1-pyrroline-5-carboxylic acid

1-Pyrroline-5-carboxylic acid is an enamine or an imino acid that forms upon the spontaneous dehydration of L-glutamate gamma-semialdehyde in aqueous solutions. The stereoisomer (S)-1-pyrroline-5-carboxylate is an intermediate in glutamate metabolism, arginine degradation, and proline biosynthesis and degradation. It can also be converted into or be formed from three amino acids: L-glutamate, L-ornithine, and L-proline. In particular, it is synthesized via the oxidation of proline by pyrroline-5-carboxylate reductase 1 (PYCR1) (EC 1.5.1.2) or by proline dehydrogenase (PRODH) (EC 1.5.99.8). It is hydrolyzed to L-glutamate by delta-1-pyrroline-5-carboxylate dehydrogenase (ALDH4A1) (EC 1.5.1.12). It is also one of the few metabolites that can act as a precursor to other metabolites of both the urea cycle and the tricarboxylic acid (TCA) cycle. Under certain conditions, pyrroline-5-carboxylate can act as a neurotoxin and a metabotoxin. A neurotoxin causes damage to nerve cells and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of pyrroline-5-carboxylate are associated with at least five inborn errors of metabolism, including hyperprolinemia type I, hyperprolinemia type II, iminoglycinuria, prolinemia type II, and pyruvate carboxylase deficiency. Hyperprolinemia type II results in high levels of pyrroline-5-carboxylate. People with hyperprolinemia type II have signs and symptoms that vary in severity, but they are more likely than type I to have seizures or intellectual disability. Pyrroline-5-carboxylate is highly reactive and excess quantities have been shown to cause cell death and apoptosis (PMID: 15548746).


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


Cysteine

Cysteine is a naturally occurring, sulfur-containing amino acid that is found in most proteins, although only in small quantities. Cysteine is unique amongst the twenty natural amino acids as it contains a thiol group. Thiol groups can undergo oxidation/reduction (redox) reactions; when cysteine is oxidized it can form cystine, which is two cysteine residues joined by a disulfide bond. This reaction is reversible since the reduction of this disulphide bond regenerates two cysteine molecules. The disulphide bonds of cystine are crucial to defining the structures of many proteins. Cysteine is often involved in electron-transfer reactions, and help the enzyme catalyze its reaction. Cysteine is also part of the antioxidant glutathione. N-Acetyl-L-cysteine (NAC) is a form of cysteine where an acetyl group is attached to cysteine's nitrogen atom and is sold as a dietary supplement. Cysteine is named after cystine, which comes from the Greek word kustis meaning bladder (cystine was first isolated from kidney stones). Oxidation of cysteine can produce a disulfide bond with another thiol and further oxidation can produce sulphfinic or sulfonic acids. The cysteine thiol group is also a nucleophile and can undergo addition and substitution reactions. Thiol groups become much more reactive when they are ionized, and cysteine residues in proteins have pKa values close to neutrality, so they are often in their reactive thiolate form in the cell. The thiol group also has a high affinity for heavy metals and proteins containing cysteine will bind metals such as mercury, lead, and cadmium tightly. Due to this ability to undergo redox reactions, cysteine has antioxidant properties. Cysteine is an important source of sulfur in human metabolism, and although it is classified as a non-essential amino acid, cysteine may be essential for infants, the elderly, and individuals with certain metabolic disease or who suffer from malabsorption syndromes. Cysteine may at some point be recognized as an essential or conditionally essential amino acid (Wikipedia). Cysteine is important in energy metabolism. As cystine, it is a structural component of many tissues and hormones. Cysteine has clinical uses ranging from baldness to psoriasis to preventing smoker's hack. In some cases, oral cysteine therapy has proved excellent for treatment of asthmatics, enabling them to stop theophylline and other medications. Cysteine also enhances the effect of topically applied silver, tin, and zinc salts in preventing dental cavities. In the future, cysteine may play a role in the treatment of cobalt toxicity, diabetes, psychosis, cancer, and seizures (http://www.dcnutrition.com/AminoAcids/).

(+)-2-amino-3-mercaptopropionic acid
(2r)-2-amino-3-mercaptopropanoate
(2r)-2-amino-3-mercaptopropanoic acid
(2r)-2-amino-3-sulfanylpropanoate
(2r)-2-amino-3-sulfanylpropanoic acid
(r)-(+)-cysteine
(r)-2-amino-3-mercaptopropanoate
(r)-2-amino-3-mercaptopropanoic acid
(r)-2-amino-3-mercapto-propanoate
(r)-2-amino-3-mercapto-propanoic acid
(r)-cysteine
2-amino-3-mercaptopropanoate
2-amino-3-mercaptopropanoic acid
2-amino-3-mercaptopropionate
2-amino-3-mercaptopropionic acid
3-mercapto-l-alanine
Acetylcysteine
B-mercaptoalanine
Carbocysteine
Cisteina
Cisteinum
Cystein
Cysteine
Cysteinum
Free cysteine
Half-cystine
L cysteine
L-(+)-cysteine
L-2-amino-3-mercaptopropanoate
L-2-amino-3-mercaptopropanoic acid
L-2-amino-3-mercaptopropionic acid
L-cystein
L-cysteine
Polycysteine
Thioserine
Alpha-amino-beta-thiolpropionic acid
Beta-mercaptoalanine
C
Cys
E920
L-zystein
(2r)-2-amino-3-sulphanylpropanoate
(2r)-2-amino-3-sulphanylpropanoic acid
L-2-amino-3-mercaptopropionate


gamma-Glutamylcysteine

gamma-Glutamylcysteine is a dipeptide composed of gamma-glutamate and cysteine, and is a proteolytic breakdown product of larger proteins. It belongs to the family of N-acyl-alpha Amino Acids and Derivatives. These are compounds containing an alpha amino acid which bears an acyl group at its terminal nitrogen atom. gamma-Glutamylcysteine is an incomplete breakdown product of protein digestion or protein catabolism. Some dipeptides are known to have physiological or cell-signaling effects although most are simply short-lived intermediates on their way to specific amino acid degradation pathways following further proteolysis. gamma-Glutamylcysteine is a product of enzyme glutamate-cysteine ligase [EC 6.3.2.2] and a substrate of enzyme glutathione synthase [EC 6.3.2.3] in the glutamate metabolism pathway (KEGG).


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).


oxiglutatione

Oxidized glutathione is a glutathione dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized. 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.


NADPH

Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5'-phosphate (NMN) coupled by pyrophosphate linkage to the 5'-phosphate adenosine 2',5'-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed.).

2'-(dihydrogen phosphate) 5'-(trihydrogen pyrophosphate) adenosine 5'-ester with 1,4-dihydro-1-b-d-ribofuranosylnicotinamide

2'-(dihydrogen phosphate) 5'-(trihydrogen pyrophosphate) adenosine 5'-ester with 1,4-dihydro-1-beta-delta-ribofuranosylnicotinamide

Adenosine 5'-(trihydrogen diphosphate) 2'-(dihydrogen phosphate) p'-5'-ester with 1,4-dihydro-1-beta-d-ribofuranosyl-3-pyridinecarboxamide

Adenosine 5'-(trihydrogen diphosphate) 2'-(dihydrogen phosphate) p'-5'-ester with 1,4-dihydro-1-beta-delta-ribofuranosyl-3-pyridinecarboxamide

Dihydronicotinamide adenine dinucleotide phosphate

Nicotinamide adenine dinucleotide phosphate - reduced


NADP(+)

Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5-phosphate (NMN) coupled by pyrophosphate linkage to the 5-phosphate adenosine 2,5-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed.) Hydrogen carrier in biochemical redox systems. In the hexose monophosphoric acid system it is reduced to Dihydrocoenzyme II and reoxidation in the presence of flavoproteins (Dictionary of Organic Compounds).

B-nicotinamide adenine dinucleotide phosphate

Beta-nicotinamide adenine dinucleotide phosphate

Oxidized nicotinamide-adenine dinucleotide phosphate

B-nicotinamide adenine dinucleotide phosphoric acid

Beta-nicotinamide adenine dinucleotide phosphoric acid

β-nicotinamide adenine dinucleotide phosphate

β-nicotinamide adenine dinucleotide phosphoric acid


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


succinic semialdehyde

Succinic acid semialdehyde (or succinate semialdehyde) is an intermediate in the catabolism of gamma-aminobutyrate or GABA (PMID: 16435183). It is formed from GABA by the action of GABA transaminase, which leads to the production of succinate semialdehyde and alanine. The resulting succinate semialdehyde is further oxidized by succinate semialdehyde dehydrogenase to become succinic acid, which also yields NADPH. Under certain situations, high levels of succinate semialdehyde can function as 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. Elevated serum levels of succinate semialdehyde are found in succinic semialdehyde dehydrogenase (SSADH) deficiency (gamma-hydroxybutyric aciduria), a rare neurometabolic disorder of gamma-aminobutyric acid (GABA) degradation. Symptoms include motor delay, hypotonia, speech delay, autistic features, seizures, and ataxia. Patients also exhibit behavioural problems such as attention deficit, hyperactivity, anxiety, or aggression (PMID: 18622364). Succinate semialdehyde is considered a reactive carbonyl and may lead to increased oxidative stress. This stress is believed to contribute to the formation of free radicals in the brain tissue of animal models induced with SSADH deficiency, which further leads to secondary cell damage and death. Additionally, oxidative stress may be responsible for the loss of striatal dopamine, which may contribute to the neuropathology of SSADH deficiency.

2-formylpropionic acid ethyl ester
3-formylpropanoate
3-formylpropanoic acid
4-oxobutanoate
4-oxobutanoic acid
Butryaldehydate
Butryaldehydic acid
Succinaldehydate
Succinate semialdehyde
Succinic acid semialdehyde
Succinic semialdehyde
Beta-formylpropionate
Beta-formylpropionic acid
Gamma-oxybutyrate
Gamma-oxybutyric acid
3-formylpropionic acid
Semialdehyde succinique
Succinaldehydic acid
3-formylpropionate
B-formylpropionate
B-formylpropionic acid
β-formylpropionate
β-formylpropionic acid


Succinic acid

Succinic acid is a dicarboxylic acid. The anion, succinate, is a component of the citric acid cycle capable of donating electrons to the electron transfer chain. Succinate dehydrogenase (SDH) plays an important role in the mitochondria, being both part of the respiratory chain and the Krebs cycle. SDH with a covalently attached FAD prosthetic group, binds enzyme substrates (succinate and fumarate) and physiological regulators (oxaloacetate and ATP). Oxidizing succinate links SDH to the fast-cycling Krebs cycle portion where it participates in the breakdown of acetyl-CoA throughout the whole Krebs cycle. The succinate can readily be imported into the mitochondrial matrix by the n-butylmalonate- (or phenylsuccinate-) sensitive dicarboxylate carrier in exchange with inorganic phosphate or another organic acid, e. g. malate. (PMID 16143825) Mutations in the four genes encoding the subunits of the mitochondrial respiratory chain succinate dehydrogenase are associated with a wide spectrum of clinical presentations (i.e.: Huntington's disease. (PMID 11803021).

