Formaldehyde

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

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


1-methyluric acid

1-Methyluric acid is one of the three main theophylline metabolites in man. 1-Methyluric acid is one of the purine components in urinary calculi. Methylated purines originate from the metabolism of methylxanthines (caffeine, theophylline, and theobromine). Methyluric acids can be distinguished from uric acid via simple methods routinely used in clinical laboratories, requiring the use of high-performance liquid chromatography (HPLC). Purine derivatives in urinary calculi could be considered markers of abnormal purine metabolism. The content of a purine derivative in stone depends on its average urinary excretion in the general population, similarity to the chemical structure of uric acid, and content of the latter in stone. This suggests that purines in stones represent a solid solution with uric acid as solvent. It is also plausible that methylxanthines, ubiquitous components of the diet and drugs, are involved in the pathogenesis of urolithiasis. Caffeine is metabolized via successive pathways mainly catalyzed by CYP1A2, xanthine oxidase, or N-acetyltransferase-2 to give 14 different metabolites. CYP1A2 activity shows an inter-individual variability among the population. CYP1A2, an isoform of the CYP1A cytochrome P450 superfamily, is involved in the metabolism of many drugs and plays a potentially important role in the induction of chemical carcinogenesis (PMID: 11712316, 15833286, 3506820, 15013152, 4039734, 9890610).


Mo-molybdopterin cofactor

Molybdenum cofactor is a cofactor required for the activity of enzymes such as sulfite oxidase, xanthine oxidoreductase, and aldehyde oxidase. It is a coordination complex formed between molybdopterin (which, despite the name, does not contain molybdenum) and an oxide of molybdenum. Molybdopterins, in turn, are synthesized from guanosine triphosphate. Molybdenum cofactor functions directly in ethylbenzene dehydrogenase, glyceraldehyde-3-phosphate ferredoxin oxidoreductase, and respiratory arsenate reductase. In animals and plants these enzymes use molybdenum bound at the active site in a tricyclic molybdenum cofactor. All molybdenum-using enzymes so far identified in nature use this cofactor The simplest structure of molybdopterin contains a pyranopterin coordinated to molybdenum. The pyranopterin structure is a fused ring system containing a pyran fused to pterin. In addition, the pyran ring is substituted with two thiols and an alkyl phosphate. In molybdopterin, the thiols coordinate to molybdenum. In some cases, the alkyl phosphate group is replaced by an alkyl diphosphate nucleotide. -- Wikipedia.


7-Methyluric acid, also known as 7-methylate, belongs to the class of organic compounds known as xanthines. These are purine derivatives with a ketone group conjugated at carbons 2 and 6 of the purine moiety. 7-Methyluric acid is slightly soluble (in water) and a very weakly acidic compound (based on its pKa). 7-Methyluric acid has been primarily detected in urine. In humans, 7-methyluric acid is involved in the caffeine metabolism pathway. 7-Methyluric acid is the minor urinary metabolites of caffeine. Caffeine is metabolized mainly in the liver undergoing demethylation and oxidation.


1,3,7-trimethyluric acid

1,3,7-Trimethyluric acid is a methyl derivative of uric acid, found occasionally in human urine. 1,3,7-Trimethyluracil is one of the purine components in urinary calculi. Methylated purines originate from the metabolism of methylxanthines (caffeine, theophylline and theobromine). Methyluric acids are indistinguishable from uric acid by simple methods routinely used in clinical laboratories, requiring the use of high-performance liquid chromatography (HPLC). Purine derivatives in urinary calculi could be considered markers of abnormal purine metabolism. The content of a purine derivative in stone depends on its average urinary excretion in the general population, similarity to the chemical structure of uric acid, and content of the latter in stone. This suggests that purines in stones represent a solid solution with uric acid as solvent. It is also plausible that methylxanthines, ubiquitous components of the diet and drugs, are involved in the pathogenesis of urolithiasis. Caffeine is metabolized via successive pathways mainly catalyzed by CYP1A2, xanthine oxidase or N-acetyltransferase-2 to give 14 different metabolites. CYP1A2 activity shows an inter-individual variability among the population. CYP1A2, an isoform of the CYP1A cytochrome P450 super-family, is involved in the metabolism of many drugs and plays a potentially important role in the induction of chemical carcinogenesis. (PMID: 11712316, 15833286, 3506820, 15013152).


1,7-dimethyluric acid

1,7-Dimethyluric acid, also known as 1,7-dimethylate, belongs to the class of organic compounds known as xanthines. These are purine derivatives with a ketone group conjugated at carbons 2 and 6 of the purine moiety. 1,7-Dimethyluric acid is slightly soluble (in water) and a very weakly acidic compound (based on its pKa). 1,7-Dimethyluric acid has been found in human liver and kidney tissues, and has also been detected in multiple biofluids, such as feces, urine, and blood. Within the cell, 1,7-dimethyluric acid is primarily located in the cytoplasm. In humans, 1,7-dimethyluric acid is involved in the caffeine metabolism pathway. 1,7 dimethyluric acid is the major urinary caffeine metabolites that is produced in the human body. 1,7 dimethyluric acid is formed during metabolism of caffeine and the process is catalyzed primarily by CYP2A6. (PMID: 18715882).


3,7-dimethyluric acid

3,7-Dimethyluric acid is a methyl derivative of uric acid, found occasionally in human urine. 3,7-Dimethyluric is one of the purine components in urinary calculi. Methylated purines originate from the metabolism of methylxanthines (caffeine, theophylline and theobromine). Methyluric acids are indistinguishable from uric acid by simple methods routinely used in clinical laboratories, requiring the use of high-performance liquid chromatography (HPLC). Purine derivatives in urinary calculi could be considered markers of abnormal purine metabolism. The content of a purine derivative in stone depends on its average urinary excretion in the general population, similarity to the chemical structure of uric acid, and content of the latter in stone. This suggests that purines in stones represent a solid solution with uric acid as solvent. It is also plausible that methylxanthines, ubiquitous components of the diet and drugs, are involved in the pathogenesis of urolithiasis. Caffeine is metabolized via successive pathways mainly catalyzed by CYP1A2, xanthine oxidase or N-acetyltransferase-2 to give 14 different metabolites. CYP1A2 activity shows an inter-individual variability among the population. CYP1A2, an isoform of the CYP1A cytochrome P450 super-family, is involved in the metabolism of many drugs and plays a potentially important role in the induction of chemical carcinogenesis. (PMID: 11712316, 15833286, 3506820, 15013152).


A4Z6T9_HUMAN arylamine N-acetyltransferase (trembl)


Trimethyllysine

N6,N6,N6-Trimethyl-L-lysine is a methylated derivative of the amino acid lysine. It is a component of histone proteins, a precursor of carnitine and a coenzyme of fatty acid oxidation. N6,N6,N6-Trimethyl-L-lysine residues are found in a number of proteins and are generated by the action of S-adenosyl-L-methionine on exposed lysine residues. When trimethyllysine is released from cognate proteins via proteolysis, it serves as a precursor for carnitine biosynthesis. Mitochondrial 6-N-trimethyllysine dioxygenase converts 6-N-trimethyllysine to 3-hydroxy-6-N-trimethyllysine as the first step for carnitine biosynthesis. Because the subsequent carnitine biosynthesis enzymes are cytosolic, 3-hydroxy-6-N-trimethyllysine must be transported out of the mitochondria by a putative mitochondrial 6-N-trimethyllysine/3-hydroxy-6-N-trimethyllysine transporter system. Plasma -N-trimethyllysine concentrations are significantly lower in systemic carnitine deficiency patients compared to normal individuals, but no significant difference in urinary -N-trimethyllysine excretion is seen between the two groups.


