene promoter of a prefrontal lobe enzyme (i.e., membrane-bound catechol-O-methyl transferase, or COMT) in post-mortem brain samples from individuals with bipolar disorder. COMT is an enzyme that metabolizes dopamine in the synapse.
ALOX12 is also distinguished from arachidonate 12-lipoxygenase, 12R type (ALOX12B), which metabolizes arachidonic acid to the R stereoisomer of 12(S)-HpETE viz., 12(R)-hydroperoxy-5Z,8Z,10E,14Z-icosatetraenoic acid (12(R)-HpETE), a product with very different pathophysiological roles than that of 12(S)-HpETE (see ALOX12B).
Levomethamphetamine is the active metabolite of the antiparkinson's drug selegiline. Selegiline, a selective monoamine oxidase B (MAOB) inhibitor at low doses,It is a selective MAOB inhibitor at normal clinical doses. MAOB is an enzyme that metabolizes dopamine, the neurotransmitter deficient in Parkinson's Syndrome. is also metabolized into levomethamphetamine and levoamphetamine.
High- viscous Dextran also has potential complications which can be physiological and mechanical. It may crystallize on instruments and obstruct the valves and channels. Coagulation abnormalities and adult respiratory distress syndrome (ARDS) have been reported. Glycine metabolizes into ammonia and can cross the blood brain barrier, causing agitation, vomiting and coma.
Mouse e-12LO metabolizes arachidonic acid predominantly to 12(S)-HETE and to a lesser extent 15(S)-HETE. Sub-human primates, although not extensively examined, appear to have 12-lipoxygenase expression patterns that resemble those of sub-primate mammals or humans depending on the closeness of there genetic relatedness to these species.
Cytochrome P4502C8 (abbreviated CYP2C8), a member of the cytochrome P450 mixed-function oxidase system, is involved in the metabolism of xenobiotics in the body. Cytochrome P4502C8 also possesses epoxygenase activity, i.e. it metabolizes long-chain polyunsaturated fatty acids, e.g. arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and Linoleic acid to their biologically active epoxides.
Trimipramine is a racemic compound with two enantiomers. CYP2C19 is responsible for the demethylation of (D)- and (L)-trimipramine to (D)- (L)-desmethyltrimipramine, respectively, and CYP2D6 is responsible for the 2-hydroxylation of (D)- and (L)-desmethyltrimipramine to (D)- and (L)-2-hydroxydesmethyltrimipramine, respectively. CYP2D6 also metabolizes (L)-trimipramine into (L)-2-hydroxytrimipramine.
Montvale, NJ: Medical Economics Company Inc; 1998:2563-5. These symptoms are often called the disulfiram-like reaction. The proposed mechanism of action for this interaction is that metronidazole can bind to an enzyme that normally metabolizes alcohol. Binding to this enzyme may impair the liver's ability to process alcohol for proper excretion.
Carbonyl reductase is one of several monomeric, NADPH-dependent oxidoreductases having wide specificity for carbonyl compounds. This enzyme is widely distributed in human tissues. Another carbonyl reductase gene, CBR3, lies close to this gene on chromosome 21q. CBR1 metabolizes many toxic environmental quinones and pharmacological relevant substrates such as the anticancer doxorubicin.
The developing salamander thus metabolizes the oxygen, producing carbon dioxide (which then the alga consumes). Photosynthetic algae are present within the somatic and possibly the germ cells of the salamander. When the eggs hatch depends on the water temperatures. Spotted Salamander (Ambystoma maculatum) Larva As larvae, they are usually light brown or greenish-yellow.
The God Eaters assemble a mass of Dreadnought cores and fire it into Arius Nova, thus crashing its defenses while it metabolizes the cores. They defeat Arius Nova and say their goodbyes to Shio. Shio's apparition returns to the real Shio, who is still on the moon, watching over and protecting humanity from afar.
Dr. Rosenthal’s first published paper provided a method for testing the health of the liver. He showed that the rate at which the liver metabolizes an ingested dye can be used to quantify how well this organ functions. His continued work on liver function tests resulted in the use of bromsulphthalein, which remains in use.
D. thesis 2007). See also Inhibition of Photosynthesis: Inhibition at Photosystem II §§ 1–4. Rice is relatively immune to propanil but most weeds are susceptible to it. The reason for the selectivity is that rice contains a high level of the enzyme aryl acylamidase (AAA), which rapidly metabolizes propanil to relatively nontoxic 3,4-dichloroaniline.
Vets and pet owners have reported the effect of nitenpyram on flea-infested pets starting within 30 minutes after administering the neonicotinoid. Nitenpyram has been reported to metabolize into 6-chloronicotinic acid. Nitenpyram in mice metabolizes into nitenpyram- COOH, nitenpyram-deschloropyridine, desmethyl-nitenpyram, nitenpyram-CN, and nitenpyram-deschloropyridine derivatives. The nitenpyram metabolites have not been through in-depth study.
Oxytocinase is a type of enzyme that metabolizes the endogenous neuropeptide, oxytocin. The most well-characterized oxytocinase is leucyl/cystinyl aminopeptidase, which is also an enkephalinase. Other oxytocinases are also known. During pregnancy, oxytocinase plays a role in balancing concentration of oxytocin by degrading the oxytocin produced by the fetus, as production of oxytocin increases with growth of fetus.
DHA can be metabolized into DHA-derived specialized pro-resolving mediators (SPMs), DHA epoxides, electrophilic oxo-derivatives (EFOX) of DHA, neuroprostanes, ethanolamines, acylglycerols, docosahexaenoyl amides of amino acids or neurotransmitters, and branched DHA esters of hydroxy fatty acids, among others. The enzyme CYP2C9 metabolizes DHA to epoxydocosapentaenoic acids (EDPs; primarily 19,20-epoxy-eicosapentaenoic acid isomers [i.e. 10,11-EDPs]).
Malondialdehyde results from lipid peroxidation of polyunsaturated fatty acids. It is a prominent product in thromboxane A2 synthesis wherein cyclooxygenase 1 or cycloxygenase 2 metabolizes arachidonic acid to prostaglandin H2 by platelets and a wide array of other cell types and tissues. This product is further metabolized by thromboxane synthase to thromboxane A2, 12-hydroxyheptadecatrienoic acid, and malonyldialdehyde.J. Biol. Chem.
Low nutrient abundance may have caused increased photosymbiosis—where one organism is capable of photosynthesis and the other metabolizes the waste product—among prokaryotes (bacteria and archaea), and the emergence of eukaryotes. Bacteria, Archaea, and Eukaryota are the three domains, the highest taxonomic ranking. Eukaryotes are distinguished from prokaryotes by a nucleus and membrane-bound organelles, and all multicellular organisms are eukaryotes.
The CYP2C19 enzyme metabolizes proton pump inhibitors (PPI) as well as clopidogrel. Various reports have stated that there is a negative clopidogrel-omeprazole drug interaction. Some studies have found that clopidogrel activity on platelets was hampered significantly by patients receiving treatment with omeprazole, a proton pump inhibitor (PPI). Another study also showed lansoprazole to have hampering effects on clopidogrel activity.
The ability to grow at is significant because medical equipment is exposed to this temperature for sterilization in an autoclave. Prior to the 2003 discovery of Strain 121, a fifteen-minute exposure to autoclave temperatures was believed to kill all living organisms. However, Strain 121 is non-infectious because it cannot grow at temperatures near . Strain 121 metabolizes by reducing iron oxide.
It metabolizes both glucose and sucrose. In addition to morphological typing, biochemical tests are commonly used to identify the species. P. canis is positive for catalase, oxidase, and ornithine decarboxylase, but negative for lysine decarboxylase, V-factor (nicotinamide adenine dinucleotide), D-mannitol, dulcitol, D-sorbitol, urease, maltose, and L-arabinose. It can also be indole positive or negative depending on the biotype.
In 2018, the FDA approved an enzyme substitute called pegvaliase which metabolizes phenylalanine. It is for adults who are poorly managed on other treatments. Tetrahydrobiopterin (BH4) (a cofactor for the oxidation of phenylalanine) when taken by mouth can reduce blood levels of this amino acid in some people. Most people, however, with the "classical" sequence of mutations, will have little or no benefit.
Phospholipase D metabolizes ethanol into phosphatidylethanol (PEtOH) in a process termed transphosphatidylation. Using fly genetics the PEtOH was shown to mediates alcohol's hyperactive response in fruit flies. And ethanol transphosphatidylation was shown to be up-regulated in alcoholics and the family members of alcoholic.s This ethanol transphosphatidylation mechanism recently emerged as an alternative theory for alcohol's effect on ion channels.
Water was once used routinely, however, problems with water intoxication and hemolysis discontinued its use by 1990. Each of these distention fluids is associated with unique physiological changes that should be considered when selecting a distention fluid. Glucose is contraindicated in patients with glucose intolerance. Sorbitol metabolizes to fructose in the liver and is contraindicated if a patient has fructose malabsorption.
Nicotine has a half-life of 1–2 hours. Cotinine is an active metabolite of nicotine that remains in the blood with a half-life of 18–20 hours, making it easier to analyze. Nicotine is metabolized in the liver by cytochrome P450 enzymes (mostly CYP2A6, and also by CYP2B6) and FMO3, which selectively metabolizes (S)-nicotine. A major metabolite is cotinine.
CYP2J2 localizes to the endoplasmic reticulum and is thought to be a prominent enzyme responsible for metabolizing endogenous polyunsaturated fatty acids to signaling molecules. It metabolizes arachidonic acid to the following eicosatrienoic acid epoxides (termed EETs): 5,6-epoxy-8Z,11Z,14Z-EET, 8,9-epoxy-8Z,11Z,14Z-EET, 11,12-epoxy-5Z,8Z,14Z-EET, and 14,15-epoxy-5Z,8Z,11Z-EET. CYP2J2 also metabolizes linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin); docosahexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs). CYP2J2, along with CYP219, CYP2C8, CYP2C9, and possibly CYP2S1 are the main producers of EETs and, very likely EEQs, EDPs, and the epoxides of linoleic acid.
Rasburicase (trade names Elitek in the US and Fasturtec in Europe) is a medication that helps to clear uric acid from the blood. It is a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin. Urate oxidase is known to be present in many mammals but does not naturally occur in humans. Rasburicase is produced by a genetically modified Saccharomyces cerevisiae strain.
While these metabolites may contribute to selegiline's ability to inhibit reuptake of the neurotransmitters dopamine and norepinephrine, they have also been associated with orthostatic hypotension and hallucinations in some people. Rasagiline metabolizes into 1(R)-aminoindan which has no amphetamine-like characteristics and has neuroprotective properties in cells and in animal models. It is selective for MAO type B over type A by a factor of fourteen.