1,2-ethanedicarboxylate
1,2-ethanedicarboxylic acid
1,4-butanedioate
1,4-butanedioic acid
Amber acid
Asuccin
Dihydrofumarate
Dihydrofumaric acid
Katasuccin
Succinate
Wormwood acid
Acide butanedioique
Acide succinique
Acidum succinicum
Bernsteinsaeure
Butandisaeure
Butanedionic acid
E363
Ethylenesuccinic acid
Hooc-ch2-ch2-cooh
Spirit of amber
Butanedionate
Ethylenesuccinate


hydron

Hydrogen ion is recommended by IUPAC as a general term for all ions of hydrogen and its isotopes.  Depending on the charge of the ion, two different classes can be distinguished: positively charged ions and negatively charged ions. Under aqueous conditions found in biochemistry, hydrogen ions exist as the hydrated form hydronium, H3O+, but these are often still referred to as hydrogen ions or even protons by biochemists. [WikiPedia])


smooth endoplasmic reticulum

biolink:CellularComponent biolink:AnatomicalEntity biolink:PhysicalEssence biolink:OrganismalEntity biolink:SubjectOfInvestigation biolink:BiologicalEntity biolink:ThingWithTaxon biolink:NamedThing biolink:PhysicalEssenceOrOccurrent


Pyroglutamic acid (5-oxoproline) is a cyclized derivative of L-glutamic acid. It is an uncommon amino acid derivative in which the free amino group of glutamic acid cyclizes to form a lactam. It is formed nonenzymatically from glutamate, glutamine, and gamma-glutamylated peptides, but it can also be produced by the action of gamma-glutamylcyclotransferase on an L-amino acid. Elevated blood levels may be associated with problems of glutamine or glutathione metabolism. This compound is found in substantial amounts in brain tissue and other tissues in bound form, especially skin. It is also present in plant tissues. It is sold, over the counter, as a "smart drug" for improving blood circulation in the brain. Pyroglutamate in the urine is a biomarker for the consumption of cheese. When present in sufficiently high levels, pyroglutamic acid 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. Chronically high levels of pyroglutamic acid are associated with at least five inborn errors of metabolism including 5-oxoprolinuria, 5-oxoprolinase deficiency, glutathione synthetase deficiency, hawkinsinuria, and propionic acidemia. Pyroglutamic acid 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). These can progress to heart, liver, and kidney abnormalities, seizures, coma, and possibly death. These are also the characteristic symptoms of the untreated IEMs mentioned above. Many affected children with organic acidemias experience intellectual disability or delayed development. In adults, acidosis or acidemia is characterized by headaches, confusion, feeling tired, tremors, sleepiness, and seizures.


bromomethane

Principally used as an insecticidal and nemacidal fumigant, especially for soil and agricultural produce. Also used as a solvent for extraction of plant oils The chemical compound bromomethane, commonly known as methyl bromide, is an organobromine compound with formula CH3Br. This colorless, odorless, nonflammable gas is produced both industrially and particularly biologically. It is a recognized ozone-depleting chemical. It was used extensively as a pesticide until being phased out by most countries in the early 2000s.Bromomethane belongs to the family of Alkyl Bromides. These are organic compounds containing the alkyl bromide functional group with formula R-Br, where R is an alkyl group.

Methyl bromide rodent fumigant (with chloropicrin)


BROMIDE

Hydrogen bromide, also known as HBr or bromure d'hydrogene, belongs to the class of inorganic compounds known as halogen hydrides. These are inorganic compounds in which the heaviest atom bonded to a hydrogen atom is a halogen. Hydrogen bromide is a potentially toxic compound.

[hbr]
Bromure d'hydrogene
Bromwasserstoff
Hbr
Hydrobromic acid
Hydrogenbromid
Hydrobromate


S-Methyl glutathione

S-Methyl-glutathione, also known as S-methyl gsh, belongs to the class of organic compounds known as oligopeptides. These are organic compounds containing a sequence of between three and ten alpha-amino acids joined by peptide bonds. S-Methyl-glutathione is slightly soluble (in water) and a moderately acidic compound (based on its pKa).


Zinc

Zinc is an essential element, necessary for sustaining all life. It is a trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Physiologically, it exists as an ion in the body. It is estimated that 3000 of the hundreds of thousands of proteins in the human body contain zinc prosthetic groups. In addition, there are over a dozen cell types in the human body that secrete zinc ions, and the roles of these secreted zinc signals in medicine and health are now being actively studied. Intriguingly, brain cells in the mammalian forebrain are one type of cell that secretes zinc, along with its other neuronal messenger substances. Cells in the salivary gland, prostate, immune system, and intestine are other types that secrete zinc. Obtaining a sufficient zinc intake during pregnancy and in young children is a problem, especially among those who cannot afford a good and varied diet. Zinc deficiency is associated with anemia, short stature, hypogonadism, impaired wound healing, and geophagia. Brain development is stunted by zinc deficiency in utero and in youth. Zinc is an activator of certain enzymes, such as carbonic anhydrase. Carbonic anhydrase is important in the transport of carbon dioxide in vertebrate blood. Even though zinc is an essential requirement for a healthy body, too much zinc can be harmful. Excessive absorption of zinc can also suppress copper and iron absorption. The free zinc ion in solution is highly toxic to plants, invertebrates, and even vertebrate fish. The Free Ion Activity Model (FIAM) is well-established in the literature and shows that just micromolar amounts of the free ion kill some organisms.


gamma-Glu-Ala

Gamma-Glutamylalanine, also known as 5-L-glutamyl-L-alanine or L-gamma-glu-L-ala, belongs to the class of organic compounds known as dipeptides. These are organic compounds containing a sequence of exactly two alpha-amino acids joined by a peptide bond. Gamma-Glutamylalanine is soluble (in water) and a moderately acidic compound (based on its pKa). In humans, Gamma-glutamylalanine is involved in the glutathione metabolism pathway. Gamma-Glutamylalanine is also involved in several metabolic disorders, some of which include glutathione synthetase deficiency, Gamma-glutamyl-transpeptidase deficiency, Gamma-glutamyltransferase deficiency, and 5-oxoprolinase deficiency.


Cys-Gly

Cysteinylglycine is a naturally occurring dipeptide composed of cysteine and glycine. It is derived from the breakdown of glutathione (a tripeptide). In plasma, cysteinylglycine is in a reduced, oxidized, and protein-bound form (aminothiol) and interacts via redox and disulphide exchange reactions in a dynamic system referred to as redox thiol status (PMID: 8642471). Spermatozoa of sub-fertile men contain significantly higher thiol concentrations as compared with those of fertile men. The detrimental effect on embryo quality of a high homocysteine (Hcy) concentration in the ejaculate and in the follicular fluid is intriguing and may suggest that Hcy is inversely associated with fertility outcome (PMID: 16556671). Rheumatoid arthritis (RA) is a chronic inflammatory disease which involves the synovial membrane of multiple diarthroidal joints causing damage to cartilage and bones. The damage process seems to be related to an overproduction of oxygen reactive species inducing an oxidative perturbation with an increase in some oxidized forms (disulfides and protein mixed disulfides) and a decrease in free thiols (PMID: 15895891). Imipenem (thienamycin formamidine) is a broad-spectrum beta-lactam antibiotic, always used in combination with cilastatin in order to avoid the premature breakdown of imipenem by renal tubular dipeptidase. As this dipeptidase also hydrolyzes the glutathione metabolite cysteinylglycine, the therapeutic association of imipenem and cilastatin causes plasma levels of cysteinylglycine to increase significantly, while cysteine levels are decreased and homocysteine levels are unaffected. Therefore, antibiotic treatment using imipenem-cilastatin induces important metabolic changes that should not remain unrecognized (PMID: 15843241).

N-Cysteinylglycine
N-L-Cysteinylglycine
Cys-Gly
L-Cys-Gly
L-Cysteinylglycine
Cysteinyl-glycine
Cysteine glycine dipeptide
Cysteine-glycine dipeptide
C-G dipeptide
CG dipeptide


Thiamine

Thiamine pyrophosphate is the active form of thiamine, and it serves as a cofactor for several enzymes involved primarily in carbohydrate catabolism. The enzymes are important in the biosynthesis of a number of cell constituents, including neurotransmitters, and for the production of reducing equivalents used in oxidant stress defenses and in biosyntheses and for synthesis of pentoses used as nucleic acid precursors. The chemical structure of TPP is that of an aromatic methylaminopyrimidine ring, linked via a methylene bridge to a methylthiazolium ring with a pyrophosphate group attached to a hydroxyethyl side chain. In non-enzymatic model studies it has been demonstrated that the thiazolium ring can catalyse reactions which are similar to those of TPP-dependent enzymes but several orders of magnitude slower. Using infrared and NMR spectrophotometry it has been shown that the dissociation of the proton from C2 of the thiazolium ring is necessary for catalysis; the abstraction of the proton leads to the formation of a carbanion (ylid) with the potential for a nucleophilic attack on the carbonyl group of the substrate. In all TPP-dependent enzymes the abstraction of the proton from the C2 atom is the first step in catalysis, which is followed by a nucleophilic attack of this carbanion on the substrate. Subsequent cleavage of a C-C bond releases the first product with formation of a second carbanion (2-greek small letter alpha-carbanion or enamine). The formation of this 2-greek small letter alpha-carbanion is the second feature of TPP catalysis common to all TPP-dependent enzymes. Depending on the enzyme and the substrate(s), the reaction intermediates and products differ. Methyl-branched fatty acids, as phytanic acid, undergo peroxisomal beta-oxidation in which they are shortened by 1 carbon atom. This process includes four steps: activation, 2-hydroxylation, thiamine pyrophosphate dependent cleavage and aldehyde dehydrogenation. In the third step, 2-hydroxy-3-methylacyl-CoA is cleaved in the peroxisomal matrix by 2-hydroxyphytanoyl-CoA lyase (2-HPCL), which uses thiamine pyrophosphate (TPP) as cofactor. The thiamine pyrophosphate dependence of the third step is unique in peroxisomal mammalian enzymology. Human pathology due to a deficient alpha-oxidation is mostly linked to mutations in the gene coding for the second enzyme of the sequence, phytanoyl-CoA hydroxylase (EC 1.14.11.18). (PMID: 12694175, 11899071, 9924800).

