QH(2), also known as ubiquinol, belongs to the class of organic compounds known as ubiquinols. These are coenzyme Q derivatives containing a 5, 6-dimethoxy-3-methylbenzene-1,4-diol moiety to which an isoprenyl group is attached at ring position 2(or 6). QH(2) is considered to be a practically insoluble (in water) and relatively neutral molecule. Within the cell, QH(2) is primarily located in the membrane (predicted from logP) and cytoplasm. QH(2) exists in all living organisms, ranging from bacteria to humans. In humans, QH(2) is involved in the congenital lactic acidosis pathway, the citric Acid cycle pathway, and the oncogenic action OF 2-hydroxyglutarate pathway. QH(2) is also involved in several metabolic disorders, some of which include fumarase deficiency, cancer (via the Warburg effect), pyruvate dehydrogenase deficiency (e3), and mitochondrial complex II deficiency. Qh(2) is part of the Oxidative phosphorylation, Cardiac muscle contraction, Alzheimer\'s disease, Parkinson\'s disease, and Huntington\'s disease pathways. It is a substrate for: Cytochrome b-c1 complex subunit Rieske, mitochondrial.


ADP

Adenosine diphosphate, abbreviated ADP, is a nucleotide. It is an ester of pyrophosphoric acid with the nucleotide adenine. ADP consists of the pyrophosphate group, the pentose sugar ribose, and the nucleobase adenine. ADP is the product of ATP dephosphorylation by ATPases. ADP is converted back to ATP by ATP synthases.

Adp
Adenosindiphosphorsaeure
Adenosine 5'-pyrophosphate
Adenosine diphosphate
Adenosine pyrophosphate
Adenosine-5'-diphosphate
Adenosine-5-diphosphate
Adenosine-diphosphate
5'-adenylphosphoric acid
Adenosine 5'-diphosphate
H3adp
5'-adenylphosphate
Adenosine 5'-diphosphoric acid
Adenosine-5'-diphosphoric acid


Labetalol

Labetalol is only found in individuals that have used or taken this drug. It is a blocker of both alpha- and beta-adrenergic receptors that is used as an antihypertensive (PubChem). Labetalol HCl combines both selective, competitive, alpha-1-adrenergic blocking and nonselective, competitive, beta-adrenergic blocking activity in a single substance. In man, the ratios of alpha- to beta- blockade have been estimated to be approximately 1:3 and 1:7 following oral and intravenous (IV) administration, respectively. The principal physiologic action of labetalol is to competitively block adrenergic stimulation of β-receptors within the myocardium (β1-receptors) and within bronchial and vascular smooth muscle (β2-receptors), and α1-receptors within vascular smooth muscle. This causes a decrease in systemic arterial blood pressure and systemic vascular resistance without a substantial reduction in resting heart rate, cardiac output, or stroke volume, apparently because of its combined α- and β-adrenergic blocking activity.


Tryptamine

Tryptamine is a monoamine compound that is common precursor molecule to many hormones and neurotransmitters. Biosynthesis generally proceeds from the amino acid tryptophan, with tryptamine in turn acting as a precursor for other compounds. Substitutions to the tryptamine molecule give rise to a group of compounds collectively known as tryptamines. The most well-known tryptamines are serotonin, an important neurotransmitter, and melatonin, a hormone involved in regulating the sleep-wake cycle.


Inositol 1,3,4,5-tetrakisphopsphate (IP4) is a second messenger responsible for mediating Ca2+ entry through plasma membrane and mobilize intracellular Ca2+ by acting synergistically with inositol 1,4,5-trisphosphate (IP3). Inositol 1,4,5-trisphosphate 3-kinase (IP3K, EC 2.7.1.127) phosphorylates IP3 to IP4. Evidence shows that IP4 can activate a protein with ras- and rap-GAP activity and finally inactivate the G protein. This indicates that IP4 regulates Ca2+ influx in a GTP-dependent way, which potentially links the IP3 signaling pathway to GTP-regulated signaling mechanisms. IP4 is demonstrated to be a common regulator in Ca2+ homeostasis. IP4 can bind with high affinity to several intracellular proteins: synaptotagmin (I and II), Gap1, Btk, and centaurin-alpha-and may interact with synaptotagmin to inhibit synaptic transmission. IP4 also acts as a mediator in neuronal death in the ischemic hippocampus. IP4 production is not always associated with modification in calcium concentration, and control of calcium mobilization is not the sole function proposed for IP4. IP4 define an essential signaling pathway for T cell precursor responsiveness and development. In the thymus, IP4 is essential during positive and negative selection of double-positive thymocytes, and in the control of thymocyte reactivity to antigens. 1D-Myo-inositol 1,3,4,5-tetrakisphosphate is also a substrate for Type I inositol-1,4,5-trisphosphate 5-phosphatase, Phosphatidylinositol 4,5-bisphosphate 5-phosphatase A and Skeletal muscle and kidney enriched inositol phosphatase. (PMID: 15740635, 14517551).


Melatonin

Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B.Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and. lowering the body temperature. Melatonin is also implicated in the regulation of mood,learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders(ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits. were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers.


Trigonellamide

1-Methylnicotinamide is a metabolite of nicotinamide and is produced primarily in the liver. It has anti-inflammatory properties (PMID 16197374). It is a product of nicotinamide N-methyltransferase [EC 2.1.1.1] in the pathway of nicotinate and nicotinamide metabolism (KEGG). 1-Methylnicotinamide may be an endogenous activator of prostacyclin production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system (PMID: 17641676).


Racemethionine

Methionine is an essential amino acid (there are 9 essential amino acids) required for normal growth and development of humans, other mammals, and avian species. In addition to being a substrate for protein synthesis, it is an intermediate in transmethylation reactions, serving as the major methyl group donor in vivo, including the methyl groups for DNA and RNA intermediates. Methionine is a methyl acceptor for 5-methyltetrahydrofolate-homocysteine methyltransferase (methionine synthase), the only reaction that allows for the recycling of this form of folate, and is also a methyl acceptor for the catabolism of betaine. Methionine is the metabolic precursor for cysteine. Only the sulfur atom from methionine is transferred to cysteine; the carbon skeleton of cysteine is donated by serine (PMID: 16702340). There is a general consensus concerning normal sulfur amino acid (SAA) requirements. WHO recommendations amount to 13 mg/kg per 24 h in healthy adults. This amount is roughly doubled in artificial nutrition regimens. In disease or after trauma, requirements may be altered for methionine, cysteine, and taurine. Although in specific cases of congenital enzyme deficiency, prematurity, or diminished liver function, hypermethioninemia or hyperhomocysteinemia may occur, SAA supplementation can be considered safe in amounts exceeding 2-3 times the minimum recommended daily intake. Apart from some very specific indications (e.g. acetaminophen poisoning) the usefulness of SAA supplementation is not yet established (PMID: 16702341). Methionine is known to exacerbate psychopathological symptoms in schizophrenic patients, but there is no evidence of similar effects in healthy subjects. The role of methionine as a precursor of homocysteine is the most notable cause for concern. Acute doses of methionine can lead to acute increases in plasma homocysteine, which can be used as an index of the susceptibility to cardiovascular disease. Sufficiently high doses of methionine can actually result in death. Longer-term studies in adults have indicated no adverse consequences of moderate fluctuations in dietary methionine intake, but intakes higher than 5 times the normal amount resulted in elevated homocysteine levels. These effects of methionine on homocysteine and vascular function are moderated by supplements of vitamins B-6, B-12, C, and folic acid (PMID: 16702346). When present in sufficiently high levels, methionine can act as an atherogen and a metabotoxin. An atherogen is a compound that when present at chronically high levels causes atherosclerosis and cardiovascular disease. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of methionine are associated with at least ten inborn errors of metabolism, including cystathionine beta-synthase deficiency, glycine N-methyltransferase deficiency, homocystinuria, tyrosinemia, galactosemia, homocystinuria-megaloblastic anemia due to defects in cobalamin metabolism, methionine adenosyltransferase deficiency, methylenetetrahydrofolate reductase deficiency, and S-adenosylhomocysteine (SAH) hydrolase deficiency. Chronically elevated levels of methionine in infants can lead to intellectual disability and other neurological problems, delays in motor skills, sluggishness, muscle weakness, and liver problems. Many individuals with these metabolic disorders tend to develop cardiovascular disease later in life. Studies on feeding rodents high levels of methionine have shown that methionine promotes atherosclerotic plaques independently of homocysteine levels (PMID: 26647293). A similar study in Finnish men showed the same effect (PMID: 16487911).


galactitol

Galactitol or dulcitol is a sugar alcohol that is a metabolic breakdown product of galactose. Galactose is derived from lactose in food (such as dairy products). When lactose is broken down by the enzyme lactase it produces glucose and galactose. Galactitol has a slightly sweet taste. It is produced from galactose in a reaction catalyzed by aldose reductase. When present in sufficiently high levels, galactitol can act as a metabotoxin, a neurotoxin, and a hepatotoxin. A neurotoxin is a compound that disrupts or attacks neural cells and neural tissue. A hepatotoxin as a compound that disrupts or attacks liver tissue or liver cells. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of galactitol are associated with at least two inborn errors of metabolism, including galactosemia and galactosemia type II. Galactosemia is a rare genetic metabolic disorder that affects an individual's ability to metabolize the sugar galactose properly. Excess lactose consumption in individuals with galactose intolerance or galactosemia activates aldose reductase to produce galactitol, thus depleting NADPH and leading to lowered glutathione reductase activity. As a result, hydrogen peroxide or other free radicals accumulate causing serious oxidative damage to various cells and tissues. In individuals with galactosemia, the enzymes needed for the further metabolism of galactose (galactose-1-phosphate uridyltransferase) are severely diminished or missing entirely, leading to toxic levels of galactose 1-phosphate, galactitol, and galactonate. High levels of galactitol in infants are specifically associated with hepatomegaly (an enlarged liver), cirrhosis, renal failure, cataracts, vomiting, seizure, hypoglycemia, lethargy, brain damage, and ovarian failure.

Ambap5938 D-dulcitol Dulcite Dulcitol Dulcose Euonymit Galactitol Hexitol Melampyrin Melampyrit Melampyrite Melampyrum Meso-galactitol D-galactitol L-galactitol


Prasterone sulfate

Dehydroepiandrosterone sulfate or DHEA-S is the sulfated form of dehydroepiandrosterone (DHEA). This sulfation is reversibly catalyzed by sulfotransferase 2A1 (SULT2A1) primarily in the adrenals, the liver, and small intestine. In the blood, most DHEA is found as DHEA-S with levels that are about 300 times higher than those of free DHEA. Orally-ingested DHEA is converted into its sulfate when passing through the intestines and liver. Whereas DHEA levels naturally reach their peak in the early morning hours, DHEAS levels show no diurnal variation. From a practical point of view, measurement of DHEA-S is preferable to DHEA since levels are more stable. DHEA (from which DHEA-S comes from) is a natural steroid prohormone produced from cholesterol by the adrenal glands, the gonads, adipose tissue, brain, and in the skin (by an autocrine mechanism). DHEA is the precursor of androstenedione, which can undergo further conversion to produce the androgen testosterone and the estrogens estrone and estradiol. DHEA is also a potent sigma-1 agonist. Serum dehydroepiandrosterone sulfate is a classic marker for adrenarche, and subsequently for the individual hormonal milieu (PMID: 10599744). Dehydroepiandrosterone sulfate is an endogenously produced sex steroid that has been hypothesized to have anti-aging effects (PMID: 16960027). It also has been inversely associated with the development of atherosclerosis (PMID: 8956025).