3-Hydroxy-N6,N6,N6-trimethyl-L-lysine is found within the Lysine degration pathway; it is the byproduct of trimethyllysine dioxygenase (EC 1.14.11.8) which converts N6-Hydroxy-trimethyl-lysine to Glycine and 4-Trimethyl-ammoniobutanal. Because carnitine is the final product of the Lysine degration pathway, this compound is often associated with carnitine defiency disorders. (PMID: 16707092) The compound is also a byproduct of glycine hydroxymethyltransferase (EC 2.1.2.1) and Lyases (EC 4.1.2.-).


Ferrous cation

Iron is a chemical element with the symbol Fe and atomic number 26. Iron makes up 5% of the Earth's crust and is second in abundance to aluminium among the metals and fourth in abundance among the elements. Physiologically, it. exists as an ion in the body. Iron (as Fe2+, ferrous ion) is a necessary trace element used by all known living organisms. Iron-containing enzymes, usually containing heme prosthetic groups, participate in catalysis of oxidation reactions in biology, and in transport of a number of soluble gases. Iron is an essential constituent of hemoglobin, cytochrome, and other components of respiratory enzyme systems. Its chief functions are in the transport of oxygen to tissue (hemoglobin) and in cellular oxidation mechanisms. Inorganic iron involved in redox reactions is also found in the iron-sulfur clusters of many enzymes, such as nitrogenase (involved in the synthesis of ammonia from nitrogen and hydrogen) and hydrogenase. A class of non-heme iron proteins is responsible for a wide range of functions such as ribonucleotide reductase (reduces ribose to deoxyribose; DNA biosynthesis) and purple acid phosphatase (hydrolysis of phosphate esters). When the body is fighting a bacterial infection, the body sequesters iron inside of cells (mostly stored in the storage molecule ferritin) so that it cannot be used by bacteria. Depletion of iron stores may result in iron-deficiency anemia. Iron is used to build up the blood in anemia. Humans experience iron toxicity above 20 milligrams of iron for every kilogram of weight, and 60 milligrams per kilogram is a lethal dose. Over-consumption of iron, often the result of children eating large quantities of ferrous sulfate tablets intended for adult consumption, is the most common toxicological cause of death in children under six. The DRI lists the Tolerable Upper Intake Level (UL) for adults as 45 mg/day. For children under fourteen years old the UL is 40 mg/day. Iron is a metal extracted from iron ore, and is almost never found in the free elemental state.

Armco iron
Carbonyl iron
Fe
Ferrovac e
Hematite
Infed
Loha
Limonite
Magnetite
Malleable iron
Metopirone
Metyrapone
Pzho
Pzh2m
Remko
Suy-b 2
Taconite
Venofer
Wrought iron
Fe (ii) ion
Fe(ii)
Fe2+
Fe(2+)
Ferrous ion
Iron ion(2+)


4-Trimethylammoniobutanal is a substrate for Serine hydroxymethyltransferase (cytosolic), Serine hydroxymethyltransferase (mitochondrial), Aldehyde dehydrogenase (mitochondrial), Fatty aldehyde dehydrogenase, 4-trimethylaminobutyraldehyde dehydrogenase, Aldehyde dehydrogenase (dimeric NADP-preferring), Aldehyde dehydrogenase family 7 member A1, Aldehyde dehydrogenase 1A3 and Aldehyde dehydrogenase X (mitochondrial).


4-(trimethylammonio)butanoic acid

4-Trimethylammoniobutanoic acid or gamma-butyrobetaine (GBB) is a highly water-soluble derivative of gamma-aminobutyric acid (GABA). It is also a precursor of L-carnitine. It is a substrate of gamma butyrobetaine hydroxylase/dioxygenase (also known as BBOX) which catalyzes the formation of L-carnitine from gamma-butyrobetaine, the last step in the L-carnitine biosynthesis pathway. Carnitine is essential for the transport of activated fatty acids across the mitochondrial membrane during mitochondrial beta-oxidation. 4-Trimethylammoniobutanoic acid is also a substrate and/or product for alpha-aminoadipic semialdehyde dehydrogenase, aldehyde dehydrogenase (dimeric NADP-preferring), aldehyde dehydrogenase family 7 member A1, aldehyde dehydrogenase 1A3, aldehyde dehydrogenase (mitochondrial), fatty aldehyde dehydrogenase, aldehyde dehydrogenase X (mitochondrial), and 4-trimethylaminobutyraldehyde dehydrogenase.


Levocarnitine

Carnitine is not an essential amino acid; it can be synthesized in the body. However, it is so important in providing energy to muscles (including the heart) that some researchers are now recommending carnitine supplements in the diet, particularly for people who do not consume much red meat (the main food source for carnitine). Carnitine has been described as a vitamin, an amino acid, or a metabimin (i.e. an essential metabolite). Like the B vitamins, carnitine contains nitrogen and is very soluble in water, and to some researchers carnitine is a vitamin (Liebovitz 1984). It was found that an animal (yellow mealworm) could not grow without carnitine in its diet. However, as it turned out, almost all other animals, including humans, do make their own carnitine; thus, it is no longer considered a vitamin. Nevertheless, in certain circumstances, such as deficiencies of methionine, lysine, or vitamin C or kidney dialysis, carnitine shortages develop. Under these conditions, carnitine must be absorbed from food, and for this reason it is sometimes referred to as a "metabimin" or a conditionally essential metabolite. Like the other amino acids used or manufactured by the body, carnitine is an amine. But like choline, which is sometimes considered to be a B vitamin, carnitine is also an alcohol (specifically, a trimethylated carboxy-alcohol). Thus, carnitine is an unusual amino acid and has different functions than most other amino acids, which are usually employed by the body in the construction of protein. Carnitine is an essential factor in fatty acid metabolism in mammals. Its most important known metabolic function is to transport fat into the mitochondria of muscle cells, including those in the heart, for oxidation. This is how the heart gets most of its energy. In humans, about 25% of carnitine is synthesized in the liver, kidney, and brain from the amino acids lysine and methionine. Most of the carnitine in the body comes from dietary sources such as red meat and dairy products. Inborn errors of carnitine metabolism can lead to brain deterioration like that of Reye's syndrome, gradually worsening muscle weakness, Duchenne-like muscular dystrophy, and extreme muscle weakness with fat accumulation in muscles. Borum et al. (1979) describe carnitine as an essential nutrient for pre-term babies and individuals who are unable to eat a normal diet (e.g. non-ketotic hypoglycemics, kidney dialysis patients) (PMID: 115309). In conditions such as kwashiorkor, cirrhosis, and heart muscle disease (cardiomyopathy) as well as in inborn errors of metabolism such as type IV hyperlipidemia and propionic or organic aciduria (acid urine resulting from genetic or other anomalies), carnitine is essential to life and carnitine supplements are valuable. Carnitine therapy may also be useful in a wide variety of clinical conditions. Carnitine supplementation has improved some patients who have angina secondary to coronary artery disease. It may also be worth a trial for patients with any form of hyperlipidemia or muscle weakness. Carnitine supplements may also be useful in many forms of toxic or metabolic liver disease and in cases of heart muscle disease. Hearts undergoing severe arrhythmia quickly deplete their stores of carnitine. Athletes, particularly in Europe, have used carnitine supplements for improved endurance. Carnitine may improve muscle building by improving fat utilization and may even be useful in treating obesity. Carnitine joins a long list of nutrients which may be of value in treating pregnant women, hypothyroid individuals, and male infertility due to the low motility of sperm. Carnitine deficiency is noted in abnormal liver function, renal dialysis patients, and severe to moderate muscular weakness with associated anorexia (http://www.dcnutrition.com). Carnitine is a biomarker for the consumption of meat.