Tpp
Thpp
Thaimine pyrophosphate
Thiamin diphosphate
Thiamin pyrophosphate
Thiamin-ppi
Thiamine diphosphate
Thiamine pyrophosphate
Thiamine-ppi
Thiamine-pyrophosphate
Thiamin diphosphoric acid
Thiamine(1+) diphosphoric acid
Thiamin pyrophosphoric acid
Thiamine diphosphoric acid


Thioctamide

Lipoamide is the oxidized form of glutathione. (PMID:8957191). Lipoamide is a trivial name for 6,8-dithiooctanoic amide. It is 6,8-dithiooctanoic acid's functional form where the carboxyl group is attached to protein (or any other amine) by an amide linkage (containing -NH2) to an amino group. Lipoamide forms a thioester bond, oxidizing the disulfide bond, with acetaldehyde (pyruvate after it has been decarboxylated). It then transfers the acetaldehyde group to CoA which can then continue in the TCA cycle. (Wikipedia). Lipoamide is an intermediate in glycolysis/gluconeogenesis, citrate cycle (TCA cycle), alanine, aspartate and pyruvate metabolism, and valine, leucine and isoleucine degradation (KEGG:C00248). It is generated from dihydrolipoamide via the enzyme dihydrolipoamide dehydrogenase (EC:1.8.1.4) and then converted to S-glutaryl-dihydrolipoamide via the enzyme oxoglutarate dehydrogenase (EC:1.2.4.2).

1,2-dithiolane-3-pentanamide
5-(1,2-dithiolan-3-yl)-pentanamide
5-(1,2-dithiolan-3-yl)pentanamide
5-(1,2-dithiolan-3-yl)valeramide
5-(dithiolan-3-yl)valeramide
Dl-lipoamide
Dl-6-thioctic amide
Lipamide
Lipoacin
Lipoamid
Lipoicin
Lipozyme
Lypoaran
Pathoclon
Thioami
Thioctamid
Thioctamide
Thioctic acid amide
Thioctic acid amide (jan)
Thiotomin
Ticolin
Vitamin n
Alpha-lipoate
Alpha-lipoic acid
Alpha-lipoic acid amide
A-lipoate amide
A-lipoic acid amide
Alpha-lipoate amide
α-lipoate amide
α-lipoic acid amide
Thioctate amide


Citric acid

Citric acid (citrate) is a weak acid that is formed in the tricarboxylic acid cycle or that may be introduced with diet. The evaluation of plasma citric acid is scarcely used in the diagnosis of human diseases. On the contrary urinary citrate excretion is a common tool in the differential diagnosis of kidney stones, renal tubular acidosis and it plays also a role in bone diseases. The importance of hypocitraturia should be considered with regard to bone mass, urine crystallization and urolithiasis. (PMID 12957820) The secretory epithelial cells of the prostate gland of humans and other animals posses a unique citrate-related metabolic pathway regulated by testosterone and prolactin. This specialized hormone-regulated metabolic activity is responsible for the major prostate function of the production and secretion of extraordinarily high levels of citrate. The key regulatory enzymes directly associated with citrate production in the prostate cells are mitochondrial aspartate aminotransferase, pyruvate dehydrogenase, and mitochondrial aconitase. testosterone and prolactin are involved in the regulation of the corresponding genes associated with these enzymes. The regulatory regions of these genes contain the necessary response elements that confer the ability of both hormones to control gene transcription. Protein kinase c (PKC) is the signaling pathway for the prolactin regulation of the metabolic genes in prostate cells. testosterone and prolactin regulation of these metabolic genes (which are constitutively expressed in all mammalian cells) is specific for these citrate-producing cells. (PMID 12198595) Citric acid is found in citrus fruits, most concentrated in lemons and limes, where it can comprise as much as 8% of the dry weight of the fruit. Citric acid is a natural preservative and is also used to add an acidic (sour) taste to foods and soft drinks. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability. Intolerance to citric acid in the diet is known to exist. Little information is available as the condition appears to be rare, but like other types of food intolerance it is often described as a "pseudo-allergic" reaction.


cis-Aconitate

cis-Aconitic acid is an intermediate in the tricarboxylic acid cycle produced by the dehydration of citric acid. The enzyme aconitase (aconitate hydratase; EC 4.2.1.3) catalyses the stereo-specific isomerization of citrate to isocitrate via cis-aconitate in the tricarboxylic acid cycle.

(1z)-1-propene-1,2,3-tricarboxylate
(1z)-1-propene-1,2,3-tricarboxylic acid
(z)-1-propene-1,2,3-tricarboxylate
(z)-1-propene-1,2,3-tricarboxylic acid
(z)-aconitate
(z)-aconitic acid
1-propene-1,2,3-tricarboxylate
1-propene-1,2,3-tricarboxylic acid
1-cis-2,3-propenetricarboxylate
1-cis-2,3-propenetricarboxylic acid
Cis-1-propene-1,2,3-tricarboxylate
Cis-1-propene-1,2,3-tricarboxylic acid
Cis-aconate
Cis-aconic acid
Cis-aconitate
Cis-aconitic acid
Cis-oxaloacetate
Cis-oxaloacetic acid


isocitric acid

The citrate oxidation to isocitrate is catalyzed by the enzyme aconitase. Human prostatic secretion is remarkably rich in citric acid and low aconitase activity will therefore play a significant role in enabling accumulation of high citrate levels (PubMed ID 8115279).


succinyl-CoA

Succinyl-CoA is an important intermediate in the citric acid cycle, where it is synthesized from α-Ketoglutarate by α-ketoglutarate dehydrogenase (EC 1.2.4.2) through decarboxylation, and is converted into succinate through the hydrolytic release of coenzyme A by succinyl-CoA synthetase (EC 6.2.1.5). Succinyl-CoA may be an end product of peroxisomal beta-oxidation of dicarboxylic fatty acids; the identification of an apparently specific succinyl-CoA thioesterase (ACOT4, EC 3.1.2.3, hydrolyzes succinyl-CoA) in peroxisomes strongly suggests that succinyl-CoA is formed in peroxisomes. Acyl-CoA thioesterases (ACOTs) are a family of enzymes that catalyze the hydrolysis of the CoA esters of various lipids to the free acids and coenzyme A, thereby regulating levels of these compounds. (PMID: 16141203).

Coa s-(hydrogen succinate)
Coa s-succinate
Coenzyme a s-(hydrogen succinate)
Coenzyme a s-succinate
S-(hydrogen butanedioate
S-(hydrogen butanedioate) coa
S-(hydrogen butanedioate) coenzyme a
S-(hydrogen butanedioic acid
S-succinoylcoenzyme a
Suc-co-a
Suc-coa
Succ-coa
Succ-coenzyme a
Succ-s-coa
Succ-s-coenzyme a
Succ-s-coenzyme-a
Succ-coenzyme-a
Succino-1-yl-coenzyme a
Succinyl coa
Succinyl coenzyme a
Succinyl-s-coa
Succinyl-s-coenzyme a
Succinyl-s-coenzyme-a
Succinylcoenzyme-a
Succinylcoenzyme a


(S)-malic acid

Malic acid is a tart-tasting organic dicarboxylic acid that plays a role in many sour or tart foods. Apples contain malic acid, which contributes to the sourness of a green apple. Malic acid can make a wine taste tart, although the amount decreases with increasing fruit ripeness. (wikipedia). In its ionized form malic acid is called malate. Malate is an intermediate of the TCA cycle along with fumarate. It can also be formed from pyruvate as one of the anaplerotic reactions. In humans, malic acid is both derived from food sources and synthesized in the body through the citric acid cycle or Krebs cycle which takes place in the mitochondria. Malate's importance to the production of energy in the body during both aerobic and anaerobic conditions is well established. Under aerobic conditions, the oxidation of malate to oxaloacetate provides reducing equivalents to the mitochondria through the malate-aspartate redox shuttle. During anaerobic conditions, where a buildup of excess of reducing equivalents inhibits glycolysis, malic acid's simultaneous reduction to succinate and oxidation to oxaloacetate is capable of removing the accumulating reducing equivalents. This allows malic acid to reverse hypoxia's inhibition of glycolysis and energy production. In studies on rats it has been found that only tissue malate is depleted following exhaustive physical activity. Other key metabolites from the citric acid cycle needed for energy production were found to be unchanged. Because of this, a deficiency of malic acid has been hypothesized to be a major cause of physical exhaustion. Notably, the administration of malic acid to rats has been shown to elevate mitochondrial malate and increase mitochondrial respiration and energy production.

(-)-(s)-malate
(-)-(s)-malic acid
(-)-hydroxysuccinate
(-)-hydroxysuccinic acid
(-)-l-malic acid
(-)-malic acid
(2s)-2-hydroxybutanedioate
(2s)-2-hydroxybutanedioic acid
(s)-(-)-hydroxysuccinate
(s)-(-)-hydroxysuccinic acid
(s)-hydroxybutanedioate
(s)-hydroxybutanedioic acid
(s)-malic acid
(s)-hydroxy-butanedioate
(s)-hydroxy-butanedioic acid
Apple acid
L-(-)-malic acid
L-apple acid
L-hydroxybutanedioate
L-hydroxybutanedioic acid
L-hydroxysuccinate
L-hydroxysuccinic acid
Malic acid
S-(-)-malate
S-(-)-malic acid
S-2-hydroxybutanedioate
S-2-hydroxybutanedioic acid
L-2-hydroxybutanedioic acid
L-malic acid
Malate
(-)-l-malate
(s)-malate
L-2-hydroxybutanedioate
L-malate