Corticosterone

Corticosterone, also known as 17-deoxycortisol, belongs to the class of organic compounds known as 21-hydroxysteroids. These are steroids carrying a hydroxyl group at the 21-position of the steroid backbone. Thus, corticosterone is considered to be a steroid lipid molecule. Corticosterone exists as a solid and is considered to be practically insoluble (in water) and relatively neutral. Corticosterone has been found throughout most human tissues, and has also been detected in multiple biofluids, such as blood and urine. Within the cell, corticosterone is primarily located in the cytoplasm, membrane (predicted from logP), mitochondria and endoplasmic reticulum. In humans, corticosterone is involved in the steroidogenesis pathway. Corticosterone is also involved in several metabolic disorders, some of which include 21-hydroxylase deficiency (cyp21), 3-Beta-hydroxysteroid dehydrogenase deficiency, 11-beta-hydroxylase deficiency (cyp11b1), and adrenal hyperplasia type 5 or congenital adrenal hyperplasia due to 17 Alpha-hydroxylase deficiency. Corticosterone is an adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman\'s The Pharmacological Basis of Therapeutics, 8th ed, p1437).


Tryptophan

Tryptophan is an essential amino acid that is the precursor of both serotonin and melatonin. Melatonin is a hormone that is produced by the pineal gland in animals, which regulates sleep and wakefulness. Serotonin is a brain neurotransmitter, platelet clotting factor, and neurohormone found in organs throughout the body. Metabolism of tryptophan into serotonin requires nutrients such as vitamin B6, niacin, and glutathione. Niacin (also known as vitamin B3) is an important metabolite of tryptophan. It is synthesized via kynurenine and quinolinic acids, which are products of tryptophan degradation. There are a number of conditions or diseases that are characterized tryptophan deficiencies. For instance, fructose malabsorption causes improper absorption of tryptophan in the intestine, which reduces levels of tryptophan in the blood and leads to depression. High corn or other tryptophan-deficient diets can cause pellagra, which is a niacin-tryptophan deficiency disease with symptoms of dermatitis, diarrhea, and dementia. Hartnup's disease is a disorder in which tryptophan and other amino acids are not absorbed properly. Symptoms of Hartnup's disease include skin rashes, difficulty coordinating movements (cerebellar ataxia), and psychiatric symptoms such as depression or psychosis. Tryptophan supplements may be useful for treating Hartnup's. Assessment of tryptophan deficiency is done through studying excretion of tryptophan metabolites in the urine or blood. Blood may be the most sensitive test because the amino acid tryptophan is transported in a unique way. Increased urination of tryptophan breakdown products (such as kynurenine) correlates with increased tryptophan degradation, which occurs with oral contraception, depression, mental retardation, hypertension, and anxiety states. The requirement for tryptophan and protein decreases with age. The minimum daily requirement for adults is 3 mg/kg/day or about 200 mg a day. There is 400 mg of tryptophan in a cup of wheat germ. A cup of low fat cottage cheese contains 300 mg of tryptophan and chicken and turkey contain up to 600 mg of tryptophan per pound (http://www.dcnutrition.com). Tryptophan plays a role in "feast-induced" drowsiness. Ingestion of a meal rich in carbohydrates triggers the release of insulin. Insulin, in turn, stimulates the uptake of large neutral branched-chain amino acids (BCAAs) into muscle, increasing the ratio of tryptophan to BCAA in the bloodstream. The increased tryptophan ratio reduces competition at the large neutral amino acid transporter (which transports both BCAAs and tryptophan), resulting in greater uptake of tryptophan across the blood-brain barrier into the cerebrospinal fluid (CSF). Once in the CSF, tryptophan is converted into serotonin and the resulting serotonin is further metabolized into melatonin by the pineal gland, which promotes sleep. Under certain situations, tryptophan can be a neurotoxin and a metabotoxin. A neurotoxin is a compound that causes damage to the brain and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of tryptophan can be found in glutaric aciduria type I (glutaric acidemia type I or GA1). GA1 is an inherited disorder in which the body is unable to completely break down the amino acids lysine, hydroxylysine, and tryptophan. Babies with glutaric acidemia type I are often born with unusually large heads (macrocephaly). Affected individuals may also have difficulty moving and may experience spasms, jerking, rigidity or decreased muscle tone, and muscle weakness. High levels of tryptophan have also been implicated in eosinophilia-myalgia syndrome (EMS), an incurable and sometimes fatal flu-like neurological condition linked to the ingestion of large amounts of L-tryptophan. The risk of developing EMS increases with larger doses of tryptophan and increasing age. Some research suggests that certain genetic polymorphisms may be related to the development of EMS. The presence of eosinophilia is a core feature of EMS, along with unusually severe myalgia (muscle pain). It is thought that both tryptophan and certain unidentified tryptophan contaminants may contribute to EMS (PMID: 1763543). It has also been suggested that excessive tryptophan or elevation of its metabolites could play a role in amplifying some of the pathological features of EMS (PMID: 10721094). This pathological damage is further augmented by metabolites of the kynurenine pathway (a tryptophan degradation pathway).


Methylamine

Methylamine occurs endogenously from amine catabolism and its tissue levels increase in some pathological conditions, including diabetes. Interestingly, methylamine and ammonia levels are reciprocally controlled by a semicarbazide-sensitive amine oxidase activity that deaminates methylamine to formaldehyde with the production of ammonia and hydrogen peroxide. Methylamine also targets the voltage-operated neuronal potassium channels, probably inducing release of neurotransmitter(s). Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the deamination of primary amines. Such deamination has been shown capable of regulating glucose transport in adipose cells. It has been independently discovered that the primary structure of vascular adhesion protein-1 (VAP-1) is identical to SSAO. Increased serum SSAO activities have been found in patients with diabetic mellitus, vascular disorders, and Alzheimer's disease. The SSAO-catalyzed deamination of endogenous substrates like methylamine led to production of toxic formaldehyde. Chronic elevated methylamine increases the excretion of malondialdehyde and microalbuminuria. Amine oxidase substrates such as methylamine have been shown to stimulate glucose uptake by increasing the recruitment of the glucose transporter GLUT4 from vesicles within the cell to the cell surface. Inhibition of this effect by the presence of semicarbazide and catalase led to the suggestion that the process is mediated by the hydrogen peroxide produced in the oxidation of these amines (PMID: 16049393, 12686132, 17406961).

Aminomethane
Anhydrous methylamine
Carbinamine
Imizin
Mma
Mercurialin
Methanamine
Methyl group
Methyl of gamma-n-methylasparagine
Methylamine
Methylamine anhydrous
Methylamine aqueous solution
Methylamine solution
Methylamine solutions
Methylaminen
Metilamine
Metyloamina
Monomethylamine
N-methylamine
Nma
Nme


3-Hexaprenyl-4-hydroxy-5-methoxybenzoic acid, also known as 3-MHHB or 3-methoxy-4-hydroxy-5-hexaprenylbenzoate, belongs to the class of organic compounds known as 2-polyprenyl-6-methoxyphenols. 2-polyprenyl-6-methoxyphenols are compounds containing a polyisoprene chain attached at the 2-position of a 6-methoxyphenol group. 3-Hexaprenyl-4-hydroxy-5-methoxybenzoic acid is considered to be a practically insoluble (in water) and relatively neutral molecule. Within the cell, 3-hexaprenyl-4-hydroxy-5-methoxybenzoic acid is primarily located in the membrane (predicted from logP) and cytoplasm. In humans, 3-hexaprenyl-4-hydroxy-5-methoxybenzoic acid is involved in ubiquinone biosynthesis pathway. 3-Hexaprenyl-4-hydroxy-5-methoxybenzoic acid is an intermediate in the biosynthesis of Ubiquinone. It is a substrate for Hexaprenyldihydroxybenzoate methyltransferase (mitochondrial).


Mycophenolic acid

Mycophenolic acid is an an immunosuppresant drug and potent anti-proliferative, and can be used in place of the older anti-proliferative azathioprine. It is usually used as part of triple therapy including a calcineurin inhibitor (ciclosporin or tacrolimus) and prednisolone. It is also useful in research for the selection of animal cells that express the E. coli gene coding for XGPRT (xanthine guanine phosphoribosyltransferase).


3alpha,11beta,21-Trihydroxy-20-oxo-5beta-pregnan-18-al is an intermediate in C21-Steroid hormone metabolism. 3alpha,11beta,21-Trihydroxy-20-oxo-5beta-pregnan-18-al is converted from 11beta,21-Dihydroxy-3,20-oxo-5beta-pregnan-18-al via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50).


Formaldehyde

Formaldehyde is a highly reactive aldehyde gas formed by oxidation or incomplete combustion of hydrocarbons. In solution, it has a wide range of uses: in the manufacture of resins and textiles, as a disinfectant, and as a laboratory fixative or preservative. Formaldehyde solution (formalin) is considered a hazardous compound, and its vapor toxic. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p717) -- Pubchem; The chemical compound formaldehyde (also known as methanal), is a gas with a pungent smell. It is the simplest aldehyde. Its chemical formula is H2CO. Formaldehyde was first synthesized by the Russian chemist Aleksandr Butlerov in 1859 but was conclusively identified by August Wilhelm van Hofmann in 1867. Although formaldehyde is a gas at room temperature, it is readily soluble in water, and it is most commonly sold as a 37% solution in water called by trade names such as formalin or formol. In water, formaldehyde polymerizes, and formalin actually contains very little formaldehyde in the form of H2CO monomer. Usually, these solutions contain a few percent methanol to limit the extent of polymerization. Formaldehyde exhibits most of the general chemical properties of the aldehydes, except that is generally more reactive than other aldehydes. Formaldehyde is a potent electrophile. It can participate in electrophilic aromatic substitution reactions with aromatic compounds and can undergo electrophilic addition reactions with alkenes. In the presence of basic catalysts, formaldehyde undergoes a Cannizaro reaction to produce formic acid and methanol. Because formaldehyde resins are used in many construction materials, including plywood, carpet, and spray-on insulating foams, and because these resins slowly give off formaldehyde over time, formaldehyde is one of the more common indoor air pollutants. At concentrations above 0.1 mg/kg in air, inhaled formaldehyde can irritate the eyes and mucous membranes, resulting in watery eyes, headache, a burning sensation in the throat, and difficulty breathing. -- Wikipedia.

Methaldehyde
Methylene glycol
Aldeide formica
Chlodithan
Chlodithane
Fannoform
Formaldehyde
Formalina
Formaline
Formalith
Formic aldehyde
Formol
Methanal
Methylene oxide
Oxomethylene
Paraform
Formaldehyd
Formalin
Oxomethane


L-dopaquinone

Dopaquinone, also known as o-dopaquinone or L-dopaquinone, is a member of the class of compounds known as L-alpha-amino acids. L-alpha-amino acids are alpha-amino acids which have the L-configuration of the alpha-carbon atom. Dopaquinone is slightly soluble (in water) and a moderately acidic compound (based on its pKa). L-Dopaquinone is a metabolite of L-DOPA and a precursor of melanin. Melanin is synthesized from tyrosine by hydroxylation to dihydroxyphenylalanine (DOPA) and subsequent oxidation to dopaquinone. Both reactions are catalyzed by the enzyme tyrosinase, which is the rate-limiting step. Dopaquinone has an ortho-quinone ring, which is known to be neurotoxic and highly reactive with many other compounds (PMID: 413870). Dopaquinone typically combines with cysteine to form pheomelanin (a pigment-polymer). Alternatively, dopaquinone can be converted to leucodopachrome and eventually to eumelanin (also a pigment-polymer). Dopaquinone can be found in skin and feces. Within the cell, dopaquinone is primarily located in the cytoplasm. Dopaquinone is involved in several metabolic disorders, some of which include transient tyrosinemia, hawkinsinuria, tyrosinemia type I, and alkaptonuria. Chronically high levels of dopaquinone are associated with Parkinson's disease (PD). Many Parkinson's patients are treated with L-DOPA. However, long-term treatment with L-DOPA may actually worsen symptoms or result in neurotic and psychotic symptoms. These may be due to dopachrome and dopaquinone accumulating in the brain of L-DOPA treated patients (PMID: 19131041, PMID: 12373519).