It was approved again on November 7, 1997, as Fortovase, a soft gel capsule reformulated for improved bioavailability. Roche announced in May 2005 that, given reduced demand, Fortovase would cease being marketed early in 2006, in favor of Invirase boosted with ritonavir,Withdrawal of Fortovase (PDF) owing to the ability of the latter co-formulated drug to inhibit the enzyme that metabolizes the AIDS drugs.
Baicalein is an inhibitor of CYP2C9, an enzyme of the cytochrome P450 system that metabolizes drugs in the body. A derivative of baicalin is a known prolyl endopeptidase inhibitor. Baicalein has been shown to inhibit Staphylococcus aureus biofilm formation and the quorum sensing system in vitro. It has also been shown to be effective in vitro against all forms of Borrelia burgdorferi and Borrelia garinii.
There is currently very little known about the mechanism of lycorine. There are tentative ideas about how lycorine metabolizes due to a study done on beagle dogs. Lycorine inhibits protein synthesis, and may inhibit ascorbic acid biosynthesis, although studies on the latter are controversial and inconclusive. Presently, it serves some interest in the study of certain yeasts, the principal organism on which lycorine is tested.
His work was published in the Journal of Biological Chemistry.Keeney D.S., Skinner C., Wei S., Friedberg T., Waterman M.R. (1998). A keratinocyte-specific epoxygenase, CYP2B12, metabolizes arachidonic acid with unusual selectivity producing a single major epoxyeicosatrienoic acid. J. Biol. Chem. 273 15:9279-9284 From 1996 to 1997 Skinner took care of his infant son, James, whilst his wife continued to work at Vanderbilt University Medical Center.
"Ambulatory detoxification of patients with alcohol dependence". Am Fam Physician 71 (3): 495–502. Some other commonly used drugs on the market include: ;Disulfiram :Disulfiram (trade name Antabuse) creates a sudden acute response to ethanol consumption by inhibiting an enzyme that metabolizes ethanol. In the liver, ethanol is metabolized by alcohol dehydrogenease to produce acetaladehye which is then metabolized by acetaldehyde dehydrogenease to produce acetic acid.
Once pathogens attach to host cells, they can cause direct damage as the pathogens use the host cell for nutrients and produce waste products. For example, Streptococcus mutans, a component of dental plaque, metabolizes dietary sugar and produces acid as a waste product. The acid decalcifies the tooth surface to cause dental caries. However, toxins produced by bacteria cause most of the direct damage to host cells.
Diauxie is a Greek word coined by Jacques Monod to mean two growth phases. The word is used in English in cell biology to describe the growth phases of a microorganism in batch culture as it metabolizes a mixture of two sugars. Rather than metabolizing the two available sugars simultaneously, microbial cells commonly consume them in a sequential pattern, resulting in two separate growth phases.
Another member of this family, CYP4F3, is approximately 18 kb away. In addition to seminal vesicles, CYP4F8 is expressed in kidney, prostate, epidermis, and corneal epithelium, and its mRNA has been found in retina; CYP4F8 is also greatly up-regulated in psoriatic skin. In addition to its ability to metabolize and presumably thereby to inactivate or reduce the activity of PGH2 and PGH1, CYP4F8 adds hydroxyl residues to carbons 18 and 19 of arachidonic acid and Dihomo-γ-linolenic acid, CYP458 possesses epoxygenase activity in that it metabolizes the omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid, (EPA) to their corresponding epoxides, the epoxydocosapentaenoic acids (EDPs) and epoxyeicosatetraenoic acids (EEQs), respectively. The enzyme metabolizes DHA primarily to 19R,20S-epoxyeicosapentaenoic acid and 19S,20R-epoxyeicosapentaenoic acid isomers (termed 19,20-EDP) and EPA primarily to 17R,18S-eicosatetraenic acid and 17S,18R-eicosatetraenic acid isomers (termed 17,18-EEQ).
Stubbe has published over 300 scientific papers and has been frequently recognized for her research achievements. Before Stubbe's work, there were no chemical mechanisms that could be written for certain enzymes. She revolutionized the biochemistry field with her first two scientific papers on enzymes enolase and pyruvate kinase. Her first two publications in scientific journals showed the mechanisms for reactions that involved the enzymes enolase that metabolizes carbohydrates, and pyruvate kinase.
Struvite stones are composed of a combination of magnesium ammonium phosphate (struvite) and calcium carbonate-apatite. Struvite stone formation can be sustained only when ammonia production is increased and the urine pH is elevated to decrease the solubility of phosphate. Both of these requirements can occur only when urine is infected with a urease-producing organism such as Proteus. Urease metabolizes urea into ammonia and carbon dioxide: urea 2 NH3 \+ CO2.
In humans, naringinase is found in the liver and rapidly metabolizes naringin into naringenin. This happens in two steps- first, naringin is hydrolyzed by α-L-rhamnosidase activity of naringinase to rhamnose and prunin. The prunin formed is then hydrolyzed by β-d-glucosidase activity of naringinase into naringenin and glucose. Naringinase is an enzyme that has a wide occurrence in nature and can be found in plants, yeasts, and fungi.
An estimated 17 million United States citizens have vasomotor rhinitis. Drinking alcohol may cause rhinitis as well as worsen asthma (see alcohol-induced respiratory reactions). In certain populations, particularly those of East Asian countries such as Japan, these reactions have a nonallergic basis. In other populations, particularly those of European descent, a genetic variant in the gene that metabolizes ethanol to acetaldehyde, ADH1B, is associated with alcohol-induced rhinitis.
Like other azapirones, gepirone acts as a selective partial agonist of the 5-HT1A receptor. Unlike its relative buspirone however, gepirone has greater efficacy in activating the 5-HT1A and has negligible affinity for the D2 receptor (30- to 50-fold lower in comparison to buspirone). However, similarly to buspirone, gepirone metabolizes into 1-(2-pyrimidinyl)piperazine, which is known to act as a potent antagonist of the α2-adrenergic receptor.
As oxygen metabolizes in the body, potentially harmful reactive oxygen species (ROS) are created. The human body implements an antioxidant defense system to protect against ROS. In the event that these defenses are overpowered by the ROS, cell damage results (which is a major cause of aging in the body). Superoxide dismutase (SOD) helps to slow the creation of ROS, ultimately playing a key role in the defense against cell damage.
Regulators, researchers, and bioethicists generally agree that clinical trials should include pregnant women. Because pregnancy changes the way the body metabolizes drugs, it is otherwise difficult to predict how drugs tested in non-pregnant adults will affect pregnant women. In order to treat illness in pregnant women, clinical research must involve them. Several projects and coalitions have formed to promote the inclusion of pregnant women in clinical research.
Retinoic acid (RA) is an important factor that causes differentiation of primordial germ cells. In males, the mesonephros releases retinoic acid. RA then goes to the gonad causing an enzyme called CYP26B1 to be released by sertoli cells. CYP26B1 metabolizes RA, and because sertoli cells surround primordial germ cells (PGCs), PGCs never come into contact with RA, which results in a lack of proliferation of PGCs and no meiotic entry.
A 15-lipoxygenase (i.e. ALOX15 or ALOX15B) metabolizes arachidonic acid to 15(S)-HpETE (see 15-Hydroxyicosatetraenoic acid); 15(S)-HpETE is then converted to its 14,15-trans-epoxide, 14,15-trans-epoxide oxido-5Z,8Z,10E,13E-eicosatetraenoic acid (i.e., Eoxin A4 (also termed EXA4) by one of the 15-lipoxygenases. 15-(S)-HpETE is then metabolized to 14(R)-glutothionyl-15(S)hydroxy-5Z,8Z,10E,13E-eicosatetraenoic acid (i.e.
Fosamprenavir (marketed by ViiV Healthcare as the calcium salt under the trade names Lexiva in the U.S. and Telzir in Europe) is a drug for the treatment of HIV infections. It is a pro-drug of the protease inhibitor and antiretroviral drug amprenavir. The FDA approved it October 20, 2003, while the EMA approved it on July 12, 2004. The human body metabolizes fosamprenavir in order to form amprenavir, which is the active ingredient.
Carbon dioxide is a by-product of the fermentation of sugar in the brewing of beer, whisky and other alcoholic beverages and in the production of bioethanol. Yeast metabolizes sugar to produce and ethanol, also known as alcohol, as follows: : → 2 + 2 All aerobic organisms produce when they oxidize carbohydrates, fatty acids, and proteins. The large number of reactions involved are exceedingly complex and not described easily. Refer to (cellular respiration, anaerobic respiration and photosynthesis).
The method usually employed is a dose of slow-acting insulin twice daily to keep the blood sugar within a recommended range for the entire day. With this method, it is important for the cat to avoid large meals or high-carbohydrate food. Meals may also be timed to coincide with peak insulin activity. Once- daily doses are not recommended, since insulin usually metabolizes faster in cats than in humans or dogs.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and the hydroxylation of fatty acids and fatty acid metabolites. CYP2U1 metabolized arachidonic acid, docosahexaenoic acid (DHA), and other long chain fatty acids which suggests that CYP2U1 may play a role in brain and immune functions. CYP2U1 also metabolizes propanone, acetone, and 2-oxypropane.
Figure 1 – Mechanism of action. A hypothetical model for the agonist activation of 5-HT2C receptor. Activation leads to accumulation of inositol phosphate and increase in intracellular Ca2+. Receptor activation also stimulates the ERK pathway and RhoA/PLD pathway. The 5-HT2C receptors are G protein–coupled receptors that are coupled to phospholipase C (PLC) via Gαq, phospholipase A2 (PLA2), and possibly Gα13. PLC metabolizes phosphatidylinositol 4,5-bisphosphate into inositol 1,4,5-triphosphate (IP3).
The mechanism behind this welcome observation was not directly known, but later it was determined that ritonavir inhibits the cytochrome P450 3A4 isozyme. Normally, this enzyme metabolizes saquinavir to an inactive form, but with the ritonavir inhibiting this enzyme, the saquinavir blood plasma levels increased considerably. Additionally, ritonavir also inhibits multidrug transporters, although to a much lower extent. Unlike other protease inhibitors, the absorption of saquinavir seems to be improved by omeprazole.
A non-curative treatment for patients with ADA-SCID is enzyme replacement therapy, in which the patient is injected with polyethyleneglycol- coupled adenosine deaminase (PEG-ADA) which metabolizes the toxic substrates of the ADA enzyme and prevents their accumulation. Treatment with PEG-ADA may be used to restore T cell function in the short term, enough to clear any existing infections before proceeding with curative treatment such as a bone marrow transplant.
The role of malate synthase in the glyoxylate cycle. The citric acid cycle (also known as the tricarboxylic acid cycle or the Krebs cycle) is used by aerobic organisms to produce energy via the oxidation of acetyl-CoA, which is derived from pyruvate (a product of glycolysis). The citric acid cycle accepts acetyl-CoA and metabolizes it to form carbon dioxide. A related cycle, called the glyoxylate cycle, is found in many bacteria and plants.