Ubidecarenone

Coenzyme Q10 (ubiquinone) is a naturally occurring compound widely distributed in animal organisms and in humans. The primary compounds involved in the biosynthesis of ubiquinone are 4-hydroxybenzoate and the polyprenyl chain. An essential role of coenzyme Q10 is as an electron carrier in the mitochondrial respiratory chain. Moreover, coenzyme Q10 is one of the most important lipophilic antioxidants, preventing the generation of free radicals as well as oxidative modifications of proteins, lipids, and DNA, it and can also regenerate the other powerful lipophilic antioxidant, alpha-tocopherol. Antioxidant action is a property of the reduced form of coenzyme Q10, ubiquinol (CoQ10H2), and the ubisemiquinone radical (CoQ10H*). Paradoxically, independently of the known antioxidant properties of coenzyme Q10, the ubisemiquinone radical anion (CoQ10-) possesses prooxidative properties. Decreased levels of coenzyme Q10 in humans are observed in many pathologies (e.g. cardiac disorders, neurodegenerative diseases, AIDS, cancer) associated with intensive generation of free radicals and their action on cells and tissues. In these cases, treatment involves pharmaceutical supplementation or increased consumption of coenzyme Q10 with meals as well as treatment with suitable chemical compounds (i.e. folic acid or B-group vitamins) which significantly increase ubiquinone biosynthesis in the organism. Estimation of coenzyme Q10 deficiency and efficiency of its supplementation requires a determination of ubiquinone levels in the organism. Therefore, highly selective and sensitive methods must be applied, such as HPLC with UV or coulometric detection. For a number of years, coenzyme Q (CoQ10 in humans) was known for its key role in mitochondrial bioenergetics; later studies demonstrated its presence in other subcellular fractions and in plasma, and extensively investigated its antioxidant role. These two functions constitute the basis on which research supporting the clinical use of CoQ10 is founded. Also at the inner mitochondrial membrane level, coenzyme Q is recognized as an obligatory co-factor for the function of uncoupling proteins and a modulator of the transition pore. Furthermore, recent data reveal that CoQ10 affects expression of genes involved in human cell signalling, metabolism, and transport and some of the effects of exogenously administered CoQ10 may be due to this property. Coenzyme Q is the only lipid soluble antioxidant synthesized endogenously. In its reduced form, CoQH2, ubiquinol, inhibits protein and DNA oxidation but it is the effect on lipid peroxidation that has been most deeply studied. Ubiquinol inhibits the peroxidation of cell membrane lipids and also that of lipoprotein lipids present in the circulation. Dietary supplementation with CoQ10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoproteins to the initiation of lipid peroxidation. Moreover, CoQ10 has a direct anti-atherogenic effect, which has been demonstrated in apolipoprotein E-deficient mice fed with a high-fat diet. (PMID: 15928598, 17914161).


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.


FADH is the reduced form of flavin adenine dinucleotide (FAD). FAD is synthesized from riboflavin and two molecules of ATP. Riboflavin is phosphorylated by ATP to give riboflavin 5-phosphate (FMN). FAD is then formed from FMN by the transfer of an AMP moiety from a second molecule of ATP. FADH is generated in each round of fatty acid oxidation, and the fatty acyl chain is shortened by two carbon atoms as a result of these reactions; because oxidation is on the beta carbon, this series of reactions is called the beta-oxidation pathway. In the citric acid cycle FADH is involved in harvesting of high-energy electrons from carbon fuels; citric acid cycle itself neither generates a large amount of ATP nor includes oxygen as a reactant. Instead, the citric acid cycle removes electrons from acetyl CoA and uses these electrons to form FADH. (Biochemistry. Berg, Jeremy M. Tymoczko, John L. and Stryer, Lubert. New York: W. H. Freeman and Co. 2002.).

1,5-dihydro-riboflavin 5'-(trihydrogen diphosphate) p'->5'-ester with adenosine

Adenosine 5'-(trihydrogen pyrophosphate), 5'-5'-ester with 5,10-dihydro-7,8-dimethyl-10-(d-ribo-2,3,4,5-tetrahydroxypentyl)alloxazine

Adenosine 5'-(trihydrogen pyrophosphate), 5'->5'-ester with 5,10-dihydro-7,8-dimethyl-10-(d-ribo-2,3,4,5-tetrahydroxypentyl)alloxazine

Adenosine pyrophosphate 5'-5'-ester with 5,10-dihydro-7,8-dimethyl-10-(d-ribo-2,3,4,5-tetrahydroxypentyl)alloxazine

Adenosine pyrophosphate, 5'-5'-ester with 5,10-dihydro-7,8-dimethyl-10-(d-ribo-2,3,4,5-tetrahydroxypentyl)alloxazine

Adenosine pyrophosphate, 5'->5'-ester with 5,10-dihydro-7,8-dimethyl-10-(d-ribo-2,3,4,5-tetrahydroxypentyl)alloxazine

Benzo[g]pteridine riboflavin 5'-(trihydrogen diphosphate) deriv

Benzo[gr]pteridine riboflavin 5'-(trihydrogen diphosphate) deriv


linolenic acid

Alpha-linolenic acid (ALA) is a polyunsaturated fatty acid (PUFA). It is a member of the group of essential fatty acids called omega-3 fatty acids. Alpha-linolenic acid, in particular, is not synthesized by mammals and therefore is an essential dietary requirement for all mammals. Certain nuts (English walnuts) and vegetable oils (canola, soybean, flaxseed/linseed, olive) are particularly rich in alpha-linolenic acid (ALA). Omega-3 fatty acids get their name based on the location of one of their first double bond. In all omega-3 fatty acids, the first double bond is located between the third and fourth carbon atom counting from the methyl end of the fatty acid (n-3). Although humans and other mammals can synthesize saturated and some monounsaturated fatty acids from carbon groups in carbohydrates and proteins, they lack the enzymes necessary to insert a cis double bond at the n-6 or the n-3 position of a fatty acid. Omega-3 fatty acids like a-linolenic acid are important structural components of cell membranes. When incorporated into phospholipids, they affect cell membrane properties such as fluidity, flexibility, permeability and the activity of membrane bound enzymes. Omega-3 fatty acids can modulate the expression of a number of genes, including those involved with fatty acid metabolism and inflammation. Alpha linolenic acid and other omega 3 fatty acids may regulate gene expression by interacting with specific transcription factors, including peroxisome proliferator activated receptors (PPARs) and liver X receptors (LXRs).


MOROCTIC ACID

Stearidonic acid is found in dietary plant oils which are metabolized to longer-chain, more unsaturated (n-3) PUFA. These oils appear to possess hypotriglyceridemic properties typically associated with fish oils.(PMID: 15173404). Stearidonic acid may be used as a precursor to increase the EPA content of human lipids and that combinations of gamma-linolenic acid and stearidonic acid eicosapentaenoic acid can be used to manipulate the fatty acid compositions of lipid pools in subtle ways. Such effects may offer new strategies for manipulation of cell composition in order to influence cellular responses and functions in desirable ways. (PMID: 15120716).

6,9,12,15-octadecatetraenoate
6,9,12,15-octadecatetraenoic acid
Stearidonic acid
Stearidonic acid c18:4
(6z,9z,12z,15z)-octadecatetraenoic acid
Sda
(6z,9z,12z,15z)-octadecatetraenoate
All-cis-octadeca-6,9,12,15-tetraenoate
Stearidonate


Linoleic acid

Linoleic acid is a doubly unsaturated fatty acid, also known as an omega-6 fatty acid, occurring widely in plant glycosides. In this particular polyunsaturated fatty acid (PUFA), the first double bond is located between the sixth and seventh carbon atom from the methyl end of the fatty acid (n-6). Linoleic acid is an essential fatty acid in human nutrition because it cannot be synthesized by humans. It is used in the biosynthesis of prostaglandins (via arachidonic acid) and cell membranes. (From Stedman, 26th ed).

C18:2 9c, 12c omega6 todos cis-9,12-octadienoico


all-cis-8,11,14,17-icosatetraenoic acid

Cis-8,11,14,17-Eicosatetraenoic acid is an eicosanoid present in marine lipids, a minor n-3 polyunsaturated fatty acid (PUFA) which is a position isomer of 20:4n-6. n-3 PUFA contained in marine lipids appear to have a protective effect against coronary heart disease and thrombosis. Human platelets metabolize 8,11,14,17-eicosatetraenoic acid primarily into 12-hydroxy-8,10,14,17-eicosatetraenoic acid. The eicosanoids are a diverse family of molecules that have powerful effects on cell function. They are best known as intercellular messengers, having autocrine and paracrine effects following their secretion from the cells that synthesize them. The diversity of possible products that can be synthesized from eicosatrienoic acid is due, in part to the variety of enzymes that can act on it. Studies have placed many, but not all, of these enzymes at or inside the nucleus. In some cases, the nuclear import or export of eicosatrienoic acid-processing enzymes is highly regulated. Furthermore, nuclear receptors that are activated by specific eicosanoids are known to exist. Taken together, these findings indicate that the enzymatic conversion of eicosatrienoic acid to specific signaling molecules can occur in the nucleus, that it is regulated, and that the synthesized products may act within the nucleus. PMID: 3109494, 8142566, 16574479, 15896193, 10037447). Trans fatty acids are characteristically produced during industrial hydrogenation of plant oils.


Icosapent

Eicosapentaenoic acid (EPA or also icosapentaenoic acid) is an important polyunsaturated fatty acid found in fish oils. It serves as the precursor for the prostaglandin-3 and thromboxane-3 families. A diet rich in eicosapentaenoic acid lowers serum lipid concentration, reduces incidence of cardiovascular disorders, prevents platelet aggregation, and inhibits arachidonic acid conversion into the thromboxane-2 and prostaglandin-2 families. Eicosapentaenoic acid is an omega-3 fatty acid. In physiological literature, it is given the name 20:5(n-3). Its systematic chemical name is all-cis-5,8,11,14,17-icosapentaenoic acid. It also has the trivial name timnodonic acid. Chemically, EPA is a carboxylic acid with a 20-carbon chain and five cis double bonds; the first double bond is located at the third carbon from the omega end. Because of the presence of double bonds, EPS is a polyunsaturated fatty acid. Metabolically it acts as a precursor for prostaglandin-3 (which inhibits platelet aggregation), thromboxane-3, and leukotriene-5 groups. It is found in fish oils of cod liver, herring, mackerel, salmon, menhaden, and sardine. It is also found in human breast milk (Wikipedia).