Glutathione

Glutathione is a compound synthesized from cysteine, perhaps the most important member of the body's toxic waste disposal team. Like cysteine, glutathione contains the crucial thiol (-SH) group that makes it an effective antioxidant. There are virtually no living organisms on this planet-animal or plant whose cells don't contain some glutathione. Scientists have speculated that glutathione was essential to the very development of life on earth. glutathione has many roles; in none does it act alone. It is a coenzyme in various enzymatic reactions. The most important of these are redox reactions, in which the thiol grouping on the cysteine portion of cell membranes protects against peroxidation; and conjugation reactions, in which glutathione (especially in the liver) binds with toxic chemicals in order to detoxify them. glutathione is also important in red and white blood cell formation and throughout the immune system. glutathione's clinical uses include the prevention of oxygen toxicity in hyperbaric oxygen therapy, treatment of lead and other heavy metal poisoning, lowering of the toxicity of chemotherapy and radiation in cancer treatments, and reversal of cataracts. (http://www.dcnutrition.com/AminoAcids/) glutathione participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It is also important as a hydrophilic molecule that is added to lipophilic toxins and waste in the liver during biotransformation before they can become part of the bile. glutathione is also needed for the detoxification of methylglyoxal, a toxin produced as a by-product of metabolism. This detoxification reaction is carried out by the glyoxalase system. Glyoxalase I (EC 4.4.1.5) catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II (EC 3.1.2.6) catalyzes the hydrolysis of S-D-Lactoyl-glutathione to glutathione and D-lactate. GSH is known as a substrate in both conjugation reactions and reduction reactions, catalyzed by glutathione S-transferase enzymes in cytosol, microsomes, and mitochondria. However, it is also capable of participating in non-enzymatic conjugation with some chemicals, as in the case of n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450-reactive metabolite formed by acetaminophen, that becomes toxic when GSH is depleted by an overdose (of acetaminophen). glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein thiol groups which would otherwise be covalently modified; when all GSH has been spent, NAPQI begins to react with the cellular proteins, killing the cells in the process. The preferred treatment for an overdose of this painkiller is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and renew the usable GSH pool. (http://en.wikipedia.org/wiki/glutathione).


Threonine

Threonine is an essential amino acid in humans. It is abundant in human plasma, particularly in newborns. Severe deficiency of threonine causes neurological dysfunction and lameness in experimental animals. Threonine is an immunostimulant which promotes the growth of thymus gland. It also can probably promote cell immune defense function. This amino acid has been useful in the treatment of genetic spasticity disorders and multiple sclerosis at a dose of 1 gram daily. It is highly concentrated in meat products, cottage cheese and wheat germ. (http://www.dcnutrition.com/AminoAcids/) The threonine content of most of the infant formulas currently on the market is approximately 20% higher than the threonine concentration in human milk. Due to this high threonine content the plasma threonine concentrations are up to twice as high in premature infants fed these formulas than in infants fed human milk. The whey proteins which are used for infant formulas are sweet whey proteins. Sweet whey results from cheese production. Threonine catabolism in mammals appears to be due primarily (70-80%) to the activity of threonine dehydrogenase (EC 1.1.1.103) that oxidizes threonine to 2-amino-3-oxobutyrate, which forms glycine and acetyl CoA, whereas threonine dehydratase (EC 4.2.1.16) that catabolizes threonine into 2-oxobutyrate and ammonia, is significantly less active. Increasing the threonine plasma concentrations leads to accumulation of threonine and glycine in the brain. Such accumulation affects the neurotransmitter balance which may have consequences for the brain development during early postnatal life. Thus, excessive threonine intake during infant feeding should be avoided. (PMID 9853925).


pantetheine 4'-phosphate

Pantetheine 4'-phosphate, or 4'-phosphopantetheine, is a metabolite in the pantothenate and coenzyme A biosynthesis pathway. It can be generated from Pantatheine (via pantothenate kinase 1) or R-4'-Phospho-pantothenoyl-L-cysteine (via phosphopantothenoylcysteine decarboxylase) or Dephospho-CoA (via 4'-phosphopantetheine adenylyl-transferase and ectonucleotide pyrophosphatase). In most mammals, coenzyme A can be hydrolyzed to pantetheine and pantothenate in the intestinal lumen via the following series of reactions: coenzyme A leads to phosphopantetheine leads to pantetheine leads to pantothenate. The conversion of 4'-phosphopantetheine (4'-PP) to dephospho-CoA, is catalyzed by 4'-phosphopantetheine adenylyl-transferase. In mammalian systems, this step may occur in the mitochondria or in the cytosol. (PMID: 1746161) It has been identified as an essential cofactor in in the biosynthesis of fatty acids, polyketides, depsipeptides, peptides, and compounds derived from both carboxylic and amino acid precursors. In particular it is a key prosthetic group of acyl carrier protein (ACP) and peptidyl carrier proteins (PCP) and aryl carrier proteins (ArCP) derived from Coenzyme A. Phosphopantetheine fulfils two demands. Firstly, the intermediates remain covalently linked to the synthases (or synthetases) in an energy-rich thiol ester linkage. Secondly, the flexibility and length of phosphopantetheine chain (approximately 2 nm) allows the covalently tethered intermediates to have access to spatially distinct enzyme active sites.


Aminobutyrates

gamma-Aminobutyric acid (GABA) is an inhibitory neurotransmitter found in the nervous systems of widely divergent species, including humans. It is the chief inhibitory neurotransmitter in the vertebrate central nervous system. In vertebrates, GABA acts at inhibitory synapses in the brain. It acts by binding to specific transmembrane receptors in the plasma membrane of both pre- and postsynaptic neurons. This binding causes the opening of ion channels to allow either the flow of negatively-charged chloride ions into the cell or positively-charged potassium ions out of the cell. This will typically result in a negative change in the transmembrane potential, usually causing hyperpolarization. Three general classes of GABA receptor are known (PMID: 10561820). These include GABA-A and GABA-C ionotropic receptors, which are ion channels themselves, and GABA-B metabotropic receptors, which are G protein-coupled receptors that open ion channels via intermediaries known as G proteins (PMID: 10561820). Activation of the GABA-B receptor by GABA causes neuronal membrane hyperpolarization and a resultant inhibition of neurotransmitter release. In addition to binding sites for GABA, the GABA-A receptor has binding sites for benzodiazepines, barbiturates, and neurosteroids. GABA-A receptors are coupled to chloride ion channels. Therefore, activation of the GABA-A receptor induces increased inward chloride ion flux, resulting in membrane hyperpolarization and neuronal inhibition (PMID: 10561820). After release into the synapse, free GABA that does not bind to either the GABA-A or GABA-B receptor complexes can be taken up by neurons and glial cells. Four different GABA membrane transporter proteins (GAT-1, GAT-2, GAT-3, and BGT-1), which differ in their distribution in the CNS, are believed to mediate the uptake of synaptic GABA into neurons and glial cells. The GABA-A receptor subtype regulates neuronal excitability and rapid changes in fear arousal, such as anxiety, panic, and the acute stress response (PMID: 10561820). Drugs that stimulate GABA-A receptors, such as the benzodiazepines and barbiturates, have anxiolytic and anti-seizure effects via GABA-A-mediated reduction of neuronal excitability, which effectively raises the seizure threshold. GABA-A antagonists produce convulsions in animals and there is decreased GABA-A receptor binding in a positron emission tomography (PET) study of patients with panic disorder. Neurons that produce GABA as their output are called GABAergic neurons and have chiefly inhibitory action at receptors in the vertebrate. Medium spiny neurons (MSNs) are a typical example of inhibitory CNS GABAergic cells. GABA has been shown to have excitatory roles in the vertebrate, most notably in the developing cortex. Organisms synthesize GABA from glutamate using the enzyme L-glutamic acid decarboxylase and pyridoxal phosphate as a cofactor (PMID: 12467378). It is worth noting that this involves converting the principal excitatory neurotransmitter (glutamate) into the principal inhibitory one (GABA). Drugs that act as agonists of GABA receptors (known as GABA analogs or GABAergic drugs), or increase the available amount of GABA typically have relaxing, anti-anxiety, and anti-convulsive effects. GABA is found to be deficient in cerebrospinal fluid and the brain in many studies of experimental and human epilepsy. Benzodiazepines (such as Valium) are useful in status epilepticus because they act on GABA receptors. GABA increases in the brain after administration of many seizure medications. Hence, GABA is clearly an antiepileptic nutrient. Inhibitors of GAM metabolism can also produce convulsions. Spasticity and involuntary movement syndromes, such as Parkinson's, Friedreich's ataxia, tardive dyskinesia, and Huntington's chorea, are all marked by low GABA when amino acid levels are studied. Trials of 2 to 3 g of GABA given orally have been effective in various epilepsy and spasticity syndromes. Agents that elevate GABA are also useful in lowering hypertension. Three grams orally have been effective in controlling blood pressure. GABA is decreased in various encephalopathies. GABA can reduce appetite and is decreased in hypoglycemics. GABA reduces blood sugar in diabetics. Chronic brain syndromes can also be marked by deficiencies of GABA. Vitamin B6, manganese, taurine, and lysine can increase both GABA synthesis and effects, while aspartic acid and glutamic acid probably inhibit GABA effects. Low plasma GABA has been reported in some depressed patients and may be a useful trait marker for mood disorders. GABA has an important role in embryonic development, especially facial development, as substantiated by the association of a cleft palate in transgenic mice deficient in GAD67 (glutamate decarboxylase). A recent Japanese population study reported linkage in patients with a nonsyndromic cleft lip with or without a cleft palate and specific GAD67 haplotypes (PMID: 23842532). Unusually high levels of GABA (especially in the brain) can be toxic and GABA can function as both a neurotoxin and a metabotoxin. A neurotoxin is a compound that damages the brain and/or nerve tissue. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of GABA are associated with at least five inborn errors of metabolism, including D-2-hydroxyglutaric aciduria, 4-hydroxybutyric aciduria/succinic semialdehyde dehydrogenase deficiency, GABA-transaminase deficiency, homocarnosinosis, and hyper beta-alaninemia. Nearly all of these conditions are associated with seizures, hypotonia, intellectual deficits, macrocephaly, encephalopathy, and other serious neurological or neuromuscular problems. Increased levels of GABA seem to alter the function of the GABA-B receptor, which may play a role in the tonic-clonic seizures that are often seen in patients with the above disorders.