In 1912 Felix Ehrlich demonstrated that yeast metabolizes the natural amino acids essentially by splitting off carbon dioxide and replacing the amino group with a hydroxyl group. By this reaction, tryptophan gives rise to tryptophol. Tryptophan affects brain serotonin synthesis when given orally in a purified form and is used to modify serotonin levels for research. Low brain serotonin level is induced by administration of tryptophan-poor protein in a technique called acute tryptophan depletion.
An offshoot of the monoamine hypothesis suggests that monoamine oxidase A (MAO-A), an enzyme which metabolizes monoamines, may be overly active in depressed people. This would, in turn, cause the lowered levels of monoamines. This hypothesis received support from a PET study, which found significantly elevated activity of MAO-A in the brain of some depressed people. In genetic studies, the alterations of MAO-A-related genes have not been consistently associated with depression.
The developing fetus is exposed to the alcohol through the placenta and umbilical cord. Alcohol metabolizes slowly in the fetus and remains for a long time when compared to an adult because of re- uptake of alcohol-containing amniotic fluid. Alcohol exposure has serious implications on the developing fetus as well as the mother. When a woman is planning for pregnancy, she should keep in mind that there is no safe limit for alcohol consumption.
Myristicin is soluble in ethanol and acetone, but insoluble in water Myristicin is additionally known to be a weak inhibitor of monoamine oxidase (MAO), a liver enzyme in humans that metabolizes neurotransmitters (e.g., serotonin, dopamine, epinephrine, and norepinephrine). It lacks the basic nitrogen atom that is typical of MAO inhibitors (MAOIs), potentially explaining a weaker inhibitory effect. While smaller concentrations of MAOIs may not cause problems, there are additional warnings regarding drug interactions.
The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and its expression is induced by glucocorticoids and some pharmacological agents. The enzyme metabolizes drugs such as nifedipine and cyclosporine as well as the steroid hormones testosterone, progesterone and androstenedione. This gene is part of a cluster of cytochrome P450 genes on chromosome 7q21.1.
AmpliChip CYP450 Test is a clinical test from Roche. The test aims to find the specific gene types (a genotype) of the patient that will determine how he or she metabolizes certain medicines, therefore guides the doctors to prescribe medicine for best effectiveness and least side effects. The AmpliChip CYP450 Test uses micro array technology from Affymetrix (GeneChip) to determine the genotype of the patient in terms of two cytochrome P450 enzymes: 2D6 and 2C19.
Antidepressants reduce symptoms of mood disorders primarily through the regulation of norepinephrine and serotonin (particularly the 5-HT receptors). After chronic use, neurons adapt to the change in biochemistry, resulting in a change in pre- and postsynaptic receptor density and second messenger function. Monoamine oxidase inhibitors (MAOIs) are the oldest class of antidepressants. They inhibit monoamine oxidase, the enzyme that metabolizes the monoamine neurotransmitters in the presynaptic terminals that are not contained in protective synaptic vesicles.
The diols thereby formed are usually not toxic or far less toxic than their epoxide predecessors, are readily further metabolized, and ultimately excreted in the urine. mEH also metabolizes certain epoxides of polyunsaturated fatty acids such as the epoxyeicosatrienoic acids (EETs) but its activity in doing this is far less than that of sEH; mEH therefore may play a minor role, compared to sEH, in limiting the bioactivity of these cell signaling compounds (see microsomal epoxide hydrolase).
Sorbitol (), less commonly known as glucitol (), is a sugar alcohol with a sweet taste which the human body metabolizes slowly. It can be obtained by reduction of glucose, which changes the converted aldehyde group (−CHO) to a primary alcohol group (−C(OH)H2). Most sorbitol is made from potato starch, but it is also found in nature, for example in apples, pears, peaches, and prunes. It is converted to fructose by sorbitol-6-phosphate 2-dehydrogenase.
The fructophilic behaviour is well known in Z. bailii. Unlike most of other yeasts, Z. bailii metabolizes fructose more rapidly than glucose and grows much faster in foods containing ≥ 1% (w/w) of fructose. In addition, it has been observed that the alcoholic fermentation under aerobic conditions (the Crabtree effect) in Z. bailii is influenced by the carbon source, i.e. ethanol is produced at a higher rate and with a higher yield on fructose than on glucose.
Sesamin, the major lignan found in sesame, inhibits CYP4A11, which leads to decrease of plasma and urinary levels of 20-HETE. A study have found that sesamin inhibits human renal and liver microsome 20-HETE synthesis. CYP4A11 also has epoxygenase activity in that it metabolizes docosahexaenoic acid to epoxydocosapentaenoic acids (EDPs; primarily 19,20-epoxy-eicosapentaenoic acid isomers [i.e. 19,20-EDPs]) and eicosapentaenoic acid to epoxyeicosatetraenoic acids (EEQs, primarily 17,18-EEQ isomers). CYP4A11 does not convert arachidonic acid to epoxides.
Sertoli cells secrete anti-mullerian hormone, which causes the paramesonephric duct to regress. The development and maintenance of the seminal vesicles, as well as their secretion and size/weight, are highly dependent on androgens. The seminal vesicles contain 5α-reductase, which metabolizes testosterone into its much more potent metabolite, dihydrotestosterone (DHT). The seminal vesicles have also been found to contain luteinizing hormone receptors, and hence may also be regulated by the ligand of this receptor, luteinizing hormone.
Due to the presence of these metabolites, people taking selegiline may test positive for "amphetamine" or "methamphetamine" on drug screening tests. While the amphetamine metabolites may contribute to selegiline's ability to inhibit reuptake of the neurotransmitters dopamine and norepinephrine, they have also been associated with orthostatic hypotension and hallucinations. The amphetamine metabolites are hydroxylated and, in phase II, conjugated by glucuronyltransferase. A newer anti-Parkinson MAO-B inhibitor, rasagiline, metabolizes into 1(R)-aminoindan, which has no amphetamine-like characteristics.
When the liver rapidly metabolizes fatty acids into acetyl-CoA, some acetyl-CoA molecules can then be converted into ketone bodies: acetoacetate, beta-hydroxybutyrate, and acetone. These ketone bodies can function as an energy source as well as signalling molecules. The liver itself cannot utilize these molecules for energy, so the ketone bodies are released into the blood for use by peripheral tissues including the brain. When ketosis is induced by carbohydrate restriction, it is sometimes referred to as nutritional ketosis.
The original 1983 Official Handbook of the Marvel Universe volume stated that Cyclops' eyes contain inter- dimensional apertures, releasing powerful energies from another dimension into his own via the beams. This account states that his body naturally metabolizes ambient energy that is used to open and focus the apertures in his eyes. The energy of the beam itself originates from this other dimension. This explanation, however, was later changed for the 1986 Official Handbook of the Marvel Universe Deluxe Edition.
They are involved in hundreds of different biochemical pathways throughout biology, and are integral to some of life's most important processes. Transferases are involved in myriad reactions in the cell. Three examples of these reactions are the activity of coenzyme A (CoA) transferase, which transfers thiol esters, the action of N-acetyltransferase, which is part of the pathway that metabolizes tryptophan, and the regulation of pyruvate dehydrogenase (PDH), which converts pyruvate to acetyl CoA. Transferases are also utilized during translation.
Ingestion of codeine or food containing poppy seeds can cause false positives. A 1999 review estimated that relatively low doses of heroin (which metabolizes immediately into morphine) are detectable by standard urine tests for 1–1.5 days after use. A 2009 review determined that, when the analyte is morphine and the limit of detection is 1ng/ml, a 20mg intravenous (IV) dose of morphine is detectable for 12–24 hours. A limit of detection of 0.6ng/ml had similar results.
5-Hydroxyeicosanoid dehydrogenase (5-HEDH) or more formally, nicotinamide adenine dinucleotide phosphate (NADP+)-dependent dehydrogenase, is an enzyme that metabolizes an eicosanoid product of arachidonate 5-lipoxygenase (5-LOX), 5(S)-hydroxy-6S,8Z,11Z,14Z-eicosatetraenoic acid (i.e. 5-(S)-HETE; see 5-HETE) to its 5-keto analog, 5-oxo-eicosatetraenoic acid (i.e. 5-oxo-6S,8Z,11Z,14Z-eicosatetraenoic acid or 5-oxo-ETE). It also acts in the reverse direction, metabolizing 5-oxo-ETE to 5(S)-HETE.
Cytochrome P450 oxidoreductase deficiency (PORD) is a rare disease and inborn error of metabolism caused by deficiency of cytochrome P450 oxidoreductase (POR). POR is a 2-flavin protein that is responsible for the transfer of electrons from NADPH to all 50 microsomal cytochrome P450 (CYP450) enzymes. This includes the steroidogenic enzymes CYP17A1 (17α-hydroxylase/17,20-lyase), CYP19A1 (aromatase), and CYP21A2 (21-hydroxylase); CYP26B1 (metabolizes retinoic acid); and the hepatic drug-metabolizing CYP450 enzymes (e.g., CYP3A4), among many other CYP450 enzymes.
The reaction catalyzed by methionine synthase (click to enlarge) Methionine synthase catalyzes the final step in the regeneration of methionine(Met) from homocysteine(Hcy). The overall reaction transforms 5-methyltetrahydrofolate(N5-MeTHF) into tetrahydrofolate (THF) while transferring a methyl group to Homocysteine to form Methionine. Methionine synthase is the only mammalian enzyme that metabolizes N5-MeTHF to regenerate the active cofactor THF. In cobalamin-dependent forms of the enzyme, the reaction proceeds by two steps in a ping-pong reaction.
The major CysLTs viz., LTC4, LTD4, and LTE4, are metabolites of arachidonic acid made by the 5-lipoxygenase enzyme, ALOX5, mainly by cells involved in regulating inflammation, allergy, and other immune responses such as neutrophils, eosinophils, basophils, monocytes, macrophages, mast cells, dendritic cells, and B-lymphocytes. ALOX5 metabolizes arachidonic acid to the 5,6-epoxide precursor, LTA4, which is then acted on by LTC4 synthase which attaches the γ-glutamyl-cysteinyl-glycine tripeptide (i.e. glutathione) to carbon 6 of the intermediate thereby forming LTC4 synthase.
Extracts and other preparations of E. arvense have served as herbal remedies, with records dating over centuries. In 2009, the European Food Safety Authority concluded there was no evidence for the supposed health effects of E. arvense, such as for invigoration, weight control, skincare, hair health or bone health. , there is insufficient scientific evidence for its effectiveness as a medicine to treat any human condition. E. arvense contains thiaminase, which metabolizes the B vitamin, thiamine, potentially causing thiamine deficiency and associated liver damage, if taken chronically.
9-HODE esterified to the sn-2 position of phosphatidylserine is subject to be released as free 9-HODE by the action of cytosol (see phospholipase A2 section on cPLA2) and therefore may serve as a storage pool that is mobilized by cell stimulation. 9-HODE may be further metabolized to 9-oxo-10(E),12(Z)-octadecadienoic acid (9-oxoODE or 9-oxo-ODE), possibly by the same hydroxy-fatty-acid dehydrogenase which metabolizes other hydroxy fatty acids, such as 13-HODE, to their oxo derivatives.