Cis, cis, cis, cis, cis-eicosa-5,8,11,14,17-pentaenoic acid

Cis, cis, cis, cis, cis-eicosa-5,8,11,14,17-pentaenoate


Docosapentaenoic acid (22n-3) (also known as clupanodonic acid) is an essential omega-3 fatty acid (EFA) which is prevalent in fish oils. Docosapentaenoic acid, commonly called DPA, is an intermediary between eicosapentaenoic acid (EPA, 20:5 ω-3) and docosahexaenoic acid (DHA, 22:6 ω-3). Seal oil is a rich source of this metabolite. There are three functions of docosapentaenoic acid. Most importantly, it is a component of phospholipids found in all animal cell membranes, and a deficiency of docosapentaenoic acid leads to faulty membranes being formed. Secondly, it is involved in the transport and oxidation of cholesterol, and clupanodonic acid tends to lower plasma cholesterol. A third function is as a precursor of prostanoids which are only formed from docosapentaenoic acid. Deficiency of this in experimental animals causes lesions mainly attributable to faulty cellular membranes. Outcomes include sudden failure of growth, lesions of the skin, kidney, and connective tissue, erythrocyte fragility, impaired fertility, and the uncoupling of oxidation and phosphorylation. In humans, pure deficiency of docosapentaenoic acid has been studied particularly in persons fed intravenously. A relative deficiency (that is, a low ratio in the body of docosapentaenoic to long-chain saturated fatty acids and isomers of docosapentaenoate) is common in Western diets and plays an important part in the causation of atherosclerosis, coronary thrombosis, multiple sclerosis, the triopathy of diabetes mellitus, hypertension, and certain forms of malignant disease. Various factors affect the dietary requirement of docosapentaenoic acid (PMID: 6469703).


Gamolenic acid

Gamma-Linolenic acid is an omega-6 fatty acid produced in the body as the delta 6-desaturase metabolite of linoleic acid. It is converted to dihomo-gamma-linolenic acid, a biosynthetic precursor of monoenoic prostaglandins such as PGE1. (From Merck Index, 11th ed) -- Pubchem.


Tetracosapentaenoic acid (24:5N-3), also known as 24:5 (N-3) or 9Z,12Z,15Z,18Z,21Z-tetracosapentaenoate, belongs to the class of organic compounds known as very long-chain fatty acids. These are fatty acids with an aliphatic tail that contains at least 22 carbon atoms. Tetracosapentaenoic acid (24:5N-3) is considered to be a practically insoluble (in water) and relatively neutral molecule. Tetracosapentaenoic acid (24:5N-3) has been primarily detected in urine. Within the cell, tetracosapentaenoic acid (24:5N-3) is primarily located in the cytoplasm, membrane (predicted from logP) and adiposome. In humans, tetracosapentaenoic acid (24:5N-3) is involved in the Alpha linolenic Acid and linoleic Acid metabolism pathway. Tetracosapentaenioc acid is intermediate of alpha-Linolenic acid metabolism.


Nisinic acid

The formation of docosahexaenoic acid(DHA) involves the production of tetracosahexaenoic acid C24:6n-3) from dietary linolenic acid (C18:3n-3) via a series of elongation and desaturation reactions, followed by beta-oxidation of C24:6n-3 to C22:6n-3. DHA is deficient in patients lacking peroxisomes.(PMID: 11734571).


diroleuton

8,11,14-Eicosatrienoic acid is a 20-carbon-chain omega-6 fatty acid unsaturated at positions 8, 11, and 14. It differs from arachidonic acid (5,8,11,14-eicosatetraenoic acid) only at position 5. 8,11,14-Eicosatrienoic acid is also known as dihomo-gamma-linolenic acid (DGLA). In physiological literature, it is given the name 20:3(n-6). DGLA is the elongation product of the 18-carbon gamma-linolenic acid (GLA). DGLA can be converted into prostaglandin E1 (PGE1). PGE1 inhibits platelet aggregation and also exerts a vasodilatory effect. DGLA competes with arachadonic acid for COX and lipoxygenase, inhibiting the production of arachadonic acid's eicosanoids.

(8z,11z,14z)-icosatrienoate
(8z,11z,14z)-icosatrienoic acid
(z,z,z)-8,11,14-eicosatrienoate
(z,z,z)-8,11,14-eicosatrienoic acid
(z,z,z)-8,11,14-icosatrienoate
(z,z,z)-8,11,14-icosatrienoic acid
(z,z,z)-icosatri-8,11,14-enoate
(z,z,z)-icosatri-8,11,14-enoic acid
8,11,14-all-cis-eicosatrienoate
8,11,14-all-cis-eicosatrienoic acid
8,11,14-eicosatrienoate
8,11,14-eicosatrienoic acid
8,11,14-icosatrienoate
8,11,14-icosatrienoic acid
8z,11z,14z-eicosatrienoate
8z,11z,14z-eicosatrienoic acid
All-cis-8,11,14-eicosatrienoate
All-cis-8,11,14-eicosatrienoic acid
Bishomo-gamma-linolenate
Bishomo-gamma-linolenic acid
Dgla
Dihomo-gamma-linolenate
Dihomo-gamma-linolenic acid
Eicosatrienoate
Eicosatrienoic acid
Homo-gamma-linolenate
Cis,cis,cis-8,11,14-eicosatrienoate
Cis,cis,cis-8,11,14-eicosatrienoic acid
Cis-8,11,14-eicosatrienoate
Cis-8,11,14-eicosatrienoic acid
Cis-8,cis-11,cis-14-eicosatrienoate
Cis-8,cis-11,cis-14-eicosatrienoic acid
Gamma-homolinolenate
Gamma-homolinolenic acid
20:3, n-6,9,12 all-cis
8c,11c,14c-eicosatrienoic acid
8c,11c,14c-eicosatriensaeure
All-cis-8,11,14-icosatrienoic acid
All-cis-eicosa-8,11,14-trienoic acid
All-cis-eicosa-8,11,14-triensaeure
C20:3, n-6,9,12 all-cis
Eicosa-8z,11z,14z-trienoic acid
Homo-gamma-linolenic acid
Homo-gamma-linolensaeure
8c,11c,14c-eicosatrienoate
All-cis-8,11,14-icosatrienoate
All-cis-eicosa-8,11,14-trienoate
Dihomo-g-linolenate
Dihomo-g-linolenic acid
Dihomo-γ-linolenate
Dihomo-γ-linolenic acid
Eicosa-8z,11z,14z-trienoate
G-homolinolenate
G-homolinolenic acid
γ-homolinolenate
γ-homolinolenic acid
Homo-g-linolenate
Homo-g-linolenic acid
Homo-γ-linolenate
Homo-γ-linolenic acid
Homo-g-linolensaeure
Homo-γ-linolensaeure
Dihomolinolenate
Dihomolinolenic acid
FA(20:3(8Z,11Z,14Z))


Arachidonate

Arachidonic acid is a polyunsaturated, essential fatty acid that has a 20-carbon chain as a backbone and four cis-double bonds at the C5, C8, C11, and C14 positions. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is synthesized from dietary linoleic acid. Arachidonic acid mediates inflammation and the functioning of several organs and systems either directly or upon its conversion into eicosanoids. Arachidonic acid in cell membrane phospholipids is the substrate for the synthesis of a range of biologically active compounds (eicosanoids) including prostaglandins, thromboxanes, and leukotrienes. These compounds can act as mediators in their own right and can also act as regulators of other processes, such as platelet aggregation, blood clotting, smooth muscle contraction, leukocyte chemotaxis, inflammatory cytokine production, and immune function. Arachidonic acid can be metabolized by cytochrome p450 (CYP450) enzymes into 5,6-, 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acids (EETs), their corresponding dihydroxyeicosatrienoic acids (DHETs), and 20-hydroxyeicosatetraenoic acid (20-HETE). The production of kidney CYP450 arachidonic acid metabolites is altered in diabetes, pregnancy, hepatorenal syndrome, and in various models of hypertension, and it is likely that changes in this system contribute to the abnormalities in renal function that are associated with many of these conditions. Phospholipase A2 (PLA2) catalyzes the hydrolysis of the sn-2 position of membrane glycerophospholipids to liberate arachidonic acid (PMID: 12736897, 12736897, 12700820, 12570747, 12432908).


adrenic acid

Adrenic acid, also known as 7,10,13,16-docosatetraenoic acid or adrenate, is a member of the class of compounds known as very long-chain fatty acids. Very long-chain fatty acids are fatty acids with an aliphatic tail that contains at least 22 carbon atoms. Adrenic acid is practically insoluble (in water) and a weakly acidic compound (based on its pKa). Adrenic acid can be found in blood and in human myelin tissue. Within the cell, adrenic acid is primarily located in the cytoplasm, in the membrane (predicted from logP), and in the peroxisome. It can also be found in the extracellular space. In humans, adrenic acid is involved in alpha-linolenic acid and linoleic acid metabolism. Docosatetraenoic acid designates any straight chain 22:4 fatty acid. In particular, all-cis-7,10,13,16-docosatetraenoic acid is an ω-6 fatty acid with the trivial name adrenic acid (AdA). This is a naturally occurring polyunsaturated fatty acid formed through a 2-carbon chain elongation of arachidonic acid. It is one of the most abundant fatty acids in the early human brain. This unsaturated fatty acid is also metabolized by cells into biologically active products, such as dihomoprostaglandins and dihomo-epoxyeicosatrienoic acids (dihomo-EETs) (Wikipedia). Adrenic acid, which is a prostacyclin inhibitor, appears to be a potential prothrombotic agent (PMID: 1642692).

7,10,13,16-docosatetraenoic acid (van) adrenate

7,10,13,16-docosatetraenoic acid (van) adrenic acid


Tetracosatetraenoic acid n-6 is metabolized to radiolabelled monohydroxylated fatty acids (predominantly the 9-hydroxy positional isomer) but not to other lipoxygenase or cyclooxygenase products by the calcium ionophore-stimulated cells. (PMID: 8049246). Oxidation of tetracosatetraenoic acid n-6 is relatively normal in adrenoleukodystrophy cells and in the cells from one PD,peroxisomal disease patient.


Tetracosapentaenoic acid (24:5N-6), also known as 6Z,9Z,12Z,15Z,18Z-tetracosapentaenoate or C24:5N-6,9,12,15,18, belongs to the class of organic compounds known as very long-chain fatty acids. These are fatty acids with an aliphatic tail that contains at least 22 carbon atoms. Tetracosapentaenoic acid (24:5N-6) is considered to be a practically insoluble (in water) and relatively neutral molecule. Tetracosapentaenoic acid (24:5N-6) has been primarily detected in urine. Within the cell, tetracosapentaenoic acid (24:5N-6) is primarily located in the cytoplasm, membrane (predicted from logP) and adiposome. In humans, tetracosapentaenoic acid (24:5N-6) is involved in the Alpha linolenic Acid and linoleic Acid metabolism pathway. Tetracosapentaenioc acid is intermediate of Linolenic acid metabolism.