3-carboxypropylamine
4-aminobutanoate
4-aminobutanoic acid
4-aminobutyrate
4-aminobutyric acid
Aminalon
Gaba
Gaballon
Gamarex
Gammalon
Gammalone
Gammar
Gammasol
Mielogen
Mielomade
Omega-aminobutyrate
Omega-aminobutyric acid
Piperidate
Piperidic acid
Piperidinate
Piperidinic acid
Gamma aminobutyrate
Gamma aminobutyric acid
Gamma-aminobutyrate
Gamma-aminobutyric acid
W-aminobutyrate
W-aminobutyric acid
G-aminobutyrate
G-aminobutyric acid
γ-aminobutyrate
γ-aminobutyric acid


4a-Methylzymosterol-4-carboxylic acid belongs to the class of organic compounds known as triterpenoids. These are terpene molecules containing six isoprene units. 4a-Methylzymosterol-4-carboxylic acid is considered to be a practically insoluble (in water) and relatively neutral molecule. Within the cell, 4a-methylzymosterol-4-carboxylic acid is primarily located in the membrane (predicted from logP) and cytoplasm. In humans, 4a-methylzymosterol-4-carboxylic acid is involved in the desmosterolosis pathway, the rosuvastatin action pathway, the atorvastatin action pathway, and the alendronate action pathway. 4a-Methylzymosterol-4-carboxylic acid is also involved in several metabolic disorders, some of which include the cholesteryl ester storage disease pathway, the chondrodysplasia punctata II, X linked dominant (CDPX2) pathway, the hypercholesterolemia pathway, and the mevalonic aciduria pathway. 4alpha-Methylzymosterol-4-carboxylic acid is a steroid derivative involved in steroid biosynthesis. It is generated from 14-demethyl-lanosterol via the enzyme methylsterol monooxygenase (EC 1.14.13.72).


Glyoxylic acid

Glyoxylic acid or oxoacetic acid is an organic compound that is both an aldehyde and a carboxylic acid. Glyoxylic acid is a liquid with a melting point of -93°C and a boiling point of 111°C. It is an intermediate of the glyoxylate cycle, which enables certain organisms to convert fatty acids into carbohydrates. The conjugate base of glyoxylic acid is known as glyoxylate (PMID: 16396466). In humans, glyoxylate is produced via two pathways: (1) through the oxidation of glycolate in peroxisomes and (2) through the catabolism of hydroxyproline in mitochondria. In the peroxisomes, glyoxylate is converted into glycine by glyoxylate aminotransferase (AGT1) or into oxalate by glycolate oxidase. In the mitochondria, glyoxylate is converted into glycine by mitochondrial glyoxylate aminotransferase AGT2 or into glycolate by glycolate reductase. A small amount of glyoxylate is converted into oxalate by cytoplasmic lactate dehydrogenase. Glyoxylic acid is found to be associated with primary hyperoxaluria I, which is an inborn error of metabolism. Under certain circumstances, glyoxylate can be a nephrotoxin and a metabotoxin. A nephrotoxin is a compound that causes damage to the kidney and kidney tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. High levels of glyoxylate are involved in the development of hyperoxaluria, a key cause of nephrolithiasis (commonly known as kidney stones). Glyoxylate is both a substrate and inductor of sulfate anion transporter-1 (SAT-1), a gene responsible for oxalate transportation, allowing it to increase SAT-1 mRNA expression, and as a result oxalate efflux from the cell. The increased oxalate release allows the buildup of calcium oxalate in the urine, and thus the eventual formation of kidney stones. As an aldehyde, glyoxylate is also highly reactive and will modify proteins to form advanced glycation products (AGEs).

Formylformate
Formylformic acid
Glyoxalate
Glyoxalic acid
Glyoxylate
Glyoxylic acid
Oxalaldehydate
Oxalaldehydic acid
Oxoacetate
Oxoacetic acid
Oxoethanoate
Oxoethanoic acid
A-ketoacetate
A-ketoacetic acid
Alpha-ketoacetate
Alpha-ketoacetic acid
Glyoxalsaeure
Glyoxylsaeure
α-ketoacetate
α-ketoacetic acid
Oxaldehydate


sphinganine 1-phosphate

Sphinganine 1-phosphate is an intermediate in the metabolism of Glycosphingolipids and sphingolipids. It is a substrate for Sphingosine kinase 1, Lipid phosphate phosphohydrolase 2, Sphingosine kinase 2, Sphingosine-1-phosphate lyase 1, Lipid phosphate phosphohydrolase 1 and Lipid phosphate phosphohydrolase 3.

(2s,3r)-2-amino-3-hydroxyoctadecyl dihydrogen phosphoric acid


3alpha,21-Dihydroxy-5beta-pregnane-11,20-dione is an intermediate in C21-Steroid hormone metabolism. 3alpha,21-Dihydroxy-5beta-pregnane-11,20-dione is converted from Tetrahydrocorticosterone via the enzyme 11beta-hydroxysteroid dehydrogenase (EC 1.1.1.146). It is then converted to 3alpha,20alpha,21-Trihydroxy-5beta-pregnane-11-one via the enzyme 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53).


Fosfructose

Fructose 1,6-bisphosphate is fructose sugar or fructosephosphate that has been phosphorylated on carbons 1 and 6. The beta-D-form of this compound is very common in cells. The vast majority of glucose and fructose entering a cell is converted to fructose 1,6-bisphosphate at some point. Fructose 1,6-bisphosphate is a key component in the glycolysis metabolic pathway and is produced by phosphorylation of fructose 6-phosphate The enzyme phosphofructokinase uses ATP to transfer a phosphate group to fructose 6-phosphate to form fructose 1, 6-bisphosphate. fructose The enzyme aldolase splits fructose 1, 6-bisphosphate into two sugars that are isomers of each other. These two sugars are dihydroxyacetone phosphate and glyceraldehyde phosphate. Fructose 1,6-bisphosphate is an allosteric activator of pyruvate kinase.


NADH

NADH is the reduced form of NAD+, and NAD+ is the oxidized form of NADH, A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). It forms NADP with the addition of a phosphate group to the 2' position of the adenosyl nucleotide through an ester linkage.(Dorland, 27th ed).

Reduced nicotinamide adenine diphosphate

Nicotinamide adenine dinucleotide (reduced)

Reduced nicotinamide adenine dinucleotide


Salicylic acid

Salicylic acid is a colorless, crystalline organic carboxylic acid. Salicylic acid is toxic if ingested in large quantities, but in small quantities is used as a food preservative and antiseptic in toothpaste. It is also the key additive in many skin-care products for the treatment of acne, psoriasis, callouses, corns, keratosis pilaris and warts. The carboxyl group (COOH) can react with alcohols, forming several useful esters. The name derives from the latin word for the willow tree (Salix), from whose bark it can be obtained. --Wikipedia.

2-carboxyphenol
2-hydroxybenzenecarboxylate
2-hydroxybenzenecarboxylic acid
2-hydroxybenzoate
2-hydroxybenzoic acid
Advanced pain relief callus removers
Advanced pain relief corn removers
Clear away wart remover
Compound w
Dr. scholl's callus removers
Dr. scholl's corn removers
Dr. scholl's wart remover kit
Duofil wart remover
Duoplant
Freezone
Ionil
Ionil plus
K 537
K 557
O-carboxyphenol
O-hydroxybenzoate
O-hydroxybenzoic acid
Phenol-2-carboxylate
Phenol-2-carboxylic acid
Psoriacid-s-stift
Retarder w
Rutranex
Salicylate
Salicylic acid
Salicylic acid soap
Salicylic acid collodion
Saligel
Salonil
Stri-dex
Trans-ver-sal


Creatine

Creatine is an amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. Creatine functions as part of the cell's energy shuttle. The high energy phosphate group of ATP is transferred to creatine to form phosphocreatine in the following reaction: Cr + ATP <-> PCr + ADP. This reaction is reversibly catalyzed by creatine kinase. In the human body, creatine is synthesized mainly in the liver by the use of parts from three different amino acids: arginine, glycine, and methionine. 95% of it is later stored in the skeletal muscles and the rest is stored in the brain, heart, and testes.


L-Saccharopine

Saccharopine is an intermediate in the degradation of lysine, formed by the condensation of lysine and alpha-ketoglutarate. The saccharopine pathway is the main route for lysine degradation in mammals, and its first two reactions are catalyzed by enzymatic activities known as lysine-oxoglutarate reductase (LOR) and saccharopine dehydrogenase (SDH), which reside on a single bifunctional polypeptide (LOR/SDH) (EC 1.5.1.8). The reactions involved with saccharopine dehydrogenases have very strict substrate specificity for L-lysine, 2-oxoglutarate, and NADPH. LOR/SDH has been detected in a number of mammalian tissues, mainly in the liver and kidney, contributing not only to the general nitrogen balance in the organism but also to the controlled conversion of lysine into ketone bodies. A tetrameric form has also been observed in human liver and placenta. LOR activity has also been detected in brain mitochondria during embryonic development, and this opens up the question of whether or not lysine degradation has any functional significance during brain development. As a result, there is now a new focus on the nutritional requirements for lysine in gestation and infancy. Finally, LOR and/or SDH deficiencies seem to be involved in a human autosomal genetic disorder known as familial hyperlysinemia, which is characterized by serious defects in the functioning of the nervous system and characterized by a deficiency in lysine-ketoglutarate reductase, saccharopine dehydrogenase, and saccharopine oxidoreductase activities. Saccharopinuria (high amounts of saccharopine in the urine) and saccharopinemia (an excess of saccharopine in the blood) are conditions present in some inherited disorders of lysine degradation (PMID: 463877, 10567240, 10772957, 4809305). If present in sufficiently high levels, saccharopine can act as an acidogen and a metabotoxin. An acidogen is an acidic compound that induces acidosis, which has multiple adverse effects on many organ systems. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Saccharopine is an organic acid. Abnormally high levels of organic acids in the blood (organic acidemia), urine (organic aciduria), the brain, and other tissues lead to general metabolic acidosis. Acidosis typically occurs when arterial pH falls below 7.35. In infants with acidosis, the initial symptoms include poor feeding, vomiting, loss of appetite, weak muscle tone (hypotonia), and lack of energy (lethargy). Many affected children with organic acidemias experience intellectual disability or delayed development.


6-phosphoglucono-delta-lactone (d-6PGL) is the immediate product of the Glucose-6-phosphate dehydrogenase (G-6-PD), the first enzyme of the hexose monophosphate pathway. (PMID 3711719). The pentose-phosphate pathway provides reductive power and nucleotide precursors to the cell through oxidative and nonoxidative branches. 6-Phosphogluconolactonase is the second enzyme of the oxidative branch and catalyzes the hydrolysis of 6-phosphogluconolactones, the products of glucose 6-phosphate oxidation by glucose-6-phosphate dehydrogenase. By efficiently catalyzing the hydrolysis of d-6PGL, 6-phosphogluconolactonase prevents the reaction between d-6PGL and intracellular nucleophiles; such a reaction would interrupt the functioning of the pentose-phosphate pathway. (PMID 11457850).

6-(dihydrogen phosphate)-(8ci)-d-gluconic acid delta-lactone

6-(dihydrogen phosphate)-(9ci)-d-gluconic acid delta-lactone

6-(dihydrogen phosphate)-d-gluconic acid delta-lactone

D-gluconic acid, delta-lactone, 6-(dihydrogen phosphate)


Kynurenine

Kynurenine is a metabolite of the amino acid tryptophan used in the production of niacin. L-Kynurenine is a central compound of the tryptophan metabolism pathway since it can change into the neuroprotective agent kynurenic acid or to the neurotoxic agent quinolinic acid. The break-up of these endogenous compounds' balance can be observable in many disorders such as stroke, epilepsy, multiple sclerosis, and amyotrophic lateral sclerosis. It can also occur in neurodegenerative disorders such as Parkinson's disease, Huntington's, and Alzheimer's disease; and in mental disorders such as schizophrenia and depression.