Regorafenib and at least one of its analogs, sorafenib, are potent inhibitors of Soluble epoxide hydrolase (sEH). sEH metabolizes, and in general thereby inactivates, epoxyeicosatrienoic acids (EETs), epoxydocosapentaenoic acids (EDPs), epoxyeicosatetraenoic acids (EEQs), and other epoxy polyunsaturated fatty acids that are made by various cytochrome P450 epoxygenases. EETs, EDPs, and EEQs have various effects in animals including vasodilation, anti-hypertensive, and anti-blood-clotting actions. However, EDPs, unlike EETs, inhibit the vascularization, growth, and metastasis of human cancer cells in vitro and in animal models.
CYP4Z1 is overexpressed in breast cancer cells. It has also been demonstrated that the expression of the CYP4Z1 gene is upregulated by activated glucocorticoid and progesterone receptors. The overexpression of CYP4Z1 is associated with the breast cancer cells' increased production of 20-Hydroxyeicosatetraenoic acid (20-HETE); it is hypothesized that CYP4Z1 metabolizes arachidonic acid to 20-HETE and that this overproduction is responsible for increasing the growth and spread of breast cancer cells in human breast cancer. CPZ4Z1 is likewise overexpressed in ovarian cancer cells.
Oxymorphone, sold under the brand names Numorphan and Opana among others, is an opioid pain medication. Pain relief after injection begins after about 5–10 minutes, after oral administration it begins after about 30 minutes, and lasts about 3–4 hours for immediate-release tablets and 12 hours for extended- release tablets. The elimination half-life of oxymorphone is much faster intravenously, and as such, the drug is most commonly used orally. Like oxycodone, which metabolizes to oxymorphone, oxymorphone has a high potential to be abused.
Entacapone is a selective and reversible inhibitor of catechol-O-methyltransferase (COMT). COMT eliminates biologically active catechols present in catecholamines (dopamine, norepinephrine, and epinephrine) and their hydroxylated metabolites. When administered with a decarboxylase inhibitor, COMT acts as the major metabolizing enzyme for levodopa and metabolizes it to 3-methoxy-4-hydroxy-L- phenylalanine (3-OMD) in the brain and in the periphery. For the treatment of Parkinson's disease, entacapone is given as an adjunct to levodopa and an aromatic amino acid decarboxylase inhibitor, carbidopa.
4-Hydroxynonenal (4HNE)—which ALDH3A1 metabolizes with Vmax of 27,754 moles NADPH/min•mg and an apparent Km of 362 micromolar —is the most abundant aldehyde produced in the LPO of arachidonic acid and linoleic acid. Its stability and multiple sites of reactivity (carbon-carbon double bond, hydroxyl group, and carbonyl) make 4HNE a potent inhibitor of cellular growth, enzyme activities, calcium sequestration, and protein synthesis. It is also involved in the consumption of glutathione and the alteration of signal transduction and gene expression.
The metabolism of glucose and insulin are also influenced. However, recent studies showed no significant correlation between hangover severity and the concentrations of various hormones, electrolytes, free fatty acids, triglycerides, lactate, ketone bodies, cortisol, and glucose in blood and urine samples. Alcohol also induces the CYP2E1 enzyme, which metabolizes ethanol and other substances into more reactive toxins. In particular, in binge drinking the enzyme is activated and plays a role in creating a harmful condition known as oxidative stress which can lead to cell death.
The triple quadrupole mass spectrometer allows for increased sensitivity and specificity yielding lower detection and quantitation limits. For these reasons, employment of the TQMS is a vital asset in the fields of drug metabolism, pharmacokinetics, environmental studies, and biological analyses. In most drug and pharmacokinetic studies, animals like rats, are subjected to a new drug in order to probe how the substance metabolizes in the body. By analyzing the rat’s urine or plasma with a triple quadrupole coupled to liquid chromatography, the concentration and fragmentation pattern of the new drug can be determined.
It metabolizes a number of substances and can release metabolic products into maternal or fetal circulations. The placenta is expelled from the body upon birth of the fetus. Mammal placentas probably first evolved about 150 million to 200 million years ago. The protein syncytin, which makes up the physical barrier between mother and baby in the syncytiotrophoblast, has a certain RNA signature in its genome that has led to the hypothesis that it originated from an ancient retrovirus: essentially a "good" virus that helped pave the transition from egg-laying to live-birth.
Activation of a wide range of serotonin receptors by serotonin itself or by certain prokinetic drugs results in enhanced gastrointestinal motility. Other prokinetic drugs may increase acetylcholine concentrations by stimulating the M1 receptor which causes acetylcholine release, or by inhibiting the enzyme acetylcholinesterase which metabolizes acetylcholine. Higher acetylcholine levels increase gastrointestinal peristalsis and further increase pressure on the lower esophageal sphincter, thereby stimulating gastrointestinal motility, accelerating gastric emptying, and improving gastro-duodenal coordination. The 5-HT4 receptor is thought to play a significant role in both the physiology and pathophysiology of GI tract motility.
Against other Marvel characters, Cyclops has been able to use his optic beam to knock Thor's Hammer from his hand.Uncanny X-Men #9 He is known to be able to overload Bishop's energy absorption power and is revealed to never have willingly used more than a small fraction of his full potential due to his anxiety regarding his optic blast. Early accounts describe Cyclops' optic beams as the product of his body metabolizing sunlight and other ambient energy.Uncanny X-Men #43 This is similar to his brother Alex (alias Havok) who metabolizes cosmic radiation.
It removes old red blood cells and holds a reserve of blood, which can be valuable in case of hemorrhagic shock, and also recycles iron. As a part of the mononuclear phagocyte system, it metabolizes hemoglobin removed from senescent red blood cells (erythrocytes). The globin portion of hemoglobin is degraded to its constitutive amino acids, and the heme portion is metabolized to bilirubin, which is removed in the liver. The spleen synthesizes antibodies in its white pulp and removes antibody-coated bacteria and antibody-coated blood cells by way of blood and lymph node circulation.
Insulinoma, a type of cancer of the islet cells of the pancreas, is the most common form of cancer in ferrets. It is most common in ferrets between the ages of 4 and 5 years but may also occur in younger ferrets. The growth of cancerous nodules on the lobes of the pancreas sometimes, but not always, leads to an increase in the production of insulin, which regulates the rate at which the ferret's body metabolizes blood glucose. Too much insulin causes blood sugar to drop, resulting in lethargy, seizures, and ultimately death.
Oxidative/fermentation glucose test (OF glucose test) is a biological technique utilized in microbiology to determine the way a microorganism metabolizes a carbohydrate such as glucose (dextrose). OF-glucose deeps contain glucose as a carbohydrate, peptones, bromothymol blue indicator for Hugh-Leifson's OF medium or phenol red for King's OF medium, and 0.5% agar. To perform the OF-glucose test, two tubes of OF-glucose medium are inoculated with the test organism. A layer of mineral oil is added to the top of the deep in one of the tubes to create anaerobic conditions.
A significant amount of research has been done on the metabolism of Thermoproteus and other hyperthermophiles as well. Thermoproteus metabolizes autotrophically through sulfur reduction, but it grows much faster by sulfur respiration in cultivation. In T. tenax, a number of metabolic pathways allow the cell to select a mode of metabolism depending on the energy requirements of the cell (depending, for example, on the cell's developmental or growth stage). Like all archaea, Thermoproteus possesses unique membrane lipids, which are ether-linked glycerol derivatives of 20 or 40 carbon branched lipids.
Symptoms typically occur between thirty minutes and four hours after ingestion and include nausea and vomiting, abdominal pain, numbness, headache, sweating, muscle weakness, bradycardia, hypotension, cardiac arrhythmia, and seizures. Treatment for poisoning includes gastrointestinal decontamination with activated charcoal followed by supportive care including antiemetics for persistent nausea and vomiting, along with atropine for treatment of bradycardia and fluid replacement and vasopressors for the treatment of hypotension. The toxins are only produced during active growth. In the winter months, the plant degrades and metabolizes most of its toxic alkaloids.
His research at NCI centered on working out how the body metabolizes environmental carcinogens, such as one of the most common in our environment, benzopyrene, which occurs in tobacco smoke, auto exhaust, and other smoke-producing sources. His laboratory identified the genes for the many cytochrome P-450 enzymes that detoxify various environmental carcinogens. These enzymes break down hazardous chemicals into molecules that can be safely excreted by the kidney. He developed the foundation for a genetic profile that could screen individuals for susceptibility to certain carcinogens, foods, and drugs.
Variation in potency of certain effects may exist amongst individual benzodiazepines. Some benzodiazepines produce active metabolites. Active metabolites are produced when a person's body metabolizes the drug into compounds that share a similar pharmacological profile to the parent compound and thus are relevant when calculating how long the pharmacological effects of a drug will last. Long- acting benzodiazepines with long-acting active metabolites, such as diazepam and chlordiazepoxide, are often prescribed for benzodiazepine or alcohol withdrawal as well as for anxiety if constant dose levels are required throughout the day.
Ethylphenidate metabolizes into methylphenidate and ritalinic acid. Tiny amounts of ethylphenidate can be formed in vivo when alcohol (also known formally as ethanol) and methylphenidate are coingested, via hepatic transesterification. Ethylphenidate formation appears to be more common when large quantities of methylphenidate and alcohol are consumed at the same time, such as in non- medical use or overdose scenarios. However, the transesterfication process of methylphenidate to ethylphenidate, as tested in mice liver, was dominant in the inactive (−)-enantiomer but showed a prolonged and increased maximal plasma concentration of the active (+)-enantiomer of methylphenidate.
Recent studies have shown that Soluble epoxide hydrolase (i.e. epoxide hydrolase 2 or EH2) readily metabolizes a) hepoxilin A3 (8-hydroxy-11S,12Sepoxy-(5Z,8Z,14Z)-eicosatrienoic acid) to trioxilin A3 (8,11,12-trihydroxy-(5Z,9E,14Z)-eicosatrienoic acid) and b) hepoxilin B3 (10-hydroxy-11S,12Sepoxy-(5Z,9E,14Z)-eicosatrienoic acid) to trioxlin B3 (10,11,12-trihydroxy-(5Z,9E,14Z)-eicosatrienoic acid. Soluble epoxide hydrolase (i.e. epoxide hydrolase 2 or EH2) sEH also appears to be the hepoxilin hydrolase that is responsible for inactivating the epoxyalcohol metabolites of arachidonic acid, hepoxilin A3 and hepoxiin B3.