Phosphatidylcholine

PC(18:3(9Z,12Z,15Z)/18:2(9Z,12Z)) is a phosphatidylcholine (PC or GPCho). It is a glycerophospholipid in which a phosphorylcholine moiety occupies a glycerol substitution site. As is the case with diacylglycerols, glycerophosphocholines can have many different combinations of fatty acids of varying lengths and saturation attached at the C-1 and C-2 positions. Fatty acids containing 16, 18 and 20 carbons are the most common. PC(18:3(9Z,12Z,15Z)/18:2(9Z,12Z)), in particular, consists of one chain of a-linolenic acid at the C-1 position and one chain of linoleic acid at the C-2 position. The a-linolenic acid moiety is derived from seed oils, especially canola and soybean oil, while the linoleic acid moiety is derived from seed oils. Phospholipids, are ubiquitous in nature and are key components of the lipid bilayer of cells, as well as being involved in metabolism and signaling.While most phospholipids have a saturated fatty acid on C-1 and an unsaturated fatty acid on C-2 of the glycerol backbone, the fatty acid distribution at the C-1 and C-2 positions of glycerol within phospholipids is continually in flux, owing to phospholipid degradation and the continuous phospholipid remodeling that occurs while these molecules are in membranes. PCs can be synthesized via three different routes. In one route, choline is activated first by phosphorylation and then by coupling to CDP prior to attachment to phosphatidic acid. PCs can also synthesized by the addition of choline to CDP-activated 1,2-diacylglycerol. A third route to PC synthesis involves the conversion of either PS or PE to PC.


Calcium cation

Calcium is essential for the normal growth and maintenance of bones and teeth, and calcium requirements must be met throughout life. Requirements are greatest during periods of growth, such as childhood, during pregnancy and when breast-feeding. Long-term calcium deficiency can lead to osteoporosis, in which the bone deteriorates and there is an increased risk of fractures. Adults need between 1,000 and 1,300 mg of calcium in their daily diet. Calcium is essential for living organisms, particularly in cell physiology, and is the most common metal in many animals. Physiologically, it exists as an ion in the body. Calcium combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. Calcium is an important component of a healthy diet. A deficit can affect bone and tooth formation, while overretention can cause kidney stones. Vitamin D is needed to absorb calcium. Dairy products, such as milk and cheese, are a well-known source of calcium. However, some individuals are allergic to dairy products and even more people, particularly those of non-European descent, are lactose-intolerant, leaving them unable to consume dairy products. Fortunately, many other good sources of calcium exist. These include: seaweeds such as kelp, wakame and hijiki; nuts and seeds (like almonds and sesame); beans; amaranth; collard greens; okra; rutabaga; broccoli; kale; and fortified products such as orange juice and soy milk. Calcium has also been found to assist in the production of lymphatic fluids.

Ca
Calcium element
Ca(2+)
Ca2+
Calcium ion
Calcium, doubly charged positive ion


Doconexent

Docosahexaenoic acid (DHA) is an omega-3 essential fatty acid. Chemically, DHA is a carboxylic acid with a 22-carbon chain and six cis double bonds with the first double bond located at the third carbon from the omega end. DHA is most often found in fish oil. It is a major fatty acid in sperm and brain phospholipids, especially in the retina. Dietary DHA can reduce the level of blood triglycerides in humans, which may reduce the risk of heart disease (Wikipedia). Docosahexaenoic acid is found to be associated with isovaleric acidemia, which is an inborn error of metabolism.


Osbond acid

Docosapentaenoic acid is an unsaturated fatty acid found in fish oils. It is a minor constituent of the total serum unsaturated fatty acids in humans. Docosapentaenoic acid (22n-6) is practically insoluble (in water) and a weakly acidic compound (based on its pKa). Docosapentaenoic acid (22n-6) can be found in blood and urine, as well as in human adipose tissue, fibroblasts, and platelet tissues. Within the cell, docosapentaenoic acid (22n-6) is primarily located in the membrane (predicted from logP). It can also be found in the extracellular space. In humans, docosapentaenoic acid (22n-6) is involved in alpha linolenic acid and linoleic acid metabolism. Docosapentaenoic acid (22n-6) is found to be associated with thyroid cancer.


Selenocysteine

Selenocysteine is an amino acid that is present in several enzymes (for example glutathione peroxidases, tetraiodothyronine 5' deiodinases, thioredoxin reductases, formate dehydrogenases, glycine reductases and some hydrogenases). Selenocysteine has a structure similar to cysteine, but with an atom of selenium taking the place of the usual sulfur. Proteins that include a selenocysteine residue are called selenoproteins (Wikipedia). Selenocysteine is a naturally occurring amino acid in both eukaryotic and prokaryotic organisms. It is found in tRNAs and in the catalytic site of some enzymes. The genes for glutathione peroxidase and formate dehydrogenase contain the TGA codon, which codes for this amino acid (Pubchem).


selane

Hydrogen selenide is a metabolite of selenium which could have potential antiangiogenic effect in the chemoprevention of cancer. The hydrogen selenide is a key intermediate in the selenium methylation metabolism of inorganic and organic selenium compounds. Accumulation of the hydrogen selenide resulting from inhibition of the selenium methylation metabolism, detoxification metabolic pathway of selenium, is found in animals following repeated administration of a toxic dose of selenocystine. The excess of the hydrogen selenide produced by inhibition of the selenium methylation metabolism contributes to the hepatotoxicity caused by selenocystine. (PMID: 9414580, 11799926).

Dihydrogen monoselenide
Dihydrogen selenide
Hydrogen selenide
Selane
Selenium dihydride
Selenium hydride
Selenium hydride (seh2)
[seh2]
H2se
Hydroselenic acid
Hydroselenate


selenophosphoric acid

Phosphoroselenoic acid, H3SePO3, is the activated selenium donor compound required for the biosynthesis of selenocysteyl-tRNA, the precursor of specific selenocysteine residues in bacterial and mammalian selenoproteins. Selenocysteine is the 21st amino acid, because Sec has a specific tRNA and codon UGA, and shares a major stop codon UGA. A number of enzymes have selenocysteine, residues and in some cases at their active sites. Proteins containing the 21st amino acid, selenocysteine (Sec), have been described in all three domains of life. (PMID: 18156471).

Monoselenophosphoric acid
Sepo3
Selenophosphoric acid
Trihydroxidoselenidophosphorus
[p(oh)3se]
Selenophosphate


selenocystathionine

Selenocystathionine is formed from Selenohomocysteine by the enzyme cystathionine beta-synthase (EC 4.2.1.22), as a by-product of cystathionine synthesis. Selenocystathionine is consumed in the diet, and is one of the main compounds present in plants that tend to hyperaccumulate selenium and use it as an elemental plant defense mechanism. (PMID: 10026151, 6456763, 16920881).


2-Ketobutyric acid is a substance that is involved in the metabolism of many amino acids (glycine, methionine, valine, leucine, serine, threonine, isoleucine) as well as propanoate metabolism and C-5 branched dibasic acid metabolism. More specifically, alpha-ketobutyric acid is a product of the lysis of cystathionine. It is also one of the degradation products of threonine. It can be converted into propionyl-CoA (and subsequently methylmalonyl CoA, which can be converted into succinyl CoA, a citric acid cycle intermediate), and thus enter the citric acid cycle.

2-ketobutanoate
2-ketobutanoic acid
2-ketobutyrate
2-oxo-butanoate
2-oxo-butanoic acid
2-oxo-butyrate
2-oxo-butyric acid
2-oxo-n-butyrate
2-oxo-n-butyric acid
2-oxobutanoate
2-oxobutanoic acid
2-oxobutyrate
2-oxobutyric acid
3-methylpyruvate
3-methylpyruvic acid
Methyl-pyruvate
Methyl-pyruvic acid
Propionyl-formate
Propionyl-formic acid
A-keto-n-butyrate
A-keto-n-butyric acid
A-ketobutyrate
A-ketobutyric acid
A-oxo-n-butyrate
A-oxo-n-butyric acid
A-oxobutyrate
A-oxobutyric acid
Alpha-keto-n-butyrate
Alpha-keto-n-butyric acid
Alpha-ketobutric acid
Alpha-ketobutyrate
Alpha-ketobutyric acid
Alpha-oxo-n-butyrate
Alpha-oxo-n-butyric acid
Alpha-oxobutyrate
Alpha-oxobutyric acid
2-ketobutyric acid
3-methyl pyruvic acid
3-methyl pyruvate
α-ketobutyrate
α-ketobutyric acid
α-oxo-n-butyrate
α-oxo-n-butyric 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).


L-selenohomocysteine zwitterion

Selenohomocysteine is the precursor of selenocysteine, which is synthesized by catalysis of cystathionine beta-synthase (EC 4.2.1.22) and cystathionine gamma-lyase (EC 4.4.1.1), in mammalian systems (both enzymes require pyridoxal phosphate). Selenohomocysteine (lactone) has been found to be a competitive and irreversible inhibitor of lysyl oxidase; this may relate to the development of connective tissue defects seen in homocystinuria. L-Selenohomocysteine also can serve as a substituent donor in the beta-replacement reaction to yield selenocystathionine. (PMID: 10609891, 9405445, 6456763, 3338973).

2-amino-4-selanyl-butanoate
2-amino-4-selanyl-butanoic acid
Se-selenocysteine


Se-Adenosylselenohomocysteine is an intermediate in Selenoamino acid metabolism. Se-Adenosylselenohomocysteine is the second to last step in the synthesis of Selenohomocystine and is converted from Se-Adenosylselenomethionine via the enzyme Transferases (EC 2.1.1.-). It is then. converted to Selenohomocysteine via the enzyme adenosylhomocysteinase (EC 3.3.1.1).


L-adenosylselenomethionine zwitterion

Se-Adenosylselenomethionine is an intermediate in Selenoamino acid metabolism. Se-Adenosylselenomethionine is converted from Selenomethionine via the enzyme S-adenosylmethionine synthetase (EC 2.5.1.6). It is then. converted to Se-Adenosylselenohomocysteine via the enzyme Transferases (EC 2.1.1.-).


selenomethionine

Selenomethionine is an amino acid containing selenium that cannot be synthesized by higher animals, but can be obtained from plant material. Selenomethionine is the major seleno-compound in cereal grains (wheat grain, maize and rice), soybeans and enriched yeast. Seleno-compounds present in plants may have a profound effect upon the health of animals and human subjects. It is now known that the total Se content cannot be used as an indication of its efficacy, but knowledge of individual selenocompounds is necessary to fully assess the significance. Thus, speciation of the seleno-compounds has moved to the forefront. Since animals and man are dependent upon plants for their nutritional requirements, this makes the types of seleno-compounds in plants even more critical. Se enters the food chain through incorporation into plant proteins, mostly as selenocysteine and selenomethionine at normal Se levels. There are two possible pathways for the catabolism of selenomethionine. One is the transsulfuration pathway via selenocystathionine to produce selenocysteine, which in turn is degraded to H2Se by the enzyme b-lyase. The other pathway is the transamination-decarboxylation pathway. It was estimated that 90% of methionine is metabolized through this pathway and thus could be also the major route for selenomethionine catabolism. (PMID: 14748935, Br J Nutr. 2004 Jan;91(1):11-28.).