GDP-4-Dehydro-6-deoxy-D-mannose is an intermediate in the fucosylation of mammalian cells. The functional significance of these fucosylated glycans is unclear, although there is evidence that the sialyl Lex determinant participaates in leukocyte adhesion and trafficking processes. GDP-4-Dehydro-6-deoxy-D-mannose is generated by GDP-D-mannose-4,6-dehydratase (GMD). This compound is then converted by the FX protein (GDP-4-keto-6-D-deoxymannose epimerase/GDP-4-keto-6-L-galactose reductase) to GDP-L-fucose. (PMID: 11698403).

Guanosine 5'-(trihydrogen diphosphate), p'-(6-deoxy-alpha-d-lyxo-hexopyranos-4-ulos-1-yl) ester


beta-Alanine

beta-Alanine is the only naturally occurring beta-amino acid - an amino acid in which the amino group is at the beta-position from the carboxylate group. It is formed in vivo by the degradation of dihydrouracil and carnosine. It is a component of the naturally occurring peptides carnosine and anserine and also of pantothenic acid (vitamin B-5), which itself is a component of coenzyme A. Under normal conditions, beta-alanine is metabolized into acetic acid. beta-Alanine can undergo a transanimation reaction with pyruvate to form malonate-semialdehyde and L-alanine. The malonate semialdehyde can then be converted into malonate via malonate-semialdehyde dehydrogenase. Malonate is then converted into malonyl-CoA and enter fatty acid biosynthesis. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, beta-alanine may act as a false transmitter replacing gamma-aminobutyric acid. When present in sufficiently high levels, beta-alanine can act as a neurotoxin, a mitochondrial toxin, and a metabotoxin. A neurotoxin is a compound that damages the brain or nerve tissue. A mitochondrial toxin is a compound that damages mitochondria and reduces cellular respiration as well as oxidative phosphorylation. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of beta-alanine are associated with at least three inborn errors of metabolism, including GABA-transaminase deficiency, hyper-beta-alaninemia, and methylmalonate semialdehyde dehydrogenase deficiency. beta-Alanine is a central nervous system (CNS) depressant and is an inhibitor of GABA transaminase. The associated inhibition of GABA transaminase and displacement of GABA from CNS binding sites can also lead to GABAuria (high levels of GABA in the urine) and convulsions. In addition to its neurotoxicity, beta-alanine reduces cellular levels of taurine, which are required for normal respiratory chain function. Cellular taurine depletion is known to reduce respiratory function and elevate mitochondrial superoxide generation, which damages mitochondria and increases oxidative stress (PMID: 27023909). Individuals suffering from mitochondrial defects or mitochondrial toxicity typically develop neurotoxicity, hypotonia, respiratory distress, and cardiac failure. beta-Alanine is a biomarker for the consumption of meat, especially red meat.

2-carboxyethylamine
3-amino-propanoate
3-amino-propanoic acid
3-aminopropanoate
3-aminopropanoic acid
3-aminopropionate
3-aminopropionic acid
Abufene
B-alanine
Omega-aminopropionate
Omega-aminopropionic acid
B-aminopropanoate
B-aminopropanoic acid
B-aminopropionate
B-aminopropionic acid
Beta alanine
Beta-alanine
Beta-aminopropanoate
Beta-aminopropanoic acid
Beta-aminopropionate
Beta-aminopropionic acid
β-alanine


ADP-D-ribose

Adenosine diphosphate ribose is a molecule formed into poly(ADP-ribose) or PAR chains by the enzyme poly ADP ribose polymerase or PARP. PARP is found in every cell nucleus. Its main role is to detect and signal single-strand DNA breaks (SSB) to the enzymatic machinery involved in the SSB repair. PARP activation is an immediate cellular response to metabolic, chemical, or radiation-induced DNA SSB damage. Once PARP detects a SSB, it binds to the DNA, and, after a structural change, begins the synthesis of a poly (ADP-ribose) chain (PAR) as a signal for the other DNA-repairing enzymes such as DNA ligase III (LigIII), DNA polymerase beta, and scaffolding proteins such as X-ray cross-complementing gene 1 (XRCC1). After repairing, the PAR chains are degraded via PAR glycohydrolase (PARG). ADP-ribose binds to and activates the TRPM2 ion channel. Adenosine diphosphate ribose is an intermediate in NAD metabolism. The enzyme NAD(P)+ nucleosidase [EC:3.2.2.6] catalyzes the production of this metabolite from nicotinamide adenine dinucleotide phosphate. This reaction is irreversible and occurs in the cytosol.


Cortisone

Cortisone is a naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver into the active metabolite cortisol (Martindale, The Extra Pharmacopoeia, 30th ed, p726). Cortisone is a corticosteroid hormone released by the adrenal gland in response to stress. One of cortisone's effects on the body, and a potentially harmful side effect when administered clinically, is the suppression of the immune system. This is an explanation for the apparent correlation between high stress and sickness (Wikipedia).


desoxycortone

11-Deoxycorticosterone (also called desoxycortone, 21-hydroxyprogesterone, DOC, or simply deoxycorticosterone) is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. It is classified as a member of the 21-hydroxysteroids. 21-hydroxysteroids are steroids carrying a hydroxyl group at the 21-position of the steroid backbone. Deoxycorticosterone is very hydrophobic, practically insoluble (in water), and relatively neutral. Deoxycorticosterone can be synthesized from progesterone by 21-beta-hydroxylase and is then converted to corticosterone by 11-beta-hydroxylase. Corticosterone is then converted to aldosterone by aldosterone synthase. Deoxycorticosterone stimulates the collecting tubules in the kidney to continue to excrete potassium in much the same way that aldosterone does. Deoxycorticosterone has about 1/20 of the sodium retaining power of aldosterone and about 1/5 the potassium excreting power of aldosterone (Wikipedia). Deoxycorticosterone can be found throughout all human tissues and has been detected in amniotic fluid and blood. When present in sufficiently high levels, deoxycorticosterone can act as a hypertensive agent and a metabotoxin. A hypertensive agent increases blood pressure and causes the production of more urine. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels.  Chronically high levels of deoxycorticosterone are associated with congenital adrenal hyperplasia (CAH) and with adrenal tumors producing deoxycorticosterone (PMID: 20671982). High levels of this mineralocorticoid are associated with resistant hypertension, which can result in polyuria, polydipsia, increased blood volume, edema, and cardiac enlargement. Deoxycorticosterone can be used to treat adrenal insufficiency. In particular, desoxycorticosterone acetate (DOCA) is used as replacement therapy in Addison's disease.


CID 28305488

Imidazoleacetic acid, also known as 4(5)-imidazoleacetate or imac, belongs to the class of organic compounds known as imidazolyl carboxylic acids and derivatives. These are organic compounds containing a carboxylic acid chain (of at least 2 carbon atoms) linked to an imidazole ring. Imidazoleacetic acid is soluble (in water) and a weakly acidic compound (based on its pKa). Imidazoleacetic acid has been primarily detected in feces, urine, blood, and cerebrospinal fluid. Within the cell, imidazoleacetic acid is primarily located in the cytoplasm and mitochondria. In humans, imidazoleacetic acid is involved in the histidine metabolism pathway. Imidazoleacetic acid is also involved in the metabolic disorder called the histidinemia pathway. Outside of the human body, imidazoleacetic acid can be found in a number of food items such as pepper (c. frutescens), black-eyed pea, rambutan, and common hazelnut. This makes imidazoleacetic acid a potential biomarker for the consumption of these food products. Imidazoleacetic acid is a metabolite product of Histamine metabolism. It is present in normal urine and increased in histidinemic patients. (PMID 6530403).

1h-imidazol-4-ylacetic acid
1h-imidazole-4-acetic acid
4(5)-imidazoleacetate
4-imidazoleacetate
4-imidazoleacetic acid
Iaa
Imac
Izc
Imidazol-4-ylacetic acid
Imidazole acetate
Imidazole-4-acetate
Imidazole-4-acetic acid
Imidazolyl-4-acetic acid
Lopac-i-0375
Imidazoleacetic acid
1h-imidazole-4-acetate
Imidazol-4-ylacetate
4(5)-imidazoleacetic acid
Imidazoleacetate


Alanine

Alanine is a non-essential amino acid made in the body from either the conversion of the carbohydrate pyruvate or the breakdown of DNA and the dipeptides carnosine and anserine. It is highly concentrated in muscle and is one of the most important amino acids released by muscle, functioning as a major energy source. Plasma alanine is often decreased when the BCAA (branched-chain amino acids) are deficient. This finding may relate to muscle metabolism. Alanine is highly concentrated in meat products and other high-protein foods like wheat germ and cottage cheese. Alanine is an important participant as well as a regulator of glucose metabolism. Alanine levels parallel blood sugar levels in both diabetes and hypoglycemia, and alanine reduces both severe hypoglycemia and the ketosis of diabetes. It is an important amino acid for lymphocyte reproduction and immunity. Alanine therapy has helped dissolve kidney stones in experimental animals. Normal alanine metabolism, like that of other amino acids, is highly dependent upon enzymes that contain vitamin B6. Alanine, like GABA, taurine, and glycine, is an inhibitory neurotransmitter in the brain (http://www.dcnutrition.com/AminoAcids/). L-Alanine has been found to be associated with glucagon deficiency, which is an inborn error of metabolism.

(2s)-2-aminopropanoate
(2s)-2-aminopropanoic acid
(s)-(+)-alanine
(s)-2-aminopropanoate
(s)-2-aminopropanoic acid
(s)-2-amino-propanoate
(s)-2-amino-propanoic acid
(s)-alanine
2-aminopropanoate
2-aminopropanoic acid
2-aminopropionate
2-aminopropionic acid
2-ammoniopropanoate
2-ammoniopropanoic acid
Ala
Alanine
L-(+)-alanine
L-2-aminopropanoate
L-2-aminopropanoic acid
L-2-aminopropionate
L-2-aminopropionic acid
L-a-alanine
L-a-aminopropionate
L-a-aminopropionic acid
L-alpha-alanine
L-alpha-aminopropionate
L-alpha-aminopropionic acid
A-alanine
A-aminopropionate
A-aminopropionic acid
Alpha-alanine
Alpha-aminopropanoate
Alpha-aminopropanoic acid
Alpha-aminopropionate
Alpha-aminopropionic acid
A
L-alanin
L-α-alanine


Leukotriene C4

Leukotriene C4 (LTC4) is a cysteinyl leukotriene (CysLT), a family of potent inflammatory mediators. Eosinophils, one of the principal cell types recruited to and activated at sites of allergic inflammation, is capable of elaborating lipid mediators, including leukotrienes derived from the oxidative metabolism of arachidonic acid (AA). Potentially 'activated' eosinophils may elaborate greater quantities of LTC4, than normal eosinophils. These activated eosinophils thus are 'primed' for enhanced LTC4 generation in response to subsequent stimuli. Some recognized priming stimuli are chemoattractants (e.g., eotaxin, PAF) that may participate in the recruitment of eosinophils to sites of allergic inflammation. The mechanisms by which chemoattractants and other activating cytokines (e.g., interleukin (IL)-5) or extracellular matrix components (e.g., fibronectin) enhance eosinophil eicosanoid formation are pertinent to the functions of these eicosanoids as paracrine mediators of allergic inflammation. Some eosinophil-derived eicosanoids may be active in down-regulating inflammation. It is increasingly likely that eicosanoids synthesized within cells, including eosinophils, may have intracellular (e.g., intracrine) roles in regulating cell functions, in addition to the more recognized activities of eicosanoids as paracrine mediators of inflammation. Acting extracellularly, the cysteinyl leukotrienes (CysLTs) LTC4 and its extracellular derivatives, LTD4 and LTE4 are key paracrine mediators pertinent to asthma and allergic diseases. Based on their receptor-mediated capabilities, they can elicit bronchoconstriction, mucous hypersecretion, bronchial hyperresponsiveness, increased microvascular permeability, and additional eosinophil infiltration. Eosinophils are a major source of CysLTs and have been identified as the principal LTC4 synthase expressing cells in bronchial mucosal biopsies of asthmatic subjects. (PMID: 12895596)Leukotrienes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs) and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes) and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signaling pathways.