3-carboxy-2-hydroxy-n,n,n-trimethyl-1-propanaminium hydroxide, inner salt


Ascorbic acid

Ascorbic acid is found naturally in citrus fruits and many vegetables and is an essential nutrient in human diets. It is necessary to maintain connective tissue and bone. The biologically active form of ascorbic acid is vitamin C. Vitamin C is a water soluble vitamin. Primates (including humans) and a few other species in all divisions of the animal kingdom, notably the guinea pig, have lost the ability to synthesize ascorbic acid and must obtain it in their food. Vitamin C functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [PubChem] Ascorbic acid is an electron donor for enzymes involved in collagen hydroxylation, biosynthesis of carnitine and norepinephrine, tyrosine metabolism, and amidation of peptide hormones. Ascrobic acid (vitamin C) deficiency causes scurvy. The amount of vitamin C necessary to prevent scurvy may not be adequate to maintain optimal health. The ability of vitamin C to donate electrons also makes it a potent water-soluble antioxidant that readily scavenges free radicals such as molecular oxygen, superoxide, hydroxyl radical, and hypochlorous acid. In this setting, several mechanisms could account for a link between vitamin C and heart disease. One is the relation between LDL oxidation and vitamins C and E. Vitamin C in vitro can recycle vitamin E, which can donate electrons to prevent LDL oxidation in vitro. As the lipid-phase vitamin E is oxidized, it can be regenerated by aqueous vitamin C. Other possibilities are that vitamin C could decrease cholesterol by mechanisms not well characterized, or could improve vasodilatation and vascular reactivity, perhaps by decreasing the interactions of nitric oxide with oxidants. (PMID: 10799361).

(+)-sodium l-ascorbate
(+)-ascorbate
(+)-ascorbic acid
3-keto-l-gulofuranolactone
3-oxo-l-gulofuranolactone
Adenex
Allercorb
Antiscorbic vitamin
Antiscorbutic vitamin
Arco-cee
Ascoltin
Ascor-b.i.d.
Ascorb
Ascorbajen
Ascorbate
Ascorbic acid
Ascorbicab
Ascorbicap
Ascorbicin
Ascorbin
Ascorbutina
Ascorin
Ascorteal
Ascorvit
C-level
C-long
C-quin
C-span
C-vimin
Cantan
Cantaxin
Catavin c
Ce lent
Ce-mi-lin
Ce-vi-sol
Cebicure
Cebid
Cebion
Cebione
Cecon
Cee-caps td
Cee-vite
Cegiolan
Ceglion
Ceklin
Celaskon
Celin
Cell c
Cemagyl
Cemill
Cenetone
Cenolate
Cereon
Cergona
Cescorbat
Cetamid
Cetane
Cetane-caps tc
Cetane-caps td
Cetebe
Cetemican
Cevalin
Cevatine
Cevex
Cevi-bid
Cevimin
Cevital
Cevitamate
Cevitamic acid
Cevitamin
Cevitan
Cevitex
Cewin
Chewcee
Ciamin
Cipca
Citriscorb
Citrovit
Colascor
Concemin
Davitamon c
Dora-c-500
Duoscorb
Ferrous ascorbate
Hicee
Hybrin
Ido-c
Juvamine
Kangbingfeng
Kyselina askorbova
L(+)-ascorbate
L(+)-ascorbic acid
L-(+)-ascorbate
L-(+)-ascorbic acid
L-3-ketothreohexuronic acid lactone
L-ascorbate
L-ascorbic acid
L-lyxoascorbate
L-lyxoascorbic acid
L-threo-ascorbic acid
L-xyloascorbate
L-xyloascorbic acid
Laroscorbine
Lemascorb
Liqui-cee
Meri-c
Natrascorb
Natrascorb injectable
Planavit c
Proscorbin
Redoxon
Ribena
Ronotec 100
Rontex 100
Roscorbic
Rovimix c
Scorbacid
Scorbu c
Scorbu-c
Secorbate
Sodascorbate
Suncoat vc 40
Testascorbic
Vasc
Vicelat
Vicin
Vicomin c
Viforcit
Viscorin
Viscorin 100m
Vitace
Vitacee
Vitacimin
Vitacin
Vitamin c
Vitamisin
Vitascorbol
Xitix
Gamma-lactone l-threo-hex-2-enonate
Gamma-lactone l-threo-hex-2-enonic acid
Acide ascorbique
Acido ascorbico
Acidum ascorbicum
Acidum ascorbinicum
Ascorbinsaeure
E 300
E-300
E300


Tyrosine

Tyrosine is an essential amino acid that readily passes the blood-brain barrier. Once in the brain, it is a precursor for the neurotransmitters dopamine, norepinephrine and epinephrine, better known as adrenalin. These neurotransmitters are an important part of the body's sympathetic nervous system, and their concentrations in the body and brain are directly dependent upon dietary tyrosine. Tyrosine is not found in large concentrations throughout the body, probably because it is rapidly metabolized. Folic acid, copper and vitamin C are cofactor nutrients of these reactions. Tyrosine is also the precursor for hormones, thyroid, catecholestrogens and the major human pigment, melanin. Tyrosine is an important amino acid in many proteins, peptides and even enkephalins, the body's natural pain reliever. Valine and other branched amino acids, and possibly tryptophan and phenylalanine may reduce tyrosine absorption. A number of genetic errors of tyrosine metabolism occur. Most common is the increased amount of tyrosine in the blood of premature infants, which is marked by decreased motor activity, lethargy and poor feeding. Infection and intellectual deficits may occur. Vitamin C supplements reverse the disease. Some adults also develop elevated tyrosine in their blood. This indicates a need for more vitamin C. More tyrosine is needed under stress, and tyrosine supplements prevent the stress-induced depletion of norepinephrine and can cure biochemical depression. However, tyrosine may not be good for psychosis. Many antipsychotic medications apparently function by inhibiting tyrosine metabolism. L-dopa, which is directly used in Parkinson's, is made from tyrosine. Tyrosine, the nutrient, can be used as an adjunct in the treatment of Parkinson's. Peripheral metabolism of tyrosine necessitates large doses of tyrosine, however, compared to L-dopa. (http://www.dcnutrition.com).


Sapropterin, also known as THBP or 6R-BH4, belongs to the class of organic compounds known as biopterins and derivatives. These are coenzymes containing a 2-amino-pteridine-4-one derivative. They are mainly synthesized in several parts of the body, including the pineal gland. Sapropterin is slightly soluble (in water) and a very weakly acidic compound (based on its pKa). Sapropterin has been detected in multiple biofluids, such as blood and cerebrospinal fluid. Within the cell, sapropterin is primarily located in the cytoplasm. In humans, sapropterin is involved in catecholamine biosynthesis pathway. Sapropterin is also involved in a couple of metabolic disorders, which include aromatic L-aminoacid decarboxylase deficiency and tyrosine hydroxylase deficiency. Sapropterin is converted from 7,8-dihydroneopterin triphosphate by 6-pyruvoyl tetrahydropterin synthase and sepiapterin reductase. It is essential in the formation of neurotransmitters and for nitric oxide synthase (PMID 16946131).