Selenic acid

Selenate, also known as sodium selenate or [seo2(OH)2], belongs to the class of inorganic compounds known as non-metal selenates. These are inorganic non-metallic compounds containing a selenate as its largest oxoanion. Selenate has been primarily detected in urine. Selenate exists in all living organisms, ranging from bacteria to humans. Outside of the human body, selenate can be found in a number of food items such as turmeric, roman camomile, savoy cabbage, and other soy product. This makes selenate a potential biomarker for the consumption of these food products. Selenate is a potentially toxic compound.


adenylyl selenate

Adenylylselenate is an intermediate in selenoamino acid metabolism. Adenylylselenate is produced from selenate via the enzyme sulfate adenylyltransferase [EC:2.7.7.4] and then converted to selenite via the enzyme adenylylsulfate reductase [EC:1.8.99.2]. The reaction between adenylselenate and adenylylsulfate kinase [EC:2.7.1.25] also gives rise to the 3'-Phosphoadenylylselenate.

Adenosine-5'-phosphoselenate
Adenylylselenic acid
Adenylylselenate
Adenosine-5'-phosphoselenic acid


3'-phosphoadenylyl selenate

3-Phosphoadenylylselenate belongs to the class of organic compounds known as purine ribonucleoside 3',5'-bisphosphates. These are purine ribobucleotides with one phosphate group attached to 3' and 5' hydroxyl groups of the ribose moiety. 3-Phosphoadenylylselenate is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). 3-Phosphoadenylylselenate exists in all living organisms, ranging from bacteria to humans. In humans, 3-phosphoadenylylselenate is involved in the selenoamino acid metabolism pathway. 3-Phosphoadenylylselenate participates in selenoamino acid metabolism. 3-phosphoadenylylselenate is converted from adenylylselenate via adenylylsulfate kinase (EC: 2.7.1.25).


Methylselenocysteine

Se-Methylselenocysteine (SeMSC) is a naturally occurring seleno-amino acid that is synthesized by plants such as garlic, astragalus, onions and broccoli. Unlike selenomethionine, which is incorporated into proteins in place of methionine, SeMSC is not incorporated into any proteins, thereby being fully available for the synthesis of selenium-containing enzymes such as glutathione peroxidase.

3-(methylseleno)-l-alanine
Methylselenocysteine
Se-methyl-l-selenocysteine
Selenium-methylselenocystine
L-methylselenocysteine
Methyl-l-selenocysteine
Se-methyl-seleno-l-cysteine
Se-methyl-selenocysteine
Se-methylselenocysteine
Selenium methyl cysteine
Selenohomocysteine
Selenomethylselenocysteine
(2r)-2-amino-3-methylselanylpropanoate


Gamma-Glutamyl-se-methylselenocysteine, also known as gamma-glutamyl-semc or GGMSC CPD, belongs to the class of organic compounds known as dipeptides. These are organic compounds containing a sequence of exactly two alpha-amino acids joined by a peptide bond. Gamma-Glutamyl-se-methylselenocysteine is soluble (in water) and a moderately acidic compound (based on its pKa). Gamma-Glutamyl-se-methylselenocysteine exists in all living organisms, ranging from bacteria to humans. In humans, Gamma-glutamyl-se-methylselenocysteine is involved in the selenoamino acid metabolism pathway. gamma-Glutamyl-Se-methylselenocysteine is an intermediate in selenoamino acid metabolism(KEGG ID C05695). It is generated from Se-methyl-selenocysteine via the enzyme gamma-glutamyltranspeptidase [EC:2.3.2.2].


The selenite anion is a selenium oxoanion with the chemical formula SeO32&#8722. A selenite (compound) is a compound that contains this ion. In slightly acid conditions, the hydrogenselenite ion, HSeO3−, is formed; in more acidic conditions selenous acid, H2SeO3, exists. Most selenite salts can be formed by heating the relevant metal oxide with selenium dioxide, e.g.:Na2O + SeO2 → Na2SeO3. Selenite is an inorganic form of selenium which may also be useful in cancer chemotherapy.(Wikipedia).

Selenite (seo32-)
Selenite ion (seo32-)
Selenite ion(2-)
Selenite(2-)
[seo3](2-)
Selenit


selenocystine

Selenocystine 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). Selenocystine is soluble (in water) and an extremely strong acidic compound (based on its pKa). Selenocystine has been primarily detected in blood. Within the cell, selenocystine is primarily located in the cytoplasm. In humans, selenocystine is involved in the selenoamino acid metabolism pathway. Selenocystine is a substrate for glutathione peroxidase 1.

3,3'-diselenobisalanine
3,3'-diselenodialanine
D,l-selenocystine
Dl-selenocystine
Selenium cystine
Seleno-dl-cystine


Potassium is an essential electrolyte. Potassium balance is crucial for regulating the excitability of nerves and muscles and so critical for regulating contractility of cardiac muscle. Although the most important changes seen in the presence of deranged potassium are cardiac, smooth muscle is also affected with increasing muscle weakness, a feature of both hyperkalaemia and hypokalaemia. Physiologically, it exists as an ion in the body. Potassium (K+) is a positively charged electrolyte, cation, which is present throughout the body in both intracellular and extracellular fluids. The majority of body potassium, >90%, are intracellular. It moves freely from intracellular fluid (ICF) to extracellular fluid (ECF) and vice versa when adenosine triphosphate increases the permeability of the cell membrane. It is mainly replaced inside or outside the cells by another cation, sodium (Na+). The movement of potassium into or out of the cells is linked to certain body hormones and also to certain physiological states. Standard laboratory tests measure ECF potassium. Potassium enters the body rapidly during food ingestion. Insulin is produced when a meal is eaten; this causes the temporary movement of potassium from ECF to ICF. Over the ensuing hours, the kidneys excrete the ingested potassium and homeostasis is returned. In the critically ill patient, suffering from hyperkalaemia, this mechanism can be manipulated beneficially by administering high concentration (50%) intravenous glucose. Insulin can be added to the glucose, but glucose alone will stimulate insulin production and cause movement of potassium from ECF to ICF. The stimulation of alpha receptors causes increased movement of potassium from ICF to ECF. A noradrenaline infusion can elevate serum potassium levels. An adrenaline infusion, or elevated adrenaline levels, can lower serum potassium levels. Metabolic acidosis causes a rise in extracellular potassium levels. In this situation, excess of hydrogen ions (H+) are exchanged for intracellular potassium ions, probably as a result of the cellular response to a falling blood pH. Metabolic alkalosis causes the opposite effect, with potassium moving into the cells. (PMID: 17883675).

K+
Kalium
Potassium
Potassium (k+)
Potassium (ion)
Potassium cation
Potassium ion
Potassium ion (k+)
Potassium ion (k1+)
Potassium ion(+)
Potassium ion(1+)
Potassium monocation
Potassium(+)
Potassium(1+)
Potassium(1+) ion
Potassium(i) cation
K(+)


CBS_HUMAN Cystathionine beta-synthase (sprot)


Chitobiose

Chitobiose, also known as CBS or chitodextrin, belongs to the class of organic compounds known as acylaminosugars. These are organic compounds containing a sugar linked to a chain through N-acyl group. Chitobiose is soluble (in water) and a weakly acidic compound (based on its pKa). Chitobiose has been found in human testicle tissue. Within the cell, chitobiose is primarily located in the cytoplasm. In humans, chitobiose is involved in the amino sugar metabolism pathway. Chitobiose is also involved in several metabolic disorders, some of which include the tay-sachs disease pathway, the sialuria or french type sialuria pathway, the g(m2)-gangliosidosis: variant b, tay-sachs disease pathway, and the salla disease/infantile sialic Acid storage disease pathway. Chitobiose is a dimer of beta-1,4-linked glucosamine units. There is ambiguity as to which structure the name refers, owing to the method by which it was first isolated.


N-acetyl-D-glucosamine

N-Acetyl-D-Glucosamine (N-acetlyglucosamine) is a monosaccharide derivative of glucose. Chemically it is an amide between glucosamine and acetic acid. A single N-acetlyglucosamine moiety linked to serine or threonine residues on nuclear and cytoplasmic proteins -O-GlcNAc, is an ubiquitous post-translational protein modification. O-GlcNAc modified proteins are involved in sensing the nutrient status of the surrounding cellular environment and adjusting the activity of cellular proteins accordingly. O-GlcNAc regulates cellular responses to hormones such as insulin, initiates a protective response to stress, modulates a cell's capacity to grow and divide, and regulates gene transcription. In humans, it exists in skin, cartilage and blood vessel as a component of hyaluronic acid, and bone tissue, cornea and aorta as a component of keratan sulfate. (PMID 16237703).


N-Acetyl-glucosamine 1-phosphate is an intermediate in aminosugar metabolism. It is a substrate for the enzymes phosphoglucomutase 3 [EC:5.4.2.2 and EC:5.4.2.3] and UDP-N-acteylglucosamine pyrophosphorylase 1 [EC:2.7.7.23] (KEGG). It is involved in UDP-N-acetyl-D-glucosamine biosynthesis and UDP-N-acetylgalactosamine biosynthesis (BioCyc).

2-(acetylamino)-2-deoxy-d-glucopyranose 1-(dihydrogen phosphoric acid)


UTP

Uridine 5'-(tetrahydrogen triphosphate). A uracil nucleotide containing three phosphate groups esterified to the sugar moiety. Uridine triphosphate has the role of a source of energy or an activator of substrates in metabolic reactions, like that of adenosine triphosphate, but more specific. When Uridine triphosphate activates a substrate, UDP-substrate is usually formed and inorganic phosphate is released. (Wikipedia).