Etiocholanedione

Etiocholanedione is a 5-beta metabolite product of the catabolism of androgens. Etiocholanedione has been identified as a ketosteroid and isolated from the urine of healthy and diseased persons. Etiocholanedione has been identified as a metabolite of an altered androgen metabolism that eventually leads hepatocellular carcinoma to impaired hormone responsiveness in human. Etiocholanedione has been identified as a metabolite of 17alpha-hydroxyprogesterone in some patients affected by congenital adrenal hyperplasia, although it doesn't appear to account for the masculinization observed in congenital hyperplasia. Etiocholanedione can be the product of microbial contamination of urine since a few organisms are able to synthesize it using endogenous steroids as substrates. Human axillary bacteria are able to produce small amounts of etiocholanedione from testosterone. (PMID: 12161001, 13795320, 11161304, 2026727).


Bilirubin

Bilirubin is a bile pigment that is a degradation product of heme. In particular, bilirubin is a yellow breakdown product of normal heme catabolism. Its levels are elevated in certain diseases and it is responsible for the yellow colour of bruises. Bilirubin is an excretion product and the body does not control its levels. Bilirubin levels reflect the balance between production and excretion. Thus, there is no "normal" level of bilirubin. Bilirubin consists of an open chain of four pyrroles (tetrapyrrole). In contrast, the heme molecule is a closed ring of four pyrroles, called porphyrin (Wikipedia). Bilirubin is found to be associated with Crigler-Najjar syndrome type I, which is an inborn error of metabolism.


Propylene glycol

Propylene glycol (1,2-propanediol) is an organic compound (a diol alcohol), usually a tasteless, odorless, and colorless clear oily liquid that is hygroscopic and miscible with water, acetone, and chloroform. It is manufactured by the hydration of propylene oxide. Propylene glycol is used as a solvent for intravenous, oral, and topical pharmaceutical preparations It is generally considered safe. However in large doses it can be toxic, especially if given over a short period of time. Intravenous lorazepam contains the largest amount of propylene glycol of commonly used drugs. In adults with normal liver and kidney function, the terminal half-life of propylene glycol ranges from 1.4 to 3.3 hours. Propylene glycol is metabolized by the liver to form lactate, acetate, and pyruvate. The nonmetabolized drug is excreted in the urine mainly as the glucuronide conjugate, approximately 12 to 45 percent is excreted unchanged in urine. Renal clearance decreases as the dose administered increases (390 ml/minute/173 m2 at a dose of 5 g/day but only 144 ml/minute/173 m2 at a dose of 21 g/day). These data suggest that renal clearance declines at higher propylene glycol doses because of saturation of proximal tubular secretion of the drug. As an acceptable level of propylene glycol has not been defined, the clinical implication of a propylene glycol level is unclear. The World Health Organization (WHO) recommends a maximum consumption of 25 mg/kg/day (1.8 g/day for a 75 kg male) of propylene glycol when used as a food additive, but this limit does not address its use as a drug solvent. No maximum dose is recommended in the literature for intravenous therapy with propylene glycol. Intoxication occurs at much higher doses than the WHO dose limit and is exclusive to pharmacologic exposure. Propylene glycol toxicity includes development of serum hyperosmolality, lactic acidosis, and kidney failure. It has been suggested that proximal tubular necrosis is the cause of acute kidney injury from propylene glycol. Along these lines, proximal tubular cell injury occurs in cultured human cells exposed to propylene glycol. Acute tubular necrosis was described with propylene glycol toxicity in a case of concomitant administration of intravenous lorazepam and trimethoprim sulfamethoxazole. Propylene glycol induced intoxication can also mimic sepsis or systemic inflammatory response syndrome (SIRS). Patients suspected of having sepsis with negative cultures should be evaluated for propylene glycol toxicity if they have been exposed to high dose lorazepam or other medications containing this solvent. (PMID: 17555487).

(rs)-1,2-propanediol
1,2-(rs)-propanediol
1,2-dihydroxypropane
1,2-propanediol
1,2-propylene glycol
1,2-propylenglykol
2,3-propanediol
2-hydroxypropanol
Aliphatic alcohol
Chilisa fe
Dl-1,2-propanediol
Dl-propylene glycol
Dowfrost
Glycol
Ilexan p
Inhibited 1,2-propylene glycol
Isopropylene glycol
Methyl glycol
Methylethyl glycol
Methylethylene glycol
Monopropylene glycol
Prolugen
Propane-1,2-diol
Propanediol
Propylene glycol
Propylene glycol usp
Propylenglycol
Sentry propylene glycol
Sirlene
Solar winter ban
Solargard p
Trimethyl glycol
Ucar 35
A-propylene glycol
Alpha-propylene glycol


7,8-dihydroneopterin (H(2)Neo) is produced by human monocyte-derived macrophages upon stimulation with Interferon-gamma. Increased amounts of H(2)Neo in human body fluids are found in many disorders, including viral infections and autoimmune diseases. (PMID 12804528 ).


cholesteryl ester

Cholesteryl docosadienoic acid is a cholesteryl ester. A cholesteryl ester is an ester of cholesterol. Fatty acid esters of cholesterol constitute about two-thirds of the cholesterol in the plasma. Cholesterol is a sterol (a combination steroid and alcohol) and a lipid found in the cell membranes of all body tissues, and transported in the blood plasma of all animals. The accumulation of cholesterol esters in the arterial intima (the innermost layer of an artery, in direct contact with the flowing blood) is a characteristic feature of atherosclerosis. Atherosclerosis is a disease affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part to the deposition of lipoproteins (plasma proteins that carry cholesterol and triglycerides).


GDP-L-fucose

GDP-L-fucose is a sugar nucleotide and a readily available source of fucose. Fucose is a deoxyhexose that is found in nearly all plant and animal species. The monosaccharide plays several important metabolic roles in complex carbohydrates and in glycoproteins. Fucosylated oligosaccharides are involved in cell-cell recognition, selectin-mediated leukocyte-endothelial adhesion, and mouse embryogenesis. They form the basis of the Lewis-type blood group antigens, are involved in the formation of atherosclerosis, and mediate host-bacterial interactions. A decrease in the availability of fucose is associated with leukocyte adhesion deficiency type-II disorder, and fucosylated glycoproteins have been implicated in memory processes. Fucose is made available during the synthesis of fucosylated glycolipids, oligosaccharides, and glycoproteins via a sugar nucleotide intermediate, specifically GDP-L-fucose. GTP-L-fucose pyrophosphorylase (GFPP, E. C. 2.7.7.30) catalyzes the reversible condensation of guanosine triphosphate and beta-L-fucose-1-phosphate to form the nucleotide-sugar GDP-L-fucose. The enzyme functions primarily in the mammalian liver and kidney to salvage free L-fucose during the breakdown of glycolipids and glycoproteins. (PMID: 16086588).

(6-deoxy-beta-l-galactopyranosyl) ester
Gdp fucose
Gdp-beta-l-fucose
Guanosine diphosphate fucose
Guanosine diphosphofucose


dTMP

5-Thymidylic acid is a thymine nucleotide. Also known as thymidine monophosphate, and abbreviated TMP, is a nucleotide that is found in DNA. It is an ester of phosphoric acid with the nucleoside thymidine. TMP consists of a phosphate group, esterified to the the pentose sugar deoxyribose moiety, and the nucleobase thymine. In mammalian cells, thymidine deprivation induces chromosome aberrations such as chromatid breaks, chromatid interchanges, and chromosome fragmentation. (PMID 3888175).

Thymidine 5'-(dihydrogen phosphoric acid)


Riboflavin

Riboflavin or vitamin B2 is an easily absorbed, water-soluble micronutrient with a key role in maintaining human health. Like the other B vitamins, it supports energy production by aiding in the metabolizing of fats, carbohydrates, and proteins. Vitamin B2 is also required for red blood cell formation and respiration, antibody production, and for regulating human growth and reproduction. It is essential for healthy skin, nails, hair growth and general good health, including regulating thyroid activity. Riboflavin is found in milk, eggs, malted barley, liver, kidney, heart, and leafy vegetables. Riboflavin is yellow or orange-yellow in color and in addition to being used as a food coloring it is also used to fortify some foods. It can be found in baby foods, breakfast cereals, sauces, processed cheese, fruit drinks and vitamin-enriched milk products. The richest natural source is yeast. It occurs in the free form only in the retina of the eye, in whey, and in urine; its principal forms in tissues and cells are as flavin mononucleotide and flavin adenine dinucleotide.


Dihydroorotic Acid

L-Dihydroorotic acid, also known as (S)-4,5-dihydroorotate or dihydro-L-orotate, belongs to the class of organic compounds known as alpha amino acids and derivatives. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon), or a derivative thereof. L-Dihydroorotic acid is soluble (in water) and a weakly acidic compound (based on its pKa). Within the cell, L-dihydroorotic acid is primarily located in the cytoplasm and mitochondria. In humans, L-dihydroorotic acid is involved in the pyrimidine metabolism pathway. L-Dihydroorotic acid is also involved in several metabolic disorders, some of which include dihydropyrimidinase deficiency, UMP synthase deficiency (orotic aciduria), the mngie (mitochondrial neurogastrointestinal encephalopathy) pathway, and Beta ureidopropionase deficiency. Outside of the human body, L-dihydroorotic acid can be found in a number of food items such as custard apple, chicory, fox grape, and tarragon. This makes L-dihydroorotic acid a potential biomarker for the consumption of these food products. L-Dihydroorotic acid is an intermediate in the metabolism of Pyrimidine. It is a substrate for Dihydroorotate dehydrogenase (mitochondrial).

(s)-4,5-dihydroorotate
(s)-dihydroorotate
Dihydro-l-orotate
Dihydro-l-orotic acid
L-dihydroorotate
L-dihydroorotic acid
(s)-4,5-dihydroorotic acid


Progesterone

The major progestational steroid that is secreted primarily by the corpus luteum and the placenta. Progesterone acts on the uterus, the mammary glands and the brain. It is required in embryo implantation, pregnancy maintenance, and the development of mammary tissue for milk production. Progesterone, converted from pregnenolone, also serves as an intermediate in the biosynthesis of gonadal steroid hormones and adrenal corticosteroids. -- Pubchem; Progesterone is a C-21 steroid hormone involved in the female menstrual cycle, pregnancy (supports gestation) and embryogenesis of humans and other species. Progesterone belongs to a class of hormones called progestagens, and is the major naturally occurring human progestagen. -- Wikipedia; During implantation and gestation, progesterone appears to decrease the maternal immune response to allow for the acceptance of the pregnancy. Progesterone decreases contractility of the uterine smooth muscle. The fetus metabolizes placental progesterone in the production of adrenal mineralo- and glucosteroids. A drop in progesterone levels is possibly one step that facilitates the onset of labor. In addition progesterone inhibits lactation during pregnancy. The fall in progesterone levels following delivery is one of the triggers for milk production. -- Wikipedia.