Levodopa

L-Dopa is the naturally occurring form of dihydroxyphenylalanine and the immediate precursor of dopamine. Unlike dopamine itself, L-Dopa can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. In particular, it is metabolized to dopamine by aromatic L-amino acid decarboxylase. Pyridoxal phosphate (vitamin B6) is a required cofactor for this decarboxylation, and may be administered along with levodopa, usually as pyridoxine. L-Dopa is used for the treatment of Parkinsonian disorders and Dopa-Responsive Dystonia and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. Peripheral tissue conversion may be the mechanism of the adverse effects of levodopa. It is standard clinical practice to co-administer a peripheral DOPA decarboxylase inhibitor - carbidopa or benserazide - and often a catechol-O-methyl transferase (COMT) inhibitor, to prevent synthesis of dopamine in peripheral tissue.


Dihydrobiopterin (BH2) is an oxidation product of tetrahydrobiopterin. Tetrahydrobiopterin is a natural occurring cofactor of the aromatic amino acid hydroxylase and is involved in the synthesis of tyrosine and the neurotransmitters dopamine and serotonin. Tetrahydrobiopterin is also essential for nitric oxide synthase catalyzed oxidation of L-arginine to L-citrulline and nitric oxide.


Dopamine

Dopamine is a member of the catecholamine family of neurotransmitters in the brain and is a precursor to epinephrine (adrenaline) and norepinephrine (noradrenaline). Dopamine is synthesized in the body (mainly by nervous tissue and adrenal glands) first by the hydration of the amino acid tyrosine to DOPA by tyrosine hydroxylase and then by the decarboxylation of DOPA by aromatic-L-amino-acid decarboxylase. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (dopamine receptors) mediates its action, which plays a major role in reward-motivated behaviour. Dopamine has many other functions outside the brain. In blood vessels, dopamine inhibits norepinephrine release and acts as a vasodilator (at normal concentrations); in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces insulin production; in the digestive system, it reduces gastrointestinal motility and protects intestinal mucosa; and in the immune system, it reduces the activity of lymphocytes. Parkinson's disease, a degenerative condition causing tremor and motor impairment, is caused by a loss of dopamine-secreting neurons in an area of the midbrain called the substantia nigra. There is evidence that schizophrenia involves altered levels of dopamine activity, and most antipsychotic drugs used to treat this are dopamine antagonists, which reduce dopamine activity. Attention deficit hyperactivity disorder, bipolar disorder, and addiction are also characterized by defects in dopamine production or metabolism. It has been suggested that animals derived their dopamine-synthesizing machinery from bacteria via horizontal gene transfer that may have occurred relatively late in evolutionary time. This is perhaps a result of the symbiotic incorporation of bacteria into eukaryotic cells that gave rise to mitochondria. Dopamine is elevated in the urine of people who consume bananas. When present in sufficiently high levels, dopamine can be a neurotoxin and a metabotoxin. A neurotoxin is a compound that disrupts or attacks neural tissue. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of dopamine are associated with neuroblastoma, Costello syndrome, leukemia, phaeochromocytoma, aromatic L-amino acid decarboxylase deficiency, and Menkes disease (MNK). High levels of dopamine can lead to hyperactivity, insomnia, agitation and anxiety, depression, delusions, excessive salivation, nausea, and digestive problems.


Norepinephrine

Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.


dehydroascorbic acid

Dehydroascorbic acid is the oxidized form of vitamin C. Reduced Vitamin C concentrations in the brain exceed those in blood by 10 fold. Dehydroascorbic acid readily enters the brain and is retained in the brain tissue in the form of ascorbic acid (ascorbic acid is not able to cross the blood-brain barrier). Therefore, transport of dehydroascorbic acid by the Glucose Transporter 1 (GLUT1, Glucose transporters are integral membrane glycoproteins involved in transporting glucose into most cells. GLUT1 is a major glucose transporter in the mammalian blood-brain barrier. It is present at high levels in primate erythrocytes and brain endothelial cells.) is a mechanism by which the brain acquires vitamin C. (OMIM 138140).


PQQ Cofactor

Enzymes containing PQQ are called quinoproteins. PQQ and quinoproteins play a role in the redox metabolism and structural integrity of cells and tissues [PMID:2558842]. It was reported that aminoadipate semialdehyde dehydrogenase (AASDH) might also use PQQ as a cofactor, suggesting a possibility that PQQ is a vitamin in mammals. [PMID:12712191].


Epinephrine

Epinephrine is a catecholamine, a sympathomimetic monoamine derived from the amino acids phenylalanine and tyrosine. It is the active sympathomimetic hormone secreted from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. Epinephrine also constricts arterioles in the skin and gut while dilating arterioles in leg muscles. It elevates the blood sugar level by increasing hydrolysis of glycogen to glucose in the liver, and at the same time begins the breakdown of lipids in adipocytes. Epinephrine has a suppressive effect on the immune system.


endocytic vesicle

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


L-cysteine-S-dioxide

3-Sulfinoalanine or cysteinesulfinic acid is a N-methyl-D-aspartate agonist. It is a product of cysteine dioxygenase or CDO [EC 1.13.11.20]. In humans cysteine catabolism is tightly regulated via regulation of cysteine dioxygenase (CDO) levels in the liver, with the turnover of CDO protein being dramatically decreased when intracellular cysteine levels increase. This occurs in response to changes in the intracellular cysteine concentration via changes in the rate of CDO ubiquitination and degradation. Expressed at high levels in the liver with lower levels in the kidney, brain, and lung, cysteine dioxygenase catalyzes the addition of molecular oxygen to the sulfhydryl group of cysteine, yielding cysteinesulfinic acid. The oxidative catabolism of cysteine to cysteinesulfinate by CDO represents an irreversible loss of cysteine from the free amino acid pool. Once generated, cysteinesulfinate is shuttled into several pathways including hypotaurine/taurine synthesis, sulfite/sulfate production, and the generation of pyruvate.

3-sulfino- alanine
3-sulfino-l-alanine
3-sulphino-l-alanine
Alanine 3-sulfinic acid
Cysteine hydrogen sulfite ester
Cysteine sulfinate
Cysteine sulfinic acid
L-cysteine sulfinic acid
L-cysteinesulfinic acid
2-amino-3-sulfino-propionic acid
Cysteine-s,s-dioxide
Cysteine-s-dioxide
L-cysteine-s,s-dioxide
2-amino-3-sulfino-propionate
2-amino-3-sulphino-propionate
2-amino-3-sulphino-propionic acid


3-sulfinylpyruvic acid

This compound is found in the mammalian cysteine metobolic pathway. It is the deaminated form of Cysteine sulfinic acid (PMID: 3925121), which subsequently spontaneously reacts to form pyruvate while releasing sulfur dioxide. It is the byproduct of oxidoreductases (EC 1.4.1.-), and aspartate transaminase (EC 2.6.1.1). It is also often associated with hepatic disease, and the presence of aspartate transaminase is used in diagnostic biochemical assays of such ailments. (PMID: 17310554).