Uridine-Diphosphate-N-Acetylglucosamine

Uridine diphosphate-N-acetylglucosamine (uridine 5'-diphosphate-GlcNAc, or UDP-Glc-NAc) is an acetylated aminosugar nucleotide. UDP-GlcNAc is the donor substrate for modification of nucleocytoplasmic proteins at serine and threonine residues with N-acetylglucosamine (O-GlcNAc). Nutrient sensing in mammals is done through the hexosamine biosynthetic pathway (HSP), which produces uridine 5'-diphospho-N-acetylglucosamine (UDP-Glc-NAc) as its end product. Mammals respond to nutrient excess by activating O-GlcNAcylation (addition of O-linked N-acetylglucosamine). O-GlcNAc addition (and removal) is key to histone remodeling, transcription, proliferation, apoptosis, and proteasomal degradation. This nutrient-responsive signaling pathway also modulates important cellular pathways, including the insulin signaling cascade in. Alterations in O-GlcNAc metabolism are associated with various human diseases including diabetes mellitus and neurodegeneration. (PMID: 16317114) Due to the chemical makeup of UDP-GlcNAc, it is well positioned to serve as a glucose sensor in that it is a high-energy compound that requires and/or responds to glucose, amino acid, fatty acid and nucleotide metabolism for synthesis. Elevated levels of O-GlcNAc have an effect on insulin-stimulated glucose uptake. (PMID: 12678487).

Uridine pyrophosphate 2-acetamido-2-deoxy-a-d-glucopyranosyl ester

Uridine pyrophosphate 2-acetamido-2-deoxy-alpha-d-glucopyranosyl ester

Uridine pyrophosphate 2-acetamido-2-deoxy-alpha-delta-glucopyranosyl ester


N-acetyl-beta-D-mannosamine

N-Acetylmannosamine is a monosaccharide that is used as a precursor in the chemical or enzymatic synthesis of the neuraminic acids found in glycolipids and glycoproteins. N-Acetyl-D-mannosamine (ManNAc) is a specific substrate for the synthesis of N-acetylneuraminic acid, the essential precursor of bacterial capsular polysialic acid (PA). N-Acetyl-D-mannosamine is used for the synthesis of sialic acid. It is also a synthetic intermediate for a number of carbohydrate-derived families of biologically active compounds and pharmaceutical candidates.

2-acetamido-2-deoxy-d-mannopyranose 2-acetamido-2-deoxy-d-mannose Mannac N-acetyl-d-mannosamine N-acetylmannosamine Beta-mannac N-acetyl-beta-mannosamine B-mannac β-mannac N-acetyl-b-d-mannosamine N-acetyl-β-d-mannosamine N-acetyl-b-mannosamine N-acetyl-β-mannosamine


UDP

Uridine 5'-diphosphate is a uracil nucleotide containing a pyrophosphate group esterified to C5 of the sugar moiety. UDP is an important extracellular pyrimidine signaling molecule that mediates diverse biological effects via P1 and P2 purinergic receptors, such as the uptake of thymidine and proliferation of gliomas. (PMID: 14558596). UDP induces intracellular Ca(2+) responses and oscillations in HeLa cells, due to the activation of P2Ys (G-protein coupled ATP receptors). (PMID: 1257952).

5'-udp
Udp
Uridine 5'-diphosphate
Uridine 5'-pyrophosphate
Uridine 5'-pyrophosphorate
Uridine 5'-pyrophosphoric acid
Uridine diphosphate
Uridine pyrophosphate
Uridine 5'-diphosphoric acid
Uridine diphosphoric acid


FRUCTOSE

Fructose, or levulose, is a levorotatory monosaccharide and an isomer of glucose (C6H12O6). The chemical composition of fructose is (C6H12O6). Pure fructose has a sweet taste similar to cane sugar, but with a "fruity" aroma. Although fructose is a hexose (6-carbon sugar), it generally exists as a 5-member hemiketal ring (a furanose). This structure is responsible for the long metabolic pathway and high reactivity compared to glucose. Fructose is found in many foods and is one of the three most important blood sugars along with glucose and galactose. Honey, tree fruits, berries, melons, and some root vegetables, such as beets, sweet potatoes, parsnips, and onions contain fructose, usually in combination with sucrose and glucose. Fructose is also derived from the digestion of sucrose, a disaccharide consisting of glucose and fructose that is broken down by enzymes during digestion. Fructose is the sweetest naturally occurring sugar, estimated to be twice as sweet as sucrose. It is used as a preservative and an intravenous infusion in parenteral feeding. Fructose is a reducing sugar, as are all monosaccharides. The spontaneous addition of single sugar molecules to proteins, known as glycation, is a significant cause of damage in diabetics. Fructose appears to be as dangerous as glucose in this regard, and therefore does not seem to be the answer for diabetes (McPherson et al, 1988). This may be an important contribution to senescence and many age-related chronic diseases (Levi & Werman 1998).

D-(-)-fructose
D-fructose
Fru
Fructon
Fructose
Levulose
Beta-d-arabino-hexulose
Beta-d-fructofuranose
Beta-d-fructose
Beta-fruit sugar
Beta-levulose
Beta-delta-arabino-hexulose
Beta-delta-fructofuranose
Beta-delta-fructose
Delta-(-)-fructose
Delta-fructose
B-d-arabino-hexulose
β-d-arabino-hexulose
B-d-fructofuranose
β-d-fructofuranose
B-d-fructose
β-d-fructose
B-fruit sugar
β-fruit sugar
B-levulose
β-levulose


Glucosamine

In the United States, glucosamine is not approved by the Food and Drug Administration for medical use in humans. Since glucosamine is classified as a dietary supplement, evidence of safety and efficacy is not required as long as it is not advertised as a treatment for a medical condition. Nevertheless, glucosamine is a popular alternative medicine used by consumers for the treatment of osteoarthritis. Glucosamine is also extensively used in veterinary medicine as an unregulated but widely accepted supplement (Nolen RS, 2002). Treatment with oral glucosamine is commonly used for the treatment of osteoarthritis. Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, supplemental glucosamine may help to rebuild cartilage and treat arthritis. However, there is little evidence that any clinical effect of glucosamine works this way (Laverty et al., 2005; Biggee et al., 2005). Its use as a therapy for osteoarthritis appears safe but there is conflicting evidence as to its effectiveness. Glucosamine (C6H14NO5) is an amino sugar that is an important precursor in the biochemical synthesis of glycosylated proteins and lipids.


CID 58114173

Phosphoenolpyruvate (PEP) is an important chemical compound in biochemistry. It has a high energy phosphate bond, and is involved in glycolysis and gluconeogenesis. In glycolysis, PEP is formed by the action of the enzyme enolase on 2-phosphoglycerate. Metabolism of PEP to pyruvate by pyruvate kinase (PK) generates 1 molecule of adenosine triphosphate (ATP) via substrate-level phosphorylation. ATP is one of the major currencies of chemical energy within cells. In gluconeogenesis, PEP is formed from the decarboxylation of oxaloacetate and hydrolysis of 1 guanosine triphosphate molecule. This reaction is catalyzed by the enzyme phosphoenolpyruvate carboxykinase (PEPCK). This reaction is a rate-limiting step in gluconeogenesis. (wikipedia).

2-hydroxy-acrylic acid dihydrogen phosphate


N-acetyl-beta-neuraminic acid

N-Acetylneuraminic acid (NeuAc) or sialic acid is an acetyl derivative of the amino sugar neuraminic acid. It occurs in many glycoproteins, glycolipids, and polysaccharides in both mammals and bacteria. The most abundant sialic acid, NeuAc, is synthesized in vivo from N-acetylated D-mannosamine (ManNAc) or D-glucosamine (GlcNAc). NeuAc and its activated form, CMP-NeuAc, are biosynthesized in five consecutive reactions: UDP-N-acetylglucosamine (UDP-GlcNAc) N-acetylmannosamine (ManNAc) ManNAc 6-phosphate NeuAc 9-phosphate NeuAc CMP-NeuAc. CMP-NeuAc is transported into the Golgi apparatus and, with the aid of specific sialyltransferases, added onto nonreducing positions on oligosaccharide chains of glycoproteins and glycolipids. NeuAc is widely distributed throughout human tissues and found in several fluids, including serum, cerebrospinal fluid, saliva, urine, amniotic fluid, and breast milk. It is found in high levels in the brain, adrenal glands, and the heart. Serum and urine levels of the free acid are elevated in individuals suffering from renal failure. Serum and saliva Neu5Ac levels are also elevated in alcoholics. A disorder known as Salla disease or infantile NeuAc storage disease is also characterized by high serum and urine levels of this compound. The negative charge of is responsible for the slippery feel of saliva and mucins coating the body's organs. This particular sialic acid is known to act as a "decoy" for invading pathogens. Along with involvement in preventing infections (mucus associated with mucous membranes  mouth, nose, GI, respiratory tract), Neu5Ac acts as a receptor for influenza viruses, allowing attachment to mucous cells via hemagglutinin (an early step in acquiring influenzavirus infection). NeuAc is also becoming known as an agent necessary for mediating ganglioside distribution and structures in the brain. Sialic acid (SA) is an N-acetylated derivative of neuraminic acid that is an abundant terminal monosaccharide of glycoconjugates. Normal human serum SA is largely bound to glycoproteins or glycolipids (Total sialic acid, TSA, 1.5-2.5 mmol/L), with small amounts of free SA (1-3 umol/L). Negatively charged SA units stabilize glycoprotein conformation in cell surface receptors to increase cell rigidity. This enables signal recognition and adhesion to ligands, antibodies, enzymes and microbes. SA residues are antigenic determinant residues in carbohydrate chains of glycolipids and glycoproteins, chemical messengers in tissue and body fluids, and may regulate glomeruli basement membrane permeability. Sialic acids are structurally unique nine-carbon keto sugars occupying the interface between the host and commensal or pathogenic microorganisms. An important function of host sialic acid is to regulate innate immunity. Sialic acid is the moiety most actively recycled for metabolic purposes in the salvage pathways in glycosphingolipid metabolism. Sialic acid is indispensable for the neuritogenic activities of gangliosides constituents which are unique in that a sialic acid directly binds to the glucose of the cerebroside, they are mutually connected in tandem, and some are located in the internal parts of the sugar chain. Sialylation (sialic acid linked to galactose, N-acetylgalactosamine, or linked to another sialic acid) represents one of the most frequently occurring terminations of the oligosaccharide chains of glycoproteins and glycolipids. The biosynthesis of the various linkages is mediated by the different members of the sialyltransferase family. (PMID: 11425186 , 11287396 , 12770781 , 16624269 , 12510390 , 15007099 ).