Heart muscle primarily metabolizes fat for energy and Acyl-CoA metabolism has been identified as a critical molecule in early stage heart muscle pump failure. Cellular acyl-CoA content correlates with insulin resistance, suggesting that it can mediate lipotoxicity in non-adipose tissues. Acyl-CoA: diacylglycerol acyltransferase (DGAT) plays an important role in energy metabolism on account of key enzyme in triglyceride biosynthesis. The synthetic role of DGAT in adipose tissue such as the liver and the intestine, sites where endogenous levels of its activity and triglyceride synthesis are high and comparatively clear.
The population designated Ara-3 (center) is more turbid because that population evolved to use the citrate present in the growth medium. E. coli is normally unable to grow aerobically on citrate due to the inability to express a citrate transporter when oxygen is present. However, E. coli has a complete citric acid cycle, and therefore metabolizes citrate as an intermediate during aerobic growth on other substances, including glucose. Most E. coli can grow anaerobically on citrate via fermentation, if a co-substrate such as glucose is available to provide reducing power.
In 2006, Fiona Apple covered the song, accompanied by Elvis Costello, as a VH1 tribute to Costello. Gavin Edwards of Rolling Stone said of the performance, "[Apple] metabolizes every molecule of the song’s poisoned atmosphere." Costello also collaborated with hip hop band the Roots to perform a version of "I Want You" in 2013; Questlove said that the song "is pretty much the soundtrack to every relationship I've ever had". In 2010, Steven Page released a cover of the song recorded with the Art of Time Ensemble for his second solo album, A Singer Must Die.
All-trans-retinoic acid can be produced in the body by two sequential oxidation steps that convert all-trans-retinol to retinaldehyde to all-trans- retinoic acid, but once produced it cannot be reduced again to all-trans- retinol. The enzymes that generate retinoic acid for regulation of gene expression include retinol dehydrogenase (Rdh10) that metabolizes retinol to retinaldehyde, and three types of retinaldehyde dehydrogenase, i.e. RALDH1 (ALDH1A1), RALDH2 (ALDH1A2), and RALDH3 (ALDH1A3) that metabolize retinaldehyde to retinoic acid. Enzymes that metabolize excess all-trans- retinol to prevent toxicity include alcohol dehydrogenase and cytochrome P450(cyp26).
According to a 2016 study, bacteria (mainly Propionibacterium and Staphylococcus) are more important to dandruff formation than fungi. Bacterial presence was in turn influenced by water and sebum amount. Older literature cites the fungus Malassezia furfur (previously known as Pityrosporum ovale) as the cause of dandruff. While this species does occur naturally on the skin surface of people both with and without dandruff, in 2007 it was discovered that the responsible agent is a scalp specific fungus, Malassezia globosa, that metabolizes triglycerides present in sebum by the expression of lipase, resulting in a lipid byproduct oleic acid.
A functional single- nucleotide polymorphism (a common normal variant) of the gene for catechol-O- methyltransferase results in a valine to methionine mutation at position 158 (Val158Met) rs4680. In vitro, the homozygous Val variant metabolizes dopamine at up to four times the rate of its methionine counterpart. However, in vivo the Met variant is overexpressed in the brain, resulting in a 40% decrease (rather than 75% decrease) in functional enzyme activity. The lower rates of catabolism for the Met allele results in higher synaptic dopamine levels following neurotransmitter release, ultimately increasing dopaminergic stimulation of the postsynaptic neuron.
Atheroma) plaques as well as inflamed tonsils. CYP2S1 is expressed in macrophages, liver, lung, intestine, and spleen; is abundant in human and mouse atherosclerosis (i.e. Atheroma) plaques as well as inflamed tonsils; and, in addition to forming epoxides of arachidonic acid (and other polyunsaturated fatty acids), CYP2S1 metabolizes prostaglandin G2 and Prostaglandin H2 to 12-Hydroxyheptadecatrienoic acid. Possibly because of metabolizing and thereby inactivating the prostaglandins and/or because forming the bioactive metabolite, 12-hyddroxyheptadecatrienoic acid, rather than EETs, CYP2S1 may act to inhibit the function of monocytes and thereby limit inflammation as well as other immune responses.
Other systematic names for ALOX12 include 12S-Lipoxygenase, platelet-type 12-lipoxygenase, arachidonate:oxygen 12-oxidoreductase, Delta12-lipoxygenase, 12Delta-lipoxygenase, and C-12 lipoxygenase. ALOX12, often termed plate platelet-type 12-lipoxygenase, is distinguished from leukocyte-type 12-lipoxygenase which is found in mice, rats, cows, and pigs but not humans. Leukocyte-type 12-lipoxygenase in these animal species shares 73-86% amino acid identity with human ALOX15 but only 57-66% identity with human platelet-type 12-lipoxygenase and, like ALOX15, metabolizes arachidonic acid primarily to 15(S)-hydroperoxy-5Z,8Z,11Z,13E-eicosatetraenoic acid (i.e. 15(S)-HpETE; see 15-Hydroxyeicosatetraenoic acid).
In 1994, the Food and Drug Administration of the United States granted Mash an Investigational New Drug license, to permit her to research the addiction-stopping capabilities of ibogaine (an oneirogen that occurs in some plants). A lack of funding and other barriers prevented the research from proceeding. Mash and her colleagues had previously discovered that ibogaine is a prodrug that metabolizes into a psychoactive called 12-hydroxyibogamine (or, noribogaine). In the late 1990s she provided some assistance to Healing Transitions Institute for Addiction, a drug detoxification clinic in Cancún where physicians oversaw patients' ibogaine treatments.
Phase I Metabolism of racemic bupropion. The carbonyl reductase enzyme that is responsible for producing erythro- bupropion is unknown as of March 2015. Bupropion is metabolized in the liver by the cytochrome P450 isoenzyme CYP2B6. It has several active metabolites: R,R-hydroxybupropion, S,S-hydroxybupropion, threo-hydrobupropion and erythro- hydrobupropion, which are further metabolized to inactive metabolites and eliminated through excretion into the urine. Both bupropion and its primary metabolite hydroxybupropion act in the liver as potent inhibitors of the enzyme CYP2D6, which metabolizes not only bupropion itself but also a variety of other drugs and biologically active substances.
3-hydroxyacyl-coenzyme A dehydrogenase deficiency is a rare condition that prevents the body from converting certain fats to energy, particularly during fasting. Normally, through a process called fatty acid oxidation, several enzymes work in a step-wise fashion to metabolize fats and convert them to energy. People with 3-hydroxyacyl-coenzyme A dehydrogenase deficiency have inadequate levels of an enzyme required for a step that metabolizes groups of fats called medium chain fatty acids and short chain fatty acids; for this reason this disorder is sometimes called medium- and short-chain 3-hydroxyacyl-coenzyme A dehydrogenase (M/SCHAD) deficiency.
NAGly has been the focus of research on the immune system because of its antinociceptive effects and inhibitory action on components of the immune system. Specifically, it significantly inhibited TNFα and IFNγ production, and it shows potential as a therapeutic treatment for chronic inflammation. Moreover, NAGly has been shown to act as a substrate for cyclooxygenase-2 (COX-2), the enzyme primarily known for producing prostaglandins associated with increases in inflammation and hyperalgesia. In many mammalian tissues that express COX-2, significant levels of NAGly are naturally present, and in these tissues COX-2 selectively metabolizes NAGly prostaglandin (PG) H2 glycine and HETE-Gly.
Mice depleted of Cyp4a10 maintain normal blood pressure on a low salt diet but become hypertensive on normal or high salt diets; this paradoxical result appears due to a decrease in kidney levels of Cyp2C44 caused by the loss of Cyp4a10. Cyp2C44 metabolizes arachidonic acid a family of vasodilation-inducing and anti-hypertensive products, the Epoxyeicosatrienoic acids (EETs). The model involves normal levels of 20-HETE, reduced expression of Cyp2c44, reduced levels of EETs, and deficiencies in kidney tubule absorption of sodium regulated by EETs, and the normalization of hypertensive blood pressure by increasing expression of Cyp2c44 by treating the mice with an inducer of its expression, an activator of PPARα.
A schematic cross-section of Blood Falls showing how subglacial microbial communities have survived in cold, darkness, and absence of oxygen for a million years in brine water below Taylor Glacier. Chemical and microbial analyses both indicate that a rare subglacial ecosystem of autotrophic bacteria developed that metabolizes sulfate and ferric ions. According to geomicrobiologist Jill Mikucki at the University of Tennessee, water samples from Blood Falls contained at least 17 different types of microbes, and almost no oxygen. An explanation may be that the microbes use sulfate as a catalyst to respire with ferric ions and metabolize the trace levels of organic matter trapped with them.
Noninvasive tests for H. pylori infection may be suitable and include blood antibody tests, stool antigen tests, or the carbon urea breath test (in which the patient drinks 14C – or 13C-labelled urea, which the bacterium metabolizes, producing labelled carbon dioxide that can be detected in the breath). It is not known which non- invasive test is more accurate for diagnosing a H. pylori infection, and the clinical significance of the levels obtained with these tests are not clear. An endoscopic biopsy is an invasive means to test for H. pylori infection. Low-level infections can be missed by biopsy, so multiple samples are recommended.
In cells, EEQs are rapidly metabolized by the same enzyme that similarly metabolizes other epoxy fatty acids including the EETs viz., cytosolic soluble epoxide hydrolase [EC 3.2.2.10.] (also termed sEH or the EPHX2), to form their corresponding Vicinal (chemistry) diol dihydroxyeicosatetraenoic acids (diHETEs). The omega-3 fatty acid epoxides, EEQs and EPAs, appear to be preferred over EETs as substates for sEH. sEH converts 17,18-EEQ isomers to 17,18-dihydroxy-eicosatrienoic acid isomers (17,18-diHETEs), 14,15-EEQ isomers to 14,15-diHETE isomers, 11,12-EEQ isomers to 11,12-diHETE isomers, 8,9-EEQ isomers to 8,9-diHETE isomers, and 5,6-EEQ isomers to 5,6-diHETE isomers.
Pollination is done by a Cyclocephala beetle species. The sterile male flowers produce and maintain a constant temperature that is 34 °C (93.2F) above that of the environment during the two days the entire flower structure is open by burning stored fatty tissue - comparable to the metabolic output of a small cat. T. bipinnatifidum metabolizes fat, instead of carbohydrate, to fuel this process. This feature indicates a possible evolutionary convergence where this plant species and animal species derived similar mechanisms to utilize fat reserves for energy consumption. The main reason for raising and maintaining the flower’s temperature is for volatilizing and dispersing insect attracting odors.
Enzyme therapy is being actively studied for genetic metabolic diseases where an enzyme is over-expressed, under-expressed, defective, or not at all there. In the case of under-expression or expression of a defective enzyme, an active form of the enzyme is introduced in the body to compensate for the deficit. On the other hand, an enzymatic over-expression may be counteracted by introduction of a competing non-functional enzyme; that is, an enzyme which metabolizes the substrate into non-active products. When placed within an artificial cell, enzymes can carry out their function for a much longer period compared to free enzymes and can be further optimized by polymer conjugation.