sulfite

Endogenous sulfite is generated as a consequence of the body's normal processing of sulfur-containing amino acids. Sulfites occur as a consequence of fermentation and also occur naturally in a number of foods and beverages. As food additives, sulfiting agents were first used in 1664 and have been approved in the United States since the 1800s. Sulfite is an allergen, a neurotoxin, and a metabotoxin.  An allergen is a compound that causes allergic reactions such as wheezing, rash, or rhinitis. A neurotoxin is a substance that causes damage to nerves or brain tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. As an allergen, sulfite is known to induce asthmatic reactions. Sulfite sensitivity occurs most often in asthmatic adults (predominantly women), but it is also occasionally reported in preschool children. Adverse reactions to sulfites in nonasthmatics are extremely rare. Asthmatics who are steroid-dependent or who have a higher degree of airway hyperreactivity may be at greater risk of experiencing a reaction to sulfite-containing foods. Sulfite sensitivity reactions vary widely, ranging from no reaction to severe. The majority of reactions are mild. These manifestations may include dermatologic, respiratory, or gastrointestinal signs and symptoms. The precise mechanisms of the sensitivity responses have not been completely elucidated: inhalation of sulfur dioxide (SO2) generated in the stomach following ingestion of sulfite-containing foods or beverages, a deficiency in a mitochondrial enzyme, and an IgE-mediated immune response have all been implicated. Exogenously supplied sulfite is detoxified by the enzyme sulfite oxidase. Sulfite oxidase (EC 1.8.3.1) is 1 of 3 enzymes in humans that require molybdenum as a cofactor. Under certain circumstances, chronically high levels of sulfite can lead to serious neurotoxicity. Sulfite oxidase deficiency (also called molybdenum cofactor deficiency) is a rare autosomal inherited disease that is typified by high concentrations of sulfite in the blood and urine. It is characterized by severe neurological symptoms such as untreatable seizures, attenuated growth of the brain, and mental retardation. It results from defects in the enzyme sulfite oxidase, which is responsible for the oxidation of sulfite to sulfate. This sulfite to sulfate reaction is the final step in the degradation of sulfur-containing metabolites (including the amino acids cysteine and methionine). The term "isolated sulfite oxidase deficiency" is used to define the deficiency caused by mutations in the sulfite oxidase gene. This differentiates it from another version of sulfite oxidase deficiency that is due to defects in the molybdenum cofactor biosynthetic pathway (with mutations in the MOCS1 or MOCS2 genes). Isolated sulfite oxidase deficiency is a rare but devastating neurologic disease that usually presents in early infancy with seizures and alterations in muscle tone (PMID: 16234925, 16140720, 8586770). Sulfite oxidase deficiency (as caused by MOCS1 or MOCS2) may be treated with cPMP, a precursor of the molybdenum cofactor (PMID: 20385644).  The mechanism behind sulfite neurotoxicity appears to be related to its ability to bind and inhibit glutamate dehydrogenase (GDH). Inhibition of GDH leads to a decrease in alpha-ketoglutarate and a diminished flux through the tricarboxylic acid cycle. This is accompanied by a decrease in NADH through the mitochondrial electron transport chain, which leads to a decrease in mitochondrial membrane potential and in ATP synthesis. Since glutamate is a major metabolite in the brain, inhibition of GDH by sulfite appears to contribute to neural damage characteristic of sulfite oxidase deficiency in human infants (PMID: 15273247).

Bisulfite
Sulfite dianion
Sulfite ion
Sulfite ions
Sulfonate
Sulfur trioxide
Sulfuric anhydride
Sulphite
Trioxosulfate(2-)
Trioxosulfate(iv)
Trioxosulphate(2-)
Trioxosulphate(iv)
[so3](2-)
So3(2-)
Sulphite ion


hydrogen sulfide

Hydrogen sulfide is a highly toxic and flammable gas. Because it is heavier than air it tends to accumulate at the bottom of poorly ventilated spaces. Although very pungent at first, it quickly deadens the sense of smell, so potential victims may be unaware of its presence until it is too late. H2S arises from virtually anywhere where elemental sulfur comes into contact with organic material, especially at high temperatures. Hydrogen sulfide is a covalent hydride chemically related to water (H2O) since oxygen and sulfur occur in the same periodic table group. It often results when bacteria break down organic matter in the absence of oxygen, such as in swamps, and sewers (alongside the process of anaerobic digestion). It also occurs in volcanic gases, natural gas and some well waters. It is also important to note that Hydrogen sulfide is a central participant in the sulfur cycle, the biogeochemical cycle of sulfur on Earth. As mentioned above, sulfur-reducing and sulfate-reducing bacteria derive energy from oxidizing hydrogen or organic molecules in the absence of oxygen by reducing sulfur or sulfate to hydrogen sulfide. Other bacteria liberate hydrogen sulfide from sulfur-containing amino acids. Several groups of bacteria can use hydrogen sulfide as fuel, oxidizing it to elemental sulfur or to sulfate by using oxygen or nitrate as oxidant. The purple sulfur bacteria and the green sulfur bacteria use hydrogen sulfide as electron donor in photosynthesis, thereby producing elemental sulfur. (In fact, this mode of photosynthesis is older than the mode of cyanobacteria, algae and plants which uses water as electron donor and liberates oxygen).

Acide sulfhydrique
Dihydrogen disulfide
Dihydrogen monosulfide
Dihydrogen sulfide
Hepatate
Hepatic acid
Hepatic gas
Hydrogen monosulfide
Hydrogen sulfide
Hydrogen-sulfide
Hydrogene sulfure
Hydrosulfurate
Hydrosulfuric acid
Idrogeno solforato
Schwefelwasserstoff
Sewer gas
Siarkowodor
Sour gas
Stink damp
Sulfur hydride
Sulfur hydroxide
Sulfureted hydrogen
Sulfuretted hydrogen
Zwavelwaterstof
[sh2]
H2s
Hydrogen sulphide
Sulfide
Sulfure d'hydrogene
Acide sulphhydrique
Dihydrogen monosulphide
Dihydrogen sulphide
Hydrogen monosulphide
Hydrogen-sulphide
Hydrogene sulphure
Hydrosulfate
Hydrosulphate
Hydrosulphuric acid
Sulphide
Sulphure d'hydrogene


3-mercaptopyruvic acid

3-Mercaptopyruvic acid is an intermediate in the metabolism of Cysteine. It is a substrate for L-lactate dehydrogenase A chain, 3-mercaptopyruvate sulfurtransferase, Aspartate aminotransferase (mitochondrial), L-lactate dehydrogenase C chain, L-lactate dehydrogenase A-like 6A, Aspartate aminotransferase (cytoplasmic), L-lactate dehydrogenase B chain and L-lactate dehydrogenase A-like 6B.

3-mercapto-pyruvate
3-mercapto-pyruvic acid
3-mercaptopyruvate
3-mercaptopyruvic acid
Mercaptopyruvate
Mercaptopyruvic acid
Thiopyruvate
Beta-3-mercapto-2-oxo-propanoate
Beta-3-mercapto-2-oxo-propanoic acid
Beta-mercaptopyruvate
Beta-mercaptopyruvic acid
Beta-thiopyruvate
Beta-thiopyruvic acid
3-mercapto-2-oxopropanoic acid
3-mercapto-2-oxopropanoate


cyanide

The cyanide ion consists of a carbon triple bonded to a nitrogen. It readily reacts with hydrogen to form hydrogen cyanide gas, which has a faint almond-like smell. Most people can smell hydrogen cyanide; however, due to an apparent genetic trait, some individuals cannot. Cyanide gas (HCN) can be generated via combustion, including the exhaust of internal combustion engines, tobacco smoke, and especially some plastics derived from acrylonitrile (because of the latter effect, house fires can result in poisonings of the inhabitants). Cyanides are also produced by certain bacteria, fungi, and algae and are found in a number of foods and plants. Small amounts of cyanide can be found in apple seeds, mangoes and bitter almonds. Hydrocyanic acid (a solution of hydrogen cyanide in water) is present in freshly distilled bitter almond oil (2-4%) prior to its removal by precipitation as calcium ferrocyanide to give food quality oil. Hydrogen cyanide and most cyanide salts readily dissolve in water (or other biofluids) and exists in solution as the cyanide ion. Cyanide ions bind to the iron atom of the enzyme cytochrome c oxidase (also known as aa3) in the fourth complex in the mitochondrial membrane in the mitochondria of cells. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted, meaning that the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Because of its respiratory chain toxicity cyanide has been used as a poison many times throughout history. Its most infamous application was the use of hydrogen cyanide by the Nazi regime in Germany for mass murder in some gas chambers during the Holocaust. Hydrogen cyanide (with the historical common name of Prussic acid) is a colorless and highly volatile liquid that boils slightly above room temperature at 26 °C (78.8 °F). Hydrogen cyanide is weakly acidic and partly ionizes in solution to give the cyanide anion, CN-. The salts of hydrogen cyanide are known as cyanides. HCN is a highly valuable precursor to many chemical compounds ranging from polymers to pharmaceuticals. Hydrogen cyanide is a linear molecule, with a triple bond between carbon and nitrogen. It is a weak acid with a pKa of 9.2. A minor tautomer of HCN is HNC, hydrogen isocyanide.