17a-progesterone
3,20-pregnene-4
4-pregnen-3,20-dione
4-pregnene-3,20-dione
Agolutin
Bio-luton
Cidr
Colprosterone
Corlutin
Corlutina
Corluvite
Corporin
Corpus luteum hormone
Crinone
Crinone progesterone gel
Curretab
Cyclogest
Cyclogesterin
D4-pregnene-3,20-dione
Delalutin
Duraprogen
Estima
Flavolutan
Fologenon
Gesterol
Gesterol 100
Gesterol 50
Gestiron
Gestone
Gestormone
Gestron
Glanducorpin
Gynlutin
Gynoluton
Gynolutone
Hormoflaveine
Hormoluton
Hydroxyprogesterone caproate
Hydroxyprogesterone caproic acid
Lingusorbs
Lipo-lutin
Lucorteum
Lucorteum sol
Lugesteron
Luteal hormone
Luteocrin normale
Luteodyn
Luteogan
Luteohormone
Luteol
Luteopur
Luteosan
Luteostab
Luteovis
Luteum
Lutex
Lutidon
Lutociclina
Lutocuclin m
Lutocyclin
Lutocyclin m
Lutocylin
Lutocylol
Lutoform
Lutogyl
Lutren
Lutromone
Mpa
Membrettes
Methylpregnone
Nalutron
Percutacrine
Percutacrine luteinique
Piaponon
Pranone
Pregn-4-en-3,20-dione
Pregn-4-ene-3,20-dione
Pregnene-3,20-dione
Pregnenedione
Primolut
Prochieve
Progeffik
Progekan
Progestan
Progestasert
Progesterol
Progesterone
Progesteronum
Progestin
Progestogel
Progestol
Progeston
Progestone
Progestosol
Progestron
Progestronol
Projestaject
Prolets
Prolidon
Prolutin
Proluton
Prolutone
Prometrium
Prontogest
Protormone
Syngesterone
Syngestrets
Synovex s
Syntolutan
Utrogest
Utrogestan
Vitarrine
Beta-progesterone
Delta(sup 4)-pregnene-3,20-dione
(s)-4-pregnene-3,20-dione
(s)-pregn-4-en-3,20-dione
(s)-progesterone
17alpha-progesterone
Akrolutin
Delta(4)-pregnene-3,20-dione
Gelbkoerperhormon
Progesteron
17α-progesterone
δ(4)-pregnene-3,20-dione


allysine

Allysine is a derivative of Lysine, used in the production of elastin and collagen. It is produced by the actions of the enzyme lysyl oxidase in the extracellular matrix and is essential in the crosslink formation that stabilizes collagen and elastin.


Chitin

Chitin is one of the main components in the cell walls of fungi, the exoskeletons of insects and other arthropods (such as crustaceans) as well as fish and frogs. It is a polysaccharide that is constructed from units of acetylglucosamine (more completely, N-acetyl-D-glucose-2-amine). These are linked together in beta-1,4 fashion (in a similar manner to the glucose units which form cellulose). In effect, chitin may be described as cellulose with one hydroxyl group on each monomer replaced by an acetylamine group. This allows for increased hydrogen bonding between adjacent polymers, giving the polymer increased strength. Chitin is the second most abundant polysaccharide in the world (after cellulose). Chitinases break down chitin and are a part of the defence mechanism of mammals against chitin-containing parasites in lower life forms. Under certain circumstances, chitin can act as an allergen. Research using murine models has shown that chitin is a size-dependent microbial-associated molecular pattern (MAMP) that can induce an immunological response via pattern recognition receptors. Medium-sized chitin micro-particles (CMPs) have been shown to induce inflammation, while small-sized CMPs reduce inflammation. Additionally, mammalian chitinases may play a key role in mediating the T-helper 2 cell-driven inflammatory response that is commonly associated with asthma. The high prevalence of asthma among people working with chitinous substances, such as crabs and fungi, suggests that chitin might be an allergen playing a significant role in the development of asthma.


biliverdin

Biliverdin is a green pigment formed as a byproduct of hemoglobin breakdown. It consists of four linearly connected pyrrole rings (a tetrapyrrole). Biliverdin is formed when the heme group in hemoglobin is cleaved at its alpha-methene bridge. The resulting biliverdin is then reduced to bilirubin, a yellow pigment, by the enzyme biliverdin reductase. The changing color of a bruise from deep purple to yellow over time is a graphical indicator of this reaction. Biliverdin occurs in the bile of amphibia and of birds, but not in normal human bile or serum.


3-phosphoglyceric acid

3-phosphoglyceric acid (3PG) is a 3-carbon molecule that is a metabolic intermediate in both glycolysis and the Calvin cycle. This chemical is often termed PGA when referring to the Calvin cycle. In the Calvin cycle, two glycerate 3-phosphate molecules are reduced to form two molecules of glyceraldehyde 3-phosphate (GALP). (wikipedia).

3-(dihydrogen phosphoric acid)glyceric acid


Aspartic acid

Aspartic acid (Asp, D), also known as aspartate, the name of its anion, is one of the 20 natural proteinogenic amino acids which are the building blocks of proteins. As its name indicates, aspartic acid is the carboxylic acid analog of asparagine. As a neurotransmitter, aspartic acid may provide resistance to fatigue and thus lead to endurance, although the evidence to support this idea is not strong (Wikipedia). Aspartic acid is a nonessential amino acid that is made from glutamic acid by enzymes using vitamin B6. The amino acid has important roles in the urea cycle and DNA metabolism. Aspartic acid is a major excitatory neurotransmitter, which is sometimes found to be increased in epileptic and stroke patients. It is decreased in depressed patients and in patients with brain atrophy. Aspartic acid supplements are being evaluated. Five grams can raise blood levels. Magnesium and zinc may be natural inhibitors of some of the actions of aspartic acid. Aspartic acid, with the amino acid phenylalanine, is a part of a new natural sweetener, aspartame. This sweetener is an advance in artificial sweeteners, and is probably safe in normal doses to all except phenylketonurics. The jury is still out on the long-term effects it has on many brain neurohormones. Aspartic acid may be a significant immunostimulant of the thymus and can protect against some of the damaging effects of radiation. Many claims have been made for the special value of administering aspartic acid in the form of potassium and magnesium salts. Since aspartic acid is relatively nontoxic, studies are now in progress to elucidate its pharmacological and therapeutic roles (http://www.dcnutrition.com/AminoAcids).

Asp
(+)-aspartate
(+)-aspartic acid
(2s)-aspartate
(2s)-aspartic acid
(l)-aspartate
(l)-aspartic acid
(r)-2-aminosuccinate
(s)-(+)-aspartate
(s)-(+)-aspartic acid
(s)-2-aminosuccinate
(s)-2-aminosuccinic acid
(s)-aminobutanedioate
(s)-aminobutanedioic acid
(s)-aspartate
(s)-aspartic acid
(s)-amino-butanedioate
(s)-amino-butanedioic acid
2-amino-3-methylsuccinate
2-amino-3-methylsuccinic acid
2-aminosuccinate
2-aminosuccinic acid
Aminosuccinate
Asparagate
Asparagic acid
Asparaginate
Asparaginic acid
Asparatate
Aspartate
H-asp-oh
L-(+)-aspartate
L-(+)-aspartic acid
L-aminosuccinate
L-aminosuccinic acid
L-asparagate
L-asparagic acid
L-asparaginate
L-asparaginic acid
L-aspartate
Alpha-aminosuccinate
Alpha-aminosuccinic acid
(s)-2-aminobutanedioic acid
Aspartic acid
D
L-asparaginsaeure
(s)-2-aminobutanedioate


(R)-3-hydroxybutyric acid

(R)-3-Hydroxybutyric acid is a butyric acid substituted with a hydroxyl group in the beta or 3 position. 3-hydroxybutyric acid, or beta-hydroxybutyrate, is involved in the synthesis and degradation of ketone bodies. Like the other ketone bodies (acetoacetate and acetone), levels of beta-hydroxybutyrate are raised in the blood and urine in ketosis. Beta-hydroxybutyrate is a typical partial-degradation product of branched-chain amino acids (primarily valine) released from muscle for hepatic and renal gluconeogenesis This acid is metabolized by 3-hydroxybutyrate dehydrogenase (catalyzes the oxidation of D-3-hydroxybutyrate to form acetoacetate, using NAD+ as an electron acceptor). The enzyme functions in nervous tissues and muscles, enabling the use of circulating hydroxybutyrate as a fuel. In the liver mitochondrial matrix, the enzyme can also catalyze the reverse reaction, a step in ketogenesis. 3-Hydroxybutyric acid is a chiral compound having two enantiomers, D-3-hydroxybutyric acid and L-3-hydroxybutyric acid. In humans, beta-hydroxybutyrate is synthesized in the liver from acetyl-CoA, and can be used as an energy source by the brain when blood glucose is low. It can also be used for the synthesis of biodegradable plastics (Wikipedia).


glycolaldehyde

Glycolaldehyde (HOCH2-CH=O, IUPAC name 2-hydroxyethanal) is a type of diose (2-carbon monosaccharide). Glycolaldehyde is readily converted to acetyl coenzyme A. It has an aldehyde and a hydroxyl group. However, it is not actually a sugar, because there is only one hydroxyl group. Glycolaldehyde is formed from many sources, including the amino acid glycine and from purone catabolism. It can form by action of ketolase on fructose 1,6-bisphosphate in an alternate glycolysis pathway. This compound is transferred by thiamin pyrophosphate during the pentose phosphate shunt.

Glycolaldehyde
2-hydroxyacetaldehyde
2-hydroxyethanal
2-oh-acetaldehyde
2-oxoethanol
Diose
Glycolic aldehyde
Glycollaldehyde
Hydroxyacetaldehyde
Hydroxyethanal
Methylol formaldehyde
Methylolformaldehyde
Monomethylolformaldehyde
Glycoaldehyde


Streptomycin

Streptomycin is an aminoglycoside antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by binding to the 30S ribosomal subunit of susceptible organisms and disrupting the initiation and elongation steps in protein synthesis. It is bactericidal due to effects that are not fully understood.


2-hydroxyglutaric acid

2-Hydroxyglutarate belongs to the class of organic compounds known as short-chain hydroxy acids and derivatives. These are hydroxy acids with an alkyl chain the contains less than 6 carbon atoms. 2-Hydroxyglutarate is soluble (in water) and a weakly acidic compound (based on its pKa). 2-Hydroxyglutarate has been found in human brain tissue, and has also been detected in most biofluids, including urine, saliva, cerebrospinal fluid, and blood. Within the cell, 2-hydroxyglutarate is primarily located in the cytoplasm and mitochondria. 2-Hydroxyglutarate exists in all living organisms, ranging from bacteria to humans. In humans, 2-hydroxyglutarate is involved in the oncogenic action OF 2-hydroxyglutarate pathway, the oncogenic action OF fumarate pathway, and the oncogenic action OF succinate pathway. 2-Hydroxyglutarate is also involved in a couple of metabolic disorders, which include the oncogenic action OF L-2-hydroxyglutarate in hydroxygluaricaciduria pathway and the oncogenic action OF D-2-hydroxyglutarate in hydroxygluaricaciduria pathway. 2-Hydroxyglutarate has been found to be associated with several diseases known as colorectal cancer, cerebrotendinous xanthomatosis, and deafness, onychodystrophy, osteodystrophy, mental retardation, and seizures syndrome; 2-hydroxyglutarate has also been linked to several inborn metabolic disorders including l-2-hydroxyglutaric aciduria and glutaric aciduria II. 2-hydroxyglutarate is part of the Amino-acid biosynthesis, and Glycine, serine and threonine metabolism pathways. It is a substrate for: D-3-phosphoglycerate dehydrogenase.