Methylisocitrate lyase is used in the methylcitrate cycle, a modified version of the Krebs cycle that metabolizes propionyl coenzyme A instead of acetyl coenzyme A. The enzyme 2-methylcitrate synthase adds propionyl coenzyme A to oxaloacetate, yielding methylcitrate instead of citrate. But isomerizing methylcitrate to methylisocitrate and then subjecting it to MICL regenerates succinate, which proceeds as in the Krebs cycle, and pyruvate, which is easily metabolized by other pathways (e.g. decarboxylated to form acetyl coenzyme A and oxidized in the Krebs cycle). This allows catabolism of propionic acid—and, using beta oxidation, other fatty acids with odd numbers of carbons—without relying on coenzyme B12, a complex cofactor often used to metabolize propionate.
Brainstem(where HSD2 neurons are located) The term "HSD2 neurons" is used in the scientific literature to refer to a subpopulation of neurons in the NTS which express both the mineralocorticoid receptor (MR) and 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2). HSD2 is an enzyme that metabolizes cortisol and other glucocorticosteroids, which typically prevent aldosterone from binding to the mineralocorticoid receptor. This pre-receptor mechanism for modifying hormone binding is necessary for cellular sensitivity to aldosterone because, under physiologic conditions, cortisol circulates at 100-1000 times higher concentrations than aldosterone. As both cortisol and aldosterone bind the mineralocorticoid receptor with equal affinity, cortisol effectively crowds out aldosterone in cells without abundant HSD2.
The differences between the substrate selectivity of the two enzymes are utilized clinically when treating specific disorders: Monoamine oxidase A inhibitors have been typically used in the treatment of depression, and monoamine oxidase B inhibitors are typically used in the treatment of Parkinson's disease. Nonspecific (i.e. MAOA/B combined) inhibitors can pose problems when taken concomitantly with tyramine- containing foods such as cheese, because the drug's inhibition of MAOA causes a dangerous elevation of serum tyramine levels, which can lead to hypertensive symptoms. Selective MAOB inhibitors bypass this problem by preferentially inhibiting MAOB, which mostly metabolizes DA. If MAOB is inhibited, then more DA is available for proper neuronal function, especially in Parkinson's Disease.
Chick embryo that was treated with methylene blue to stain the skeleton, then cleansed with two or three ethanol washes, and treated with methyl salicylate to make the surrounding tissues transparent Methyl salicylate is used in high concentrations as a rubefacient and analgesic in deep heating liniments (such as Bengay) to treat joint and muscular pain. Randomised double blind trials report that evidence of its effectiveness is weak, but stronger for acute pain than chronic pain, and that effectiveness may be due entirely to counterirritation. However, in the body it metabolizes into salicylates, including salicylic acid, a known NSAID. Methyl salicylate is used in low concentrations (0.04% and under)Wintergreen at Drugs.
Cyclooxygenase-1 and cyclooxygenase-2 metabolize arachidonic acid to the 15-hydroperoxy, 20 carbon prostaglandin (PG) intermediate, PGG2, and then to the 15-hydroxy, 20 carbon intermediate, prostaglandin H2 (PGH2). Thromboxane synthase further metabolizes PGH2 to the 20 carbon product, Thromboxane A2, the 17 carbon product, 12-HHT, and the 3 carbon product Malonyldialdehyde. Platelets express cycloxygenase and thromboxane synthase enzymes, producing PGG2, PGH2, and TXA2 in response to platelet aggregating agents such as thrombin; these metabolites act as autocrines by feeding back to promote further aggregation of their cells of origin and as paracrines by recruiting nearby platlets into the response as well as exerting effects on other nearby tissues such as contracting blood vessels. These effects combine to trigger blood clotting and limiting blood loss.
Grapefruit and grapefruit juice have been found to interact with numerous drugs, in many cases resulting in adverse effects. This happens in two ways: one is that grapefruit can block an enzyme which metabolizes medication, and if the drug is not metabolized, then the level of the drug in the blood can become too high, leading to an adverse effect; the other effect is that grapefruit can block the absorption of drugs in the intestine, and if the drug is not absorbed, then not enough of it is in the blood to have a therapeutic effect. One whole grapefruit or a glass of of grapefruit juice can cause drug overdose toxicity. Drugs which are incompatible with grapefruit are typically labeled on the container or package insert.
It is suggested that this variant metabolizes ethanol to acetaldehyde too quickly for further processing by ALDH2 and thereby leads to the accumulation of acetaldehyde and rhinitis symptoms. In these cases, alcohol-induced rhinitis may be of the mixed rhinitis type and, it seems likely, most cases of alcohol- induced rhinitis in non-Asian populations reflect true allergic response to the non-ethanol and/or contaminants in alcoholic beverages, particularly when these beverages are wines or beers. Alcohol-exacerbated rhinitis is more frequent in individuals with a history of rhinitis exacerbated by aspirin. Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), particularly those that inhibit cyclooxygenase 1 (COX1), can worsen rhinitis and asthma symptoms in individuals with a history of either one of these diseases.
Splenda usually contains 95% dextrose (D-glucose) and maltodextrin (by volume) which the body readily metabolizes, combined with a small amount of mostly indigestible sucralose. Sucralose is made by replacing three select hydrogen-oxygen groups on sucrose (table sugar) molecules with three chlorine atoms. The tightly bound chlorine atoms create a molecular structure that is stable under intense conditions. Sucralose itself is recognized as safe to ingest as a diabetic sugar substitute, but the sugars or other carbohydrates used as bulking agents in Splenda products should be evaluated individually. The recommended amount of sucralose that can be consumed on a daily basis over a person's lifetime without any adverse effects is 900 mg/kg BW/day, or about 60 g for a 70 kg (150 lb) person.
Alcohol dehydrogenase and aldehyde dehydrogenase are present at their highest concentrations in the liver, but are widely expressed throughout the body, and alcohol dehydrogenase may also be present in the stomach and small intestine. Aside from alcohol dehydrogenase, the microsomal ethanol-oxidizing system (MEOS), specifically mediated by the cytochrome P450 enzyme CYP2E1, is the other major route of ethanol metabolism. CYP2E1 is inducible by ethanol, so while alcohol dehydrogenase handles acute or low concentrations of ethanol, MEOS is predominant with higher concentrations or with repeated/chronic use. A small amount of ethanol undergoes conjugation to form ethyl glucuronide and ethyl sulfate. There may also be another metabolic pathway that metabolizes as much as 25 to 35% of ethanol at typical concentrations.
In the best known of these metabolic pathways, cellular CYP epoxygenases metabolize the 20-carbon straight-chain omega-6 fatty acid, arachidonic acid, to epoxyeicosatrienoic acids (EETs); another CYP epoxygenase pathway metabolizes the 20-carbon omega-3 fatty acid, eicosapentaenoic acid (EPA), to epoxyeicosatetraenoic acids (EEQs). CYP epoxygenases similarly convert various other PUFAs to epoxides (see epoxygenase) These epoxide metabolites have a variety of activities. However, essentially all of them are rapidly converted to their corresponding, but in general far less active, Vicinal (chemistry) dihydroxy fatty acids by ubiquitous cellular Soluble epoxide hydrolase (sEH; also termed Epoxide hydrolase 2). Consequently, these epoxides, including EDPs, operate as short-lived signaling agents that regulate the function of their parent or nearby cells.
RvEs are di- or tri- hydroxyl metabolites of EPA. To date, four RvEs have been described: RvE1 (5S,12R,18R-trihydroxy-EPA), 18S-Rv1 (5S,12R,18S-trihydroxy-EPA), RvE2 (5S,18R-dihydroxy-EPA), and RvE3 (17R,18R/S-dihydroxy-EPA). (Structures of the RvEs are further defined at Specialized proresolving mediators#EPA-derived Resolvins.) Resolvin Es are formed in manner similar to AT resolving Ts. COX-2 modified in activity by aspirin or atorvastatin or, alternatively, a microbial or possibly mammalian cytochrome P450 monoxygenase metabolizes EPA to its 18R-hydroperoxy derivative; this intermediate is then further metabolized by ALOX5 to a 5,6 epoxide which is hydrolyzed enzymatically or non-enzymatically to RvE1 and 18S-RvE1 or reduced to RvE2; alternatively the 18R-hydroperoxide is converted to the 17R,18S vicinal diol product, RvE3.
The human brain is one of the most metabolically active organs in the body and metabolizes a large amount of glucose to produce cellular energy in the form of adenosine triphosphate (ATP). Despite its high energy demands, the brain is relatively inflexible in its ability to utilize substrates for energy production and relies almost entirely on circulating glucose for its energy needs. This dependence on glucose puts the brain at risk if the supply of glucose is interrupted, or if its ability to metabolize glucose becomes defective. If the brain is not able to produce ATP, synapses cannot be maintained and cells cannot function, ultimately leading to impaired cognition. Imaging studies have shown decreased utilization of glucose in the brains of Alzheimer’s disease patients early in the disease, before clinical signs of cognitive impairment occur.
While both MAO-A and MAO-B metabolize tyramine, only MAO-A is present in the gastrointestinal tract and singularly metabolizes the majority of consumed tyramine. (The small portion normally passing into circulation is mostly degraded in the liver where both MAO types act.) Consequently, MAOIs that irreversibly inhibit MAO-A will permit high levels of circulating tyramine able to cause tyramine-induced hypertensive crisis. Aged cheese, beer, red wine, some mushrooms, and fermented products such as pickles are foods containing high levels of tyramine that passed into circulation can cause such a hypertensive crisis. Adrenergic storms are not provoked often from MAOI-tyramine interactions; hypertensive crisis alone does not diagnose adrenergic storm, although there will always be hypertension in an adrenergic storm, along with tachycardia and rapid, shallow breathing.
Hepoxilin-epoxide hydrolase or hepoxilin hydrolase is currently best defined as an enzyme activity that converts the biologically active monohydroxy-epoxide metabolites of arachidonic acid hepoxilin A3s and hepoxilin B3s to essentially inactive trihydroxy products, the trioxilins. That is, hepoxilin A3s (8-hydroxy-11,12-oxido-5Z,9E,14Z-eicosatrienoic acid) are metabolized to trioxilin A3s (8,11,12-trihydroxy-5Z,9E,14Z-eicosatrienoic acids) and hepoxilins B3s (10-hydroxy-11,12-oxido-5Z,8Z,14Z-eicosatrienoic acids) are metabolized to trioxilin B3s (10,11,12-trihydroxy-5Z,8Z,14Z-eicosatrienoic acids). However, this activity has not been characterized at the purified protein or gene level and recent work indicate that sEH readily metabolizes an hepoxilin A3 to a trioxilin A3 and that hepoxilin-epoxide hydrolase activity is due to sEH, at least as it is detected in mouse liver.