Carbon nitride ion
Chuck norrisium
Cyanide
Cyanide ion
Cyanide(1-) ion
Cyano
Cyanure
Isocyanide
Prussiate


thiocyanate

Thiocyanate is analogous to the cyanate ion, [OCN]-, wherein oxygen is replaced by sulfur. [SCN]- is one of the pseudohalogens, due to the similarity of its reactions to that of halide ions. Thiocyanate was formerly known as rhodanide (from a Greek word for rose) because of the red color of its complexes with iron. Thiocyanates are typically colorless. Cyanide ions can react with cystine to yield thicocyanate. This reaction occurs to a slight extent even in neutral solution, but is more pronounced in alkaline solutions of cystine. In addition to this non-enzymatic route, cyanide produced in vivo can be converted in part to thiocyanate by sulfur transferase systems. The thiocyanate ion can be oxidized at acid pH by hydrogen peroxide to generate sulfate and cyanide. The reaction is catalyzed by hemoglobin acting as a peroxidase.

Rhodanide
Scn
Ammonium rhodanate
Ammonium rhodanide
Ammonium sulfocyanate
Hscn
Hydrogen thiocyanate
Nitridosulfanidocarbon
Rhodanid
Silver thiocyanate agscn
Thallium thiocyanate
Thiocyanate ion
Thiocyanic acid
Thiocyanid
Weedazol tl
[s-c#n](-)
N#c-s(-)
Scn(-)
Thiocyanate ion (1-)
Thiozyanat


3-mercaptolactic acid

3-Mercaptolactic acid, also known as 3-mercaptolactate, belongs to the class of organic compounds known as monosaccharides. Monosaccharides are compounds containing one carbohydrate unit not glycosidically linked to another such unit, and no set of two or more glycosidically linked carbohydrate units. Monosaccharides have the general formula CnH2nOn. 3-Mercaptolactic acid is soluble (in water) and a weakly acidic compound (based on its pKa). Within the cell, 3-mercaptolactic acid is primarily located in the cytoplasm. In humans, 3-mercaptolactic acid is involved in the cysteine metabolism pathway and the cystinosis, ocular nonnephropathic pathway. 3-Mercaptolactic acid is also involved in the metabolic disorder called the Beta-mercaptolactate-cysteine disulfiduria pathway. 3-Mercaptolactic acid is a thiol that has been confirmed to be found in urine (PMID 8852041).

3-mercaptolactate
B-mercaptolactate
B-mercaptolactic acid
Beta-mercaptolactate
Beta-mercaptolactic acid


D-ornithine

D-Ornithine is an amino acid produced in the urea cycle by the splitting off of urea from arginine. Ornithine is one of the products of the action of the enzyme arginase on L-arginine, creating urea. Therefore, ornithine is a central part of the urea cycle, which allows for the disposal of excess nitrogen.

(2r)-2,5-diaminopentanoate
(2r)-2,5-diaminopentanoic acid
(r)-ornithine
Ornithine


5-amino-2-oxopentanoic acid

5-Amino-2-oxopentanoic acid, also known as 2-oxo-5-amino-pentanoate or alpha-keto-delta-aminopentanoate, belongs to the class of organic compounds known as short-chain keto acids and derivatives. These are keto acids with an alkyl chain the contains less than 6 carbon atoms. 5-Amino-2-oxopentanoic acid is soluble (in water) and a weakly acidic compound (based on its pKa). 5-Amino-2-oxopentanoic acid has been primarily detected in saliva. Within the cell, 5-amino-2-oxopentanoic acid is primarily located in the peroxisome. In humans, 5-amino-2-oxopentanoic acid is involved in the D-arginine and D-ornithine metabolism pathway. 5-Amino-2-oxopentanoic acid is also involved in the metabolic disorder called the fatty acid elongation in mitochondria pathway. 5-Amino-2-oxopentanoic acid is a breakdown product of D-proline. D-proline is first converted to 1-pyrroline-2-carboxylic acid via D-amino acid oxidase, which then spontaneously breaks down into 5-amino-2-oxopentanoic acid.

2-oxo-5-amino-pentanoate
2-oxo-5-amino-pentanoic acid
2-oxo-5-aminopentanoate
2-oxo-5-aminopentanoic acid
2-oxo-5-aminovalerate
5-amino-2-oxopentanoate
5-amino-2-oxopentanoic acid
Alpha-keto-delta-aminopentanoate
Alpha-keto-delta-aminopentanoic acid
5-amino-2-oxovaleric acid
2-oxo-5-aminovaleric acid
5-amino-2-oxovalerate
A-keto-delta-aminopentanoate
A-keto-delta-aminopentanoic acid
α-keto-δ-aminopentanoate
α-keto-δ-aminopentanoic acid
A-keto-δ-aminopentanoate
A-keto-δ-aminopentanoic acid


D-arginine

D-Arginine, also known as D-2-amino-5-guanidinovaleric acid or (2R)-2-amino-5-guanidinopentanoate, is a member of the class of compounds known as D-alpha-amino acids. D-alpha-Amino acids are alpha amino acids which have the D-configuration of the alpha-carbon atom. D-Arginine is slightly soluble (in water) and a moderately acidic compound (based on its pKa). D-Arginine can be found in human epidermis and platelet tissues. Within the cell, D-arginine is primarily located in the peroxisome. In humans, D-arginine is involved in D-arginine and D-ornithine metabolism. Arginine (abbreviated as Arg or R) is an alpha-amino acid that is used in the biosynthesis of proteins. It is encoded by the codons CGU, CGC, CGA, CGG, AGA, and AGG. It contains an alpha-amino group, an alpha-carboxylic acid group, and a side chain consisting of a 3-carbon aliphatic straight chain ending in a guanidino group. At physiological pH, the carboxylic acid is deprotonated (−COO−), the amino group is protonated (−NH3+), and the guanidino group is also protonated to give the guanidinium form (-C-(NH2)2+), making arginine a charged, aliphatic amino acid. It is the precursor for the biosynthesis of nitric oxide (Wikipedia). D-Arginine is an essential amino acid that is physiologically active in the L-form.