Alpha-hydroxyglutaric acid
A-hydroxyglutarate
A-hydroxyglutaric acid
Alpha-hydroxyglutarate
α-hydroxyglutarate
α-hydroxyglutaric acid
2-hydroxyglutarate


Phosphoribosyl pyrophosphate (PRPP) is a pentosephosphate. The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides. It is formed from ribose 5-phosphate by the enzyme ribose-phosphate diphosphokinase. It plays a role in transferring phosphate groups in several reactions. (Wikipedia).

A-d-5-(dihydrogen phosphate) 1-(trihydrogen pyrophosphate) ribofuranose

A-d-ribofuranose, 5-(dihydrogen phosphate) 1-(trihydrogen diphosphate)

Alpha-d-5-(dihydrogen phosphate) 1-(trihydrogen pyrophosphate) ribofuranose

Alpha-d-ribofuranose, 5-(dihydrogen phosphate) 1-(trihydrogen diphosphate)

Alpha-delta-5-(dihydrogen phosphate) 1-(trihydrogen pyrophosphate) ribofuranose

Alpha-d-ribofuranose 5-(dihydrogen phosphate) 1-(trihydrogen diphosphate)

A-d-ribofuranose 5-(dihydrogen phosphate) 1-(trihydrogen diphosphate)

A-d-ribofuranose 5-(dihydrogen phosphoric acid) 1-(trihydrogen diphosphoric acid)

Alpha-d-ribofuranose 5-(dihydrogen phosphoric acid) 1-(trihydrogen diphosphoric acid)

α-d-ribofuranose 5-(dihydrogen phosphate) 1-(trihydrogen diphosphate)

α-d-ribofuranose 5-(dihydrogen phosphoric acid) 1-(trihydrogen diphosphoric acid)


Serine

Serine is a nonessential amino acid derived from glycine. Like all the amino acid building blocks of protein and peptides, serine can become essential under certain conditions, and is thus important in maintaining health and preventing disease. Low-average concentration of serine compared to other amino acids is found in muscle. Serine is highly concentrated in all cell membranes. (http://www.dcnutrition.com/AminoAcids/) L-Serine may be derived from four possible sources: dietary intake; biosynthesis from the glycolytic intermediate 3-phosphoglycerate; from glycine ; and by protein and phospholipid degradation. Little data is available on the relative contributions of each of these four sources of l-serine to serine homoeostasis. It is very likely that the predominant source of l-serine will be very different in different tissues and during different stages of human development. In the biosynthetic pathway, the glycolytic intermediate 3-phosphoglycerate is converted into phosphohydroxypyruvate, in a reaction catalyzed by 3-phosphoglycerate dehydrogenase (3- PGDH; EC 1.1.1.95). Phosphohydroxypyruvate is metabolized to phosphoserine by phosphohydroxypyruvate aminotransferase (EC 2.6.1.52) and, finally, phosphoserine is converted into l-serine by phosphoserine phosphatase (PSP; EC 3.1.3.3). In liver tissue, the serine biosynthetic pathway is regulated in response to dietary and hormonal changes. Of the three synthetic enzymes, the properties of 3-PGDH and PSP are the best documented. Hormonal factors such as glucagon and corticosteroids also influence 3-PGDH and PSP activities in interactions dependent upon the diet. L-serine plays a central role in cellular proliferation. L-Serine is the predominant source of one-carbon groups for the de novo synthesis of purine nucleotides and deoxythymidine monophosphate. It has long been recognized that, in cell cultures, L-serine is a conditional essential amino acid, because it cannot be synthesized in sufficient quantities to meet the cellular demands for its utilization. In recent years, L-serine and the products of its metabolism have been recognized not only to be essential for cell proliferation, but also to be necessary for specific functions in the central nervous system. The findings of altered levels of serine and glycine in patients with psychiatric disorders and the severe neurological abnormalities in patients with defects of L-serine synthesis underscore the importance of L-serine in brain development and function. (PMID 12534373).


dehydroalanine

2-Aminoacrylic acid, also known as 2,3-didehydroalanine or 2-aminoacrylate, belongs to the class of organic compounds known as alpha amino acids. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon). 2-Aminoacrylic acid is soluble (in water) and a moderately acidic compound (based on its pKa). In humans, 2-aminoacrylic acid is involved in thyroid hormone synthesis pathway. Outside of the human body, 2-aminoacrylic acid can be found in a number of food items such as evergreen huckleberry, welsh onion, japanese pumpkin, and lemon grass. This makes 2-aminoacrylic acid a potential biomarker for the consumption of these food products. Dehydroalanine (or (alpha)-(beta)-di-dehydroalanine) is an uncommon amino acid found in peptides of microbial origin (an unsaturated amino acid).

(alpha)-(beta)-di-dehydroalanine
2-aminoacrylate
2-aminoacrylic acid
Dehydroalanine
A-b-di-dehydroalanine
Alpha-beta-di-dehydroalanine
2-aminoprop-2-enoate
2-aminoprop-2-enoic acid


Roxatidine acetate is only found in individuals that have used or taken this drug. It is a specific and competitive H2 receptor antagonist. It is currently approved in South Africa under the tradename Roxit.The H2 antagonists are competitive inhibitors of histamine at the parietal cell H2 receptor. They suppress the normal secretion of acid by parietal cells and the meal-stimulated secretion of acid. They accomplish this by two mechanisms: histamine released by ECL cells in the stomach is blocked from binding on parietal cell H2 receptors which stimulate acid secretion, and other substances that promote acid secretion (such as gastrin and acetylcholine) have a reduced effect on parietal cells when the H2 receptors are blocked.

Roxatidine
Aceroxatidine
Roxatidina
Roxatidinum
Pifatidine
Roxatidine acetic acid


glyceraldehyde 3-phosphate

Glyceraldehyde 3-phosphate (G3P) or triose phosphate is an aldotriose, an important metabolic intermediate in both glycolysis and gluconeogenesis, and in tryptophan biosynthesis. G3P is formed from Fructose-1,6-bisphosphate, Dihydroxyacetone phosphate (DHAP),and 1,3-bisphosphoglycerate, (1,3BPG), and this is how glycerol (as DHAP) enters the glycolytic and gluconeogenesis pathways.

(2-hydroxy-3-oxopropyl) dihydrogen phosphoric acid

Glyceraldehyde 3-(dihydrogen phosphoric acid)


Cysteamine

Cysteamine is a product of the constitutive degradation of coenzyme A, a process that occurs in all tissues, although some tissues such as brain and heart may have exceptionally high coenzyme A turnover rates. Cysteamine has only one known function, and that is as a precursor for the formation of hypotaurine, which is subsequently oxidized to taurine. The rate of cysteamine production as a result of coenzyme A breakdown is not well understood but it is clear that cysteamine levels are not as dramatically affected by dietary habits as are cysteine levels. Cysteamine is generated from hypotaurine by cysteamine dioxygenase (EC:1.13.11.19), an enzyme that was recently identified in mammals (PMID: 17581819). Cysteamine is the simplest stable aminothiol found in the body. It is used in the treatment of disorders of cystine excretion. Cysteamine cleaves the disulfide bond with cysteine to produce molecules that can escape the metabolic defect in cystinosis and cystinuria. Cyst(e)amine may also serve as an endogenous regulator of immune system activity as well as a potential therapeutic agent for the treatment of Huntington disease. Cysteamine is also used as a radiation-protective agent that oxidizes in air to form cystamine. It can be given intravenously or orally to treat radiation sickness. -- Wikipedia.

(2-mercaptoethyl)amine
2-amino-1-ethanethiol
2-aminoethanethiol
2-aminoethyl mercaptan
2-mercaptoethanamine
Aminoethyl mercaptan
Becaptan
Cash
Cisteamina
Cysteamide
Cysteamin
Cysteamine
Cysteinamine
Decarboxycysteine
Ethanethiolamine
Lambraten
Lambratene
Mecramine
Mercamin
Mercamine
Mercaptamin
Mercaptamine
Merkamin
Riacon
Thioethanolamine
B-aminoethanethiol
B-aminoethylthiol
B-mercaptoethylamine
Beta-aminoethanethiol
Beta-aminoethylthiol
Beta-mercaptoethylamine
2-amino-ethanethiol
Beta-mea
Mea
Mercaptamina
Mercaptaminum
β-aminoethanethiol
β-aminoethylthiol
B-mea
β-mea
β-mercaptoethylamine
Cysteaminium


Putrescine

Putrescine is a polyamine. Putrescine is related to cadaverine (another polyamine). Both are produced by the breakdown of amino acids in living and dead organisms and both are toxic in large doses. Putrescine and cadaverine are largely responsible for the foul odor of putrefying flesh, but also contribute to the odor of such processes as bad breath and bacterial vaginosis. Putrescine is also found in semen. Putrescine attacks s-adenosyl methionine and converts it to spermidine. Spermidine in turn attacks another s-adenosyl methionine and converts it to spermine. Putrescine is synthesized in small quantities by healthy living cells by the action of ornithine decarboxylase. The polyamines, of which putrescine is one of the simplest, appear to be growth factors necessary for cell division. Putrescine apparently has specific role in skin physiology and neuroprotection. (PMID: 15009201, 16364196). Pharmacological interventions have demonstrated convincingly that a steady supply of polyamines is a prerequisite for cell proliferation to occur. Genetic engineering of polyamine metabolism in transgenic rodents has shown that polyamines play a role in spermatogenesis, skin physiology, promotion of tumorigenesis and organ hypertrophy as well as neuronal protection. Transgenic activation of polyamine catabolism not only profoundly disturbs polyamine homeostasis in most tissues, but also creates a complex phenotype affecting skin, female fertility, fat depots, pancreatic integrity and regenerative growth. Transgenic expression of ornithine decarboxylase antizyme has suggested that this unique protein may act as a general tumor suppressor. Homozygous deficiency of the key biosynthetic enzymes of the polyamines, ornithine and S-adenosylmethionine decarboxylase is not compatible with murine embryogenesis.


phosphatidyl-N,N-dimethylethanolamine

PE-NMe2(14:0/14:0) is a dimethylphosphatidylethanolamine. It is a glycerophospholipid, and is formed by sequential methylation of phosphatidylethanolamine as part of a mechanism for biosynthesis of phosphatidylcholine. Dimethylphosphatidylethanolamines are usually found at trace levels in animal or plant tissues. They can have many different combinations of fatty acids of varying lengths and saturation attached at the C-1 and C-2 positions.PE-NMe2(14:0/14:0), in particular, consists of two tetradecanoyl chain at positions C-1 and C2. Fatty acids containing 16, 18 and 20 carbons are the most common. Phospholipids, are ubiquitous in nature and are key components of the lipid bilayer of cells, as well as being involved in metabolism and signaling.

dimethylphosphatidylethanolamine DMPE N-dimethylphosphatidylethanolamine phosphatidyl-N-dimethylethanolamine phosphatidyl-N,N-dimethylethanolamine