CYP2C8 also possesses epoxygenase activity: it is one of the principal enzymes responsible for attacking various long-chain polyunsaturated fatty acids at their double (i.e. alkene) bonds to form epoxide products that act as signaling agents. It metabolizes: 1) arachidonic acid to various epoxyeicosatrienoic acids (also termed EETs); 2) linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin); 3) docosahexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and 4) eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs). Along with CYP2C8, CYP2C9, CYP2C19, CYP2J2, and possibly CYP2S1 are the main producers of EETs and, very likely, EEQs, EDPs, and the epoxides of linoleic acid.
As about the biologic species, the HNMT enzyme is found in vertebrates, including birds, reptiles and amphibian, but not in invertebrates and plants. The NHMT enzyme resides in the cytosol intracellular fluid. Whereas DAO metabolizes extracellular free histamine, be it either exogenous came with food or mostly endogenous released from granules of mast cells and basophils as a result of allergic reactions, in view of the fact that DAO is mainly expressed in the cells of intestinal epithelium, HNMT is involved in metabolism of the persistently present intracellular primarily endogenous histamine, mainly in kidneys and liver, but also in bronchi, large intestine, ovary, prostate, spinal cord, spleen, trachea and peripheral tissues. In the case of flawed HNMT activity, the organs which are most affected are brain, liver and mucous membrane of bronchus.
Since platelets have no DNA, they are unable to synthesize new PTGS once aspirin has irreversibly inhibited the enzyme, an important difference with reversible inhibitors. Furthermore, aspirin, while inhibiting the ability of COX-2 to form pro-inflammatory products such as the prostaglandins, converts this enzyme's activity from a prostaglandin-forming cyclooxygenase to a lipoxygenase-like enzyme: aspirin-treated COX-2 metabolizes a variety of polyunsaturated fatty acids to hydroperoxy products which are then further metabolized to specialized proresolving mediators such as the aspirin- triggered lipoxins, aspirin-triggered resolvins, and aspirin-triggered maresins. These mediators possess potent anti-inflammatory activity. It is proposed that this aspirin-triggered transition of COX-2 from cyclooxygenase to lipoxygenase activity and the consequential formation of specialized proresolving mediators contributes to the anti-inflammatory effects of aspirin.
The prevalence of ethanol-induced allergic symptoms in non-Asian genotypes commonly ranges above 5% even though many of these non-Asian populations have no or very low levels of individuals bearing the glu487lys allele. These "ethanol reactors" may have other gene-based abnormalities that cause the accumulation of acetaldehyde following the ingestion of ethanol or ethanol- containing beverages. For example, the surveyed incidence of self-reported ethanol-induced flushing reactions in Scandinavians living in Copenhagen as well as Australians of European descent is about ~16% in individuals homozygous for the "normal" ADH1B gene but runs to ~23% in individuals with the ADH1-Arg48His Single-nucleotide polymorphism variant; in vitro, this variant metabolizes ethanol rapidly and, it is proposed but not proven, in humans forms acetaldehyde at levels exceeding ALDH2's acetaldehyde- metabolizing capacity.Int Arch Allergy Immunol. 2010;153(1):86-94.
This gene encodes a member of the lipoxygenase family of structurally related nonheme iron dioxygenases involved in the production of fatty acid hydroperoxides. 15-LOX-2 has 38-39% amino acid sequence identity to human 15-LOX-1 and 12-lipoxygenase and 44% amino acid sequence identity to human 5-lipoxygenase. 15-LOX-2 converts arachidonic acid almost exclusively to the S stereoisomer of 15-Hydroperoxyicosatetraenoic acid which is commonly reduced to the S stereoisomer 15-Hydroxyeicosatetraenoic acid by ubiquitous cellular peroxidases; it metabolizes linoleic acid less effectively, converting this fatty acid to the S stereoisomer of 13-hydroperoxyoctadecadienoic acid which is likewise rapidly reduced to the S stereoisomer of 13-Hydroxyoctadecadienoic acid. The ALOX15B gene is located in a cluster of related genes and a pseudogene that spans approximately 100 kilobases on the short arm of chromosome 17.
ALOX12B targets Linoleic acid (LA). LA is the most abundant fatty acid in the skin epidermis, being present mainly esterified to the omega-hydroxyl residue of amide-linked omega- hydroxylated very long chain fatty acids (VLCFAs) in a unique class of ceramides termed esterified omega-hydroxyacyl-sphingosine (EOS). EOS is an intermediate component in a proposed multi-step metabolic pathway which delivers VLCFAs to the cornified lipid envelop in the skin's Stratum corneum; the presence of these wax-like, hydrophobic VLCFAs is needed to maintain the skin's integrity and functionality as a water barrier (see Lung microbiome#Role of the epithelial barrier). ALOX12B metabolizes the LA in EOS to its 9-hydroperoxy derivative; ALOXE3 then converts this derivative to three products: a) 9R,10R-trans-epoxide,13R-hydroxy-10E-octadecenoic acid, b) 9-keto-10E,12Z-octadecadienoic acid, and c) 9R,10R-trans- epoxy-13-keto-11E-octadecenoic acid.
Szára, who later worked for the US National Institutes of Health, had turned his attention to DMT after his order for LSD from the Swiss company Sandoz Laboratories was rejected on the grounds that the powerful psychotropic could be dangerous in the hands of a communist country. () DMT is generally not active orally unless it is combined with a monoamine oxidase inhibitor (MAOI) such as a reversible inhibitor of monoamine oxidase A (RIMA), for example, harmaline. Without a MAOI, the body quickly metabolizes orally administered DMT, and it therefore has no hallucinogenic effect unless the dose exceeds monoamine oxidase's metabolic capacity. Other means of ingestion such as vaporizing, injecting, or insufflating the drug can produce powerful hallucinations for a short time (usually less than half an hour), as the DMT reaches the brain before it can be metabolized by the body's natural monoamine oxidase.
After years of research proved that drugs deposited in the hair can be accurately measured, the company was formed in 1987 and pioneered the use of hair testing in commercial markets including banks, manufacturers, retailers, mining operations, hotels and casinos. The technology capitalizes on the way the body metabolizes ingested drugs as they flow through the blood stream and deposit in the cortex of the hair. Hair is stable and the deposits are permanently embedded in the hair, so hair acts like a tape recorder — “recording” drug deposits in proportion to use over time as drugs are deposited in proportion to use. Hair grows at approximately the rate of ½ an inch per month and takes about 5 days to grow out past the external layer of skin. Psychemedics’ standard test uses a 1 ½ inch sample of head hair, which provides an approximate 3 month history of drug use.
LA is the most abundant fatty acid in the skin epidermis, being present mainly esterified to the omega- hydroxyl residue of amide-linked omega-hydroxylated very long chain fatty acids (VLCFAs) in a unique class of ceramides termed esterified omega- hydroxyacyl-sphingosine (EOS). EOS is an intermediate component in a proposed multi-step metabolic pathway which delivers VLCFAs to the cornified lipid envelop in the skin's Stratum corneum; the presence of these wax-like, hydrophobic VLCFAs is needed to maintain the skin's integrity and functionality as a water barrier (see Lung microbiome#Role of the epithelial barrier). ALOX12B metabolizes the LA in EOS to its 9R-hydroperoxy derivative which ALOXE3 then converts to three ceramide-esterified products: a) 9R,10R-trans-epoxide,13R-hydroxy-10E-octadecenoic acid, b) 9-keto-10E,12Z-octadecadienoic acid, and c) 9R,10R-trans- epoxy-13-keto-11E-octadecenoic acid. The ALOX12B/ALOE3-oxidized products, it is proposed, signal for their hydrolysis (i.e.
CYP4F22, like other CYP4F proteins, is a Cytochrome P450 omega hydroxylase, i.e. an enzyme that metabolizes fatty acids to their omega hydroxyl derivatives (see Omega oxidation). This hydroxylation may: a) produce a biologically important signaling molecule such as occurs in the metabolism of 20-carbon straight chain polyunsaturated fatty acid, arachidonic acid, to 20-Hydroxyeicosatetraenoic acid, b) inactivate a biologically important product such as the metabolism of the arachidonic acid metabolite, 5-oxo- eicosatetraenoic acid, to its ~100-fold less potent product, 5-oxo-20-hydroxy- eicosatetraenoic acid, or c) be the first step in the further metabolism of xenobiotics or natural compounds CYP4F22 serves the latter function. It is a type 1 Integral membrane protein located in the endoplasmic reticulum of cells in the stratum granulosum of mammalian, including human, skin where it functions to attach an omega hydroxyl residue to fatty acids that are exceptionally long, 28 or more carbons, i.e.
5(Z),8(Z),11(Z),14(Z),17(Z)-eicosapentaenoic acid (EPA) is metabolized by the same CYP epoxygenases that metabolize arachidonic acid primarily to 17,18-epoxy-5(Z),8(Z),11(Z),14(Z)-eicosatetranoic acid and usually far smaller or undetectable amounts of EPA's 5,6-, 8,9-, 11,12-, or 14,15-epoxides; however, CYP2C9 metabolizes EPA primarily to 14,15-epoxy-5(Z),8(Z),11(Z),17(Z)-eicosatetranoic acid, CYP2C11 forms appreciable amounts of this 14,15-epoxide in addition to the 17,18-epoxide, and CYP2C18 forms appreciable amounts of the 11,12 epoxide (11,12-epoxy-5(Z),8(Z),14(Z),17(Z)-eicosatetranoic acid) in addition to the 17,18-epoxide. Furthermore, CYP4A11, CYP4F8, and CYP4F12, which are CYP monooxygenase rather than CYP epoxygeanse in that they metabolize arachidonic acid to monohydroxy eicosatetraenoic acid products (see 20-Hydroxyeicosatetraenoic acid), i.e. 19-hydroxy- and/or 18-hydroxy- eicosatetranoic acids, takes on epoxygenase activity in converting EPA primarily to its 17,18-epoxy metabolite (see epoxyeicosatetraenoic acid).
CYP2C9 attacks various long-chain polyunsaturated fatty acids at their double (i.e. alkene) bonds to form epoxide products that act as signaling molecules. It along with CYP2C8, CYP2C19, CYP2J2, and possibly CYP2S1 are the principle enzymes which metabolizes 1) arachidonic acid to various epoxyeicosatrienoic acids (also termed EETs); 2) linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin); 3) docosahexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and 4) eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs). Animal model studies implicate these epoxides in regulating: hypertension, Myocardial infarction and other insults to the heart, the growth of various cancers, inflammation, blood vessel formation, and pain perception; limited studies suggest but have not proven that these epoxides may function similarly in humans (see epoxyeicosatrienoic acid and epoxygenase pages).