2-Oxoarginine is a guanidino compound metabolite of arginine catabolism. 2-Oxoarginine levels are increased in patients with argininemia (OMIM:207800). Argininemia, characterized by arginase deficiency (EC 3.5.3.1, catalyzes the last step of the urea cycle) is an autosomal recessive inborn error of metabolism caused by a defect in the final step in the urea cycle, the hydrolysis of arginine to urea and ornithine. Accumulation of arginine metabolites (such as guanidino compounds) especially 2-oxoarginine, may produce the central nervous system damage in argininemia. (PMID: 3433275, 1588833, 1690873, 819629).


superoxide

Superoxide is the anionic form O2. It is important as the product of the one-electron reduction of dioxygen (oxygen gas), which occurs widely in nature. With one unpaired electron, the superoxide ion is a free radical. It is also paramagnetic. The biological toxicity of superoxide is due to its capacity to inactivate iron-sulfur cluster containing enzymes (which are critical in a wide variety of metabolic pathways), thereby liberating free iron in the cell, which can undergo fenton-chemistry and generate the highly reactive hydroxyl radical. In its HO2 form, superoxide can also initiate lipid peroxidation of polyunsaturated fatty acids. It also reacts with carbonyl compounds and halogenated carbons to create toxic peroxy radicals. As such, superoxide is a main cause of oxidative stress. Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to Methemoglobin. Because superoxide is toxic, nearly all organisms living in the presence of oxygen contain isoforms of the superoxide scavenging enzyme, superoxide dismutase, or SOD. SOD is an extremely efficient enzyme; it catalyzes the neutralization of superoxide nearly as fast as the two can diffuse together spontaneously in solution. Genetic inactivation ("knockout") of SOD produces deleterious phenotypes in organisms ranging from bacteria to mice. The latter species dies around 21 days after birth if the mitochondrial variant of SOD (Mn-SOD) is inactivated, and suffers from multiple pathologies, including reduced lifespan, liver cancer, muscle atrophy, cataracts and female infertility when the cytoplasmic (Cu, Zn -SOD) variant is inactivated. With one unpaired electron, the superoxide ion is a free radical and therefore paramagnetic. In living organisms, superoxide dismutase protects the cell from the deleterious effects of superoxides.

Dioxidanidyl
Dioxide(1-)
Hyperoxid
Superoxide
Superoxide anion
Superoxide radical
Superoxide radical anion
(o2)(.-)
Hyperoxide
O2(.-)
O2(-)
Superoxide anion radical
Superoxyde


Ethanol

Ethanol is a clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. Indeed, ethanol has widespread use as a solvent of substances intended for human contact or consumption, including scents, flavorings, colorings, and medicines. Ethanol has a depressive effect on the central nervous system and because of its psychoactive effects, it is considered a drug. Ethanol has a complex mode of action and affects multiple systems in the brain, most notably it acts as an agonist to the GABA receptors. Death from ethanol consumption is possible when blood alcohol level reaches 0.4%. A blood level of 0.5% or more is commonly fatal. Levels of even less than 0.1% can cause intoxication, with unconsciousness often occurring at 0.3-0.4 %. Ethanol is metabolized by the body as an energy-providing carbohydrate nutrient, as it metabolizes into acetyl CoA, an intermediate common with glucose metabolism, that can be used for energy in the citric acid cycle or for biosynthesis. Ethanol within the human body is converted into acetaldehyde by alcohol dehydrogenase and then into acetic acid by acetaldehyde dehydrogenase. The product of the first step of this breakdown, acetaldehyde, is more toxic than ethanol. Acetaldehyde is linked to most of the clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver,[77] multiple forms of cancer, and alcoholism. Industrially, ethanol is produced both as a petrochemical, through the hydration of ethylene, and biologically, by fermenting sugars with yeast. Small amounts of ethanol are endogenously produced by gut microflora through anaerobic fermentation. However most ethanol detected in biofluids and tissues likely comes from consumption of alcoholic beverages. Absolute ethanol or anhydrous alcohol generally refers to purified ethanol, containing no more than one percent water. Absolute alcohol is not intended for human consumption. It often contains trace amounts of toxic benzene (used to remove water by azeotropic distillation). Consumption of this form of ethanol can be fatal over a short time period. Generally absolute or pure ethanol is used as a solvent for lab and industrial settings where water will disrupt a desired reaction. Pure ethanol is classed as 200 proof in the USA and Canada, equivalent to 175 degrees proof in the UK system.

1-hydroxyethane
Absolute alcohol
Absolute ethanol
Absolute ethyl alcohol
Aethanol
Aethylalkohol
Alcare hand degermer
Alcohol
Alcohols
Alcool ethylique
Alcool etilico
Algrain
Alkohol
Alkoholu etylowego
Anhydrol
Anhydrous alcohol
Cologne spirit
Cologne spirits
Dehydrated alcohol
Dehydrated ethanol
Denatured alcohol
Denatured ethanol
Desinfektol el
Diluted alcohol
Distilled spirits
Ethanol 200 proof
Ethanol solution
Ethicap
Ethyl alc
Ethyl alcohol
Ethyl alcohol anhydrous
Ethyl alcohol in alcoholic beverages
Ethyl alcohol usp
Ethyl hydrate
Ethyl hydroxide
Fermentation alcohol
Grain alcohol
Hinetoless
Hydroxyethane
Infinity pure
Jaysol
Jaysol s
Lux
Methylcarbinol
Molasses alcohol
Potato alcohol
Punctilious ethyl alcohol
Pyro
Silent spirit
Spirit
Spirits of wine
Spirt
Synasol
Tecsol
Tecsol c
Thanol
Undenatured ethanol
[ch2me(oh)]
[oeth]
Alcohol etilico
C2h5oh
Etanol
Etoh
Spiritus vini


acetaldehyde

Acetaldehyde is a colorless, flammable liquid used in the manufacture of acetic acid, perfumes, and flavors. It is also an intermediate in the metabolism of alcohol. It has a general narcotic action and also causes irritation of mucous membranes. Large doses may cause death from respiratory paralysis. Small amounts of acetaldehyde are produced naturally through gut microbial fermentation. Acetaldehyde is produced through the action of alcohol dehydrogenase on ethanol and is somewhate more toxic than ethanol. Acetaldehyde is linked to most of the negative clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver, multiple forms of cancer, and alcoholism.

Acetaldehyde
Acetic aldehyde
Aldehyde
Ethanal
Ethyl aldehyde
Acetaldehyd
Acetaldehydes
Azetaldehyd


3-Oxohexanoyl-CoA is an intermediate in Fatty acid elongation in mitochondria. 3-Oxohexanoyl-CoA is the 3rd to last step in the synthesis of Hexanoyl-CoA and is converted from Butanoyl-CoA via the enzyme acetyl-CoA acyltransferase 2 (EC 2.3.1.16). It is then converted to (S)-Hydroxyhexanoyl-CoA via the 3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.35).

3-ketohexanoyl coa.
3-ketohexanoyl coenzyme a.
3-oxohexanoyl-coa
3-oxohexanoyl-coenzyme a
Ketohexanoyl-coa
Ketohexanoyl-coenzyme a


(S)-Hydroxyhexanoyl-CoA is an intermediate in fatty acid metabolism, being the substrate of the enzymes beta-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.211) and 3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.35). (S)-Hydroxyhexanoyl-CoA is also an intermediate in fatty acid elongation in mitochondria, the substrate of the enzymes enoyl-CoA hydratase (EC 4.2.1.17) and long-chain-enoyl-CoA hydratase (EC 4.2.1.74) (KEGG).


trans-Hexenoyl-CoA is an intermediate in fatty acid metabolism. Beta-oxidation occurs in both mitochondria and peroxisomes. Mitochondria catalyze the beta-oxidation of the bulk of short-, medium-, and long-chain fatty acids derived from diet, and this pathway constitutes the major process by which fatty acids are oxidized to generate energy. Peroxisomes are involved in the beta-oxidation chain shortening of long-chain and very-long-chain fatty acyl-coenzyme (CoAs), long-chain dicarboxylyl-CoAs, the CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid intermediates di- and trihydroxycoprostanoic acids, and in the process they generate H2O2. Long-chain and very-long-chain fatty acids (VLCFAs) are also metabolized by the cytochrome P450 CYP4A omega-oxidation system to dicarboxylic acids that serve as substrates for peroxisomal beta-oxidation. The peroxisomal beta-oxidation system consists of (a) a classical peroxisome proliferator-inducible pathway capable of catalyzing straight-chain acyl-CoAs by fatty acyl-CoA oxidase, L-bifunctional protein, and thiolase, and (b) a second noninducible pathway catalyzing the oxidation of 2-methyl-branched fatty acyl-CoAs by branched-chain acyl-CoA oxidase (pristanoyl-CoA oxidase/trihydroxycoprostanoyl-CoA oxidase), D-bifunctional protein, and sterol carrier protein (SCP)x.  trans-Hexenoyl-CoA is the substrate of the enzymes enoyl-coenzyme A reductase, acyl-CoA oxidase [EC 1.3.99.2-1.3.3.6], acyl-CoA dehydrogenase, long-chain-acyl-CoA dehydrogenase [EC 1.3.99.3-1.3.99.13], and Oxidoreductases [EC 1.3.99.-]; trans-Hexenoyl-CoA is an intermediate in fatty acid elongation in mitochondria, being the substrate of the enzymes enoyl-CoA hydratase and long-chain-enoyl-CoA hydratase [EC 4.2.1.17-4.2.1.74]. (PMID: 11375435).