5(S)-HETE is a product of the cellular metabolism of the n-6 polyunsaturated fatty acid, arachidonic acid (i.e. 5Z,8Z,11Z,14Z-eicosatetraenoic acid), by ALOX5 (also termed arachidonate-5-lipoxygenase, 5-lipoxygenase, 5-LO, and 5-LOX). ALOX5 metabolizes arachidonic acid to its hydroperoxide derivative, arachidonic acid 5-hydroperoxide i.e. 5S-hydroperoxy-6E,8Z,11Z,14Z-eicosatetraenoic acid (5(S)-HpETE). 5-(S)-HpETE may then be released and rapidly converted to 5(S)-HETE by ubiquitous cellular peroxidases: Arachidonic acid) + O2 → 5(S)-HpETE → 5(S)-HETE Alternatively, 5(S)-HpETE may be further metabolized to its epoxide, 5(6)-oxido-eicosatetraenoic acid viz., leukotriene A4 (i.e. S,6S-oxido-7E,9E,11Z,14Z-eicosatetraenoic acid). Leukotriene A4 may then be further metabolized either to leukotriene B4 by leukotriene A4 hydrolase or to leukotriene C4 by leukotriene C4 synthase. Finally, leukotriene C4 may be metabolized to leukotriene D4 and then to leukotriene E4.
In the maturation of the red blood cell lineage (see erythropoiesis) from mitochondria-bearing reticulocytes to mature mitochondria-free erythrocytes in rabbits, the mitochondria accumulate phospholipid-bound 13(S)-HODE in their membranes due to the action of a lipoxygenase which (in rabbits, mice, and other sub-primate vertebrates) directly metabolizes linoleic acid-bound phospholipid to 13(S)-HpODE-bound phospholipid which is rapidly reduced to 13(S)-HODE-bound phospholipid. It is suggested that the accumulation of phospholipid-bound 13(S)-HpODE and/or 13(S)-HODE is a critical step in rendering mitochondria more permeable thereby triggering their degradation and thence maturation to erythrocytes. However, functional inactivation of the phospholipid-attacking lipoxygenase gene in mice does not cause major defects in erythropoiesis. It is suggested that mitochondrial degradation proceeds through at least two redundant pathways besides that triggered by lipoxygenase-dependent formation of 13(S)-HpODE- and 13(S)-HODE-bound phospholipids viz.
The brain metabolizes as much as a fifth of consumed oxygen, and reactive oxygen species produced by oxidative metabolism are a major source of DNA damage in the brain. Damage to a cell’s DNA is particularly harmful because DNA is the blueprint for protein production and unlike other molecules it cannot simply be replaced by re-synthesis. The vulnerability of post-mitotic neurons to DNA damage (such as oxidative lesions or certain types of DNA strand breaks), coupled with a gradual decline in the activities of repair mechanisms, could lead to accumulation of DNA damage with age and contribute to brain aging and neurodegeneration. DNA single-strand breaks are common and are associated with the neurodegenerative disease ataxia-oculomotor apraxia. Increased oxidative DNA damage in the brain is associated with Alzheimer’s disease and Parkinson’s disease. Defective DNA repair has been linked to neurodegenerative disorders such as Alzheimer’s disease, amyotrophic lateral sclerosis, ataxia telangiectasia, Cockayne syndrome, Parkinson’s disease and xeroderma pigmentosum.
These decompositions may occur during tissue isolation procedures. Recent studies indicate that the metabolism by ALOXE3 of the R stereoisomer of 12-HpETE made by ALOX12B and therefore possibly the S stereoisomer of 12-HpETE made by ALOX12 or ALOX15 is responsible for forming various hepoxilins in the epidermis of human and mouse skin and tongue and possibly other tissues. Human skin metabolizes 12(S)-HpETE in reactions strictly analogous to those of 12(R)-HpETE; it metabolized 12(S)-HpETE by eLOX3 to 8R-hydroxy-11S,12S-epoxy-5Z,9E,14Z-eicosatetraenoic acid and 12-oxo-ETE, with the former product then being metabolized by sEH to 8R,11S,12S-trihydroxy-5Z,9E,14Z-eicosatetraenoic acid. 12(S)-HpETE also spontaneously decomposes to a mixture of hepoxilins and trihydroxy- eicosatetraenoic acids (trioxillins) that possess R or S hydroxy and R,S or S,R epoxide residues at various sites while 8R-hydroxy-11S,12S-epoxy-hepoxilin A3 spontaneously decomposes to 8R,11S,12S-trihydroxy-5Z,9E,14Z-eicosatetraenoic acid.
It was raised in defense that 1,4-B and GHB contain different functional groups, and that the food additive monosodium glutamate (MSG) also metabolizes into GHB in the body, but these were not held to be grounds to consider 1,4-B not substantially similar to GHB. It was also raised in the case of Washam that the Federal Analogue Act was unconstitutionally vague, but in this case the court rejected this argument on the grounds that the defendant's actions in concealing her activities and lying to DEA agents showed that she knew her actions were illegal, and furthermore that “…a person of common intelligence has sufficient notice under the statute that 1,4-Butanediol is a controlled substance analogue.” The court in Washam construed the Analogue Act to require parts A(i) and either A(ii) or A(iii), and concluded the Act was constitutionally permissible upon this construction. As a result of Washam, the Federal Analogue Act has been upheld (at least for the states and territories comprising the eighth judicial circuit) and can be considered valid at the present time.
5-LOX may also work in series with cytochrome P450 oxygenases or aspirin-treated COX2 to form Resolvins RvE1, RvE2, and 18S-RvE1 (see Specialized pro-resolving mediators#EPA-derived resolvins). The enzyme arachidonate 12-lipoxygenase (12-LO or ALOX12) metabolizes arachidonic acid to the S stereoisomer of 12-hydroperoxyeicosatetraenoic acid (12-HPETE) which is rapidly reduced by cellular peroxidases to the S stereoisomer of 12-hydroxyeicosatetraenoic acid (12-HETE) or further metabolized to hepoxilins (Hx) such as HxA3 and HxB. The enzymes 15-lipoxygenase-1 (15-LO-1 or ALOX15) and 15-lipoxygenase-2 (15-LO-2, ALOX15B) metabolize arachidonic acid to the S stereoisomer of 15-Hydroperoxyeicosatetraenoic acid (15(S)-HPETE) which is rapidly reduced by cellular peroxidases to the S stereoisomer of 15-Hydroxyicosatetraenoic acid (15(S)-HETE). The 15-lipoxygenases (particularly ALOX15) may also act in series with 5-lipoxygenase, 12-lipoxygenase, or aspirin-treated COX2 to form the lipoxins and epi-lipoxins or with P450 oxygenases or aspirin-treated COX2 to form Resolvin E3 (see Specialized pro-resolving mediators#EPA-derived resolvins.
Finch's research on how iron metabolizes in the blood helped with blood disorders characterized by either an excess or inadequate supply of iron in the blood stream, such as anemia and hemochromatosis, and also focused his work on further understanding Erythropoiesis, a process by which red blood cells are produced. During a period in which little was known about iron-deficiency anemia, how often it occurred or the principles of iron metabolism, Finch made significant findings in his research at the University of Washington throughout his 60-year tenure using radioisotopes to measure the body's production of red cells and their life span. He was able to discover how iron is incorporated in hemoglobin, and was able to aid doctors in expanding their abilities from simply detecting iron-deficiency anemia to detecting different types of anemia in an increasingly accurate manner. Finch has published Scientific Journal articles specifically pertaining to Erythropoiesis and anemia such as Erythropoiesisin Pernicious Anemia (1953), Treatment of Iron Deficiency Anemia in the Adult (1957), The Diagnosing of Iron deficiency Anemia (1964), Pathophysiologic Aspects of Sickle Cell Anemia (1972), and Erythroid Marrow Function in Anemic Patients (1987).
As the medical wisdom at the time stated that bacteria could not survive in the stomach's acidic environment, his research was largely ignored. It was not until the 1980s, when researchers Dr. Barry Marshall and Dr. Robin Warren identified the bacteria Helicobacter pylori in the stomach as a cause of ulcers and stomach cancer, for which they won the 2005 Nobel Prize in Physiology or Medicine. He pushed the National Council on Alcoholism and Drug Dependence to create the journal Alcoholism: Clinical and Experimental Research in 1977 as an academic journal for articles regarding alcohol abuse and its treatment, to disseminate research in a field that was minimized by other medical professionals who did not believe that alcohol research was a legitimate avenue for research and that there was nothing medicine could do to address the problems of alcoholism. A 1990 study published in the New England Journal of Medicine showed that women feel greater effects than men from equivalent amounts of alcohol adjusted for body size due to lower amounts of a stomach enzyme that metabolizes the alcohol and keeps it from entering the bloodstream, though the study did not explain the cause of this enzymatic discrepancy.
Accordingly, rodent leukocyte 12-lipoxygenase is deemed an ortholog of ALOX15 and is designated as Alox15. Human ALOX12 and ALOX15 along with rodent leukocyte-type Alox12 and Alox15 are commonly termed 12/15-lipoxygenases based on their ability to metabolize arachidonic acid to both 12(S)-HpETE and 15(S)-HpETE and to conduct this same metabolism on arachidonic acid that is esterified to membrane phospholipids; human ALOX15B makes 15(S)-HpETE but not 12(S)-HpETE and therefore is not regarded as a 12/15-lipoxygenase. Studies on the role of ALOX12 in pathophysiology using the main models for such functional studies, rats and mice, are complicated because neither species possesses a lipoxygenase that makes a predominance of 12(S)-HETE and therefore is metabolically equivalent to ALOX12. For example, the functions inferred for Alox12 in mice made deficient in Alox12 using knockout methods may not indicate a similar function for ALOX12 in humans due to differences in these two enzymes' metabolic activities. The function of ALOX12 is further clouded by human ALOX15 which metabolizes arachidonic acid primarily to 15(S)-HpETE but also makes lesser but still significant amounts of 12(S)-HpETE (see ALOX15).
In guinea pigs, 13(S)-HODE, when injected intravenously, causes a narrowing of lung airways and, when inhaled as an aerosol, mimics the asthmatic hypersensitivity to agents that cause bronchoconstriction by increasing airway narrowing responses to methacholine and histamine. In a mouse model of allergen-induced asthma, 13-HODE levels are elevated, in the latter mouse model, the injection of antibody directed against 13(S)-HODE reduced many of the pathological and physiological features of asthma,. mouse forced to overexpress in lung the mouse enzyme (12/15-lipoxygenase) that metabolizes linoleic acid to 13(S)-HODE exhibited elevated levels of this metabolite in lung as well as various pathological and physiological features of asthma, and the instillation of 13(S)HODE replicated many of these features of asthma, In the mouse model of asthma and in the human disease, epithelial cells of lung airways show various pathological changes including disruption of their mitochondria 13(S)-HODE causes similar disruptive changes in the mitochondria of cultured Beas 2B human airway epithelial cells. Furthermore, human suffers of asthma exhibit increased levels of 13-HODE in their blood, sputum, and washings form their lung alveola (i.e.

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