Hexanoyl-CoA

Hexanoyl-CoA, also known as hexanoyl-coenzyme A or caproyl-CoA, is a medium-chain fatty acyl-CoA having hexanoyl as the acyl group. Hexanoyl-CoA is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). Within the cell, hexanoyl-CoA is primarily located in the membrane (predicted from logP). It can also be found in the extracellular space. Hexanoyl-CoA exists in all living organisms, ranging from bacteria to humans. In humans, hexanoyl-CoA is involved in the biosynthesis and oxidation of fatty acids as well as in ceramide formation. Hexanoyl-CoA is also involved in few metabolic disorders, such as fatty acid elongation in mitochondria, mitochondrial beta-oxidation of medium chain saturated fatty acids, and mitochondrial beta-oxidation of short chain saturated fatty acids.

Caproyl-CoA
Caproyl coenzyme A
Caproyl-coenzyme A
Hexanoyl coenzyme A
Hexanoyl-coenzyme A
CoA(6:0)


3-Oxooctanoyl-CoA is the substrate of the acetyl-CoA C-acyltransferase/oxoacyl-CoA thiolase A (EC 2.3.1.16, SCP2/3-oxoacyl-CoA thiolase) present in peroxisomes from normal liver. Peroxisomes beta -oxidize a wide variety of substrates including straight chain fatty acids, 2-methyl-branched fatty acids, and the side chain of the bile acid intermediates di- and trihydroxycoprostanic acids. Peroxisomes contain several beta -oxidation pathways with different substrate specificities; or example, straight chain acyl-CoAs are desaturated by palmitoyl-CoA oxidase, and their enoyl-CoAs are then converted to 3-oxoacyl-CoAs by MFP-1, which forms (hydration) and dehydrogenates L-3(3S)-hydroxyacyl-CoAs; for example, straight chain acyl-CoAs are desaturated by palmitoyl-CoA oxidase (23), and their enoyl-CoAs are then converted to 3-oxoacyl-CoAs by 3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.35), which forms (hydration) and dehydrogenates L-3(3S)-hydroxyacyl-CoAs and their enoyl-CoAs are then converted to the corresponding 3-oxoacyl-CoAs by long-chain-enoyl-CoA hydratase(EC 4.2.1.74), which forms and dehydrogenates D-3(3R)-hydroxyacyl-CoAs. (PMID: 9325339).

3-ketooctanoyl-coa
3-ketooctanoyl-coenzyme a
3-oxooctanoyl coenzyme a
3-oxooctanoyl-coenzyme a
S-(3-oxooctanoate
S-(3-oxooctanoate) coa
S-(3-oxooctanoate) coenzyme a
S-(3-oxooctanoic acid


Coenzyme A is notable for its role in the synthesis and oxidation of fatty acids. Since coenzyme A is chemically a thiol, it can react with carboxylic acids to form thioesters, thus functioning as an acyl group carrier. It assists in transferring fatty acids from the cytoplasm to mitochondria. Specifically (S)-Hydroxyoctanoyl-CoA is involved in fatty acid metabolism. It is the product of a reaction between 3-Oxooctanoyl-CoA and two enzymes; 3-hydroxyacyl-CoA Dehydrogenase and long-chain- 3-hydroxyacyl-CoA dehydrogenase.


(2E)-Octenoyl-CoA is the main metabolite produced in medium-chain acyl-CoA dehydrogenase (EC 1.3.99.3, MCAD) deficiency; however the product of the enzymatic reaction is not directly detected in several methods for screening of inborn errors of fatty acid oxidation. In order to aid the timely follow-up of screening results that suggest abnormalities in MCAD, rapid and simple confirmatory tests for the enzyme activity and/or gene mutation analysis should be available. Medium-chain fatty acyl-CoA dehydrogenase (MCAD) catalyzes the conversion of different chain length fatty acyl- CoAs into their corresponding trans-enoyl-CoA moieties via two consecutive sequences of steps. The first step involves the concerted abstraction of a proton and a hydride ion from the a- and 8-carbon chains of the fatty acyl-CoA substrates, concomitant with the reduction of the enzyme (E)-bound FAD to FADH2. The reoxidation of EFADH2, to propagate further rounds of catalysis, is accomplished via transfer of electrons to a variety of organic electron acceptors; the natural electron acceptor for this process, under physiological conditions, is the electron-transferring flavoprotein. Of the different chain length fatty acyl-CoA substrates, octanoyl-CoA/octenoyl-CoA have been known as the most efficient (and physiological) substrates for the medium-chain fatty acyl-CoA dehydrogenase (MCAD)-catalyzed reaction. (PMID: 16046200, 1390638, 8038175).

(e)-s-2-octenoate
(e)-s-2-octenoate coa
(e)-s-2-octenoate coenzyme a
(e)-s-2-octenoic acid
2,3-trans-octenoyl coenzyme a
Oct-2-trans-enoyl-coa
Oct-2-trans-enoyl-coenzyme a
Oct-trans-2-enoyl coenzyme a
S-(2e)-2-octenoate
S-(2e)-2-octenoate coa
S-(2e)-2-octenoate coenzyme a
S-(2e)-2-octenoic acid
Trans-d2,3-octenoyl-coa
Trans-d2,3-octenoyl-coenzyme a
Trans-oct-2-enoyl-coa
Trans-oct-2-enoyl-coenzyme a


octanoyl-CoA

Octanoyl-CoA is a substrate for Trifunctional enzyme beta subunit (mitochondrial), Acyl-coenzyme A oxidase 1 (peroxisomal), 3-ketoacyl-CoA thiolase (mitochondrial), 3-ketoacyl-CoA thiolase (peroxisomal), Nuclear receptor-binding factor 1, Acyl-CoA dehydrogenase (long-chain specific, mitochondrial), Acyl-coenzyme A oxidase 3 (peroxisomal), HPDHase, Acyl-CoA dehydrogenase (medium-chain specific, mitochondrial), Acyl-coenzyme A oxidase 2 (peroxisomal) and Peroxisomal carnitine O-octanoyltransferase.

Capryloyl-coa
Capryloyl-coenzyme a
Octanoyl-coa
Octanoyl-coenzyme a
CoA(8:0)


3-Oxodecanoyl-CoA is an intermediate in fatty acid metabolism, the substrate of the enzyme acetyl-Coenzyme A acetyltransferase 1 and 2 [EC:2.3.1.16-2.3.1.9]; 3-Oxodecanoyl-CoA is an intermediate in fatty acid elongation in mitochondria, being the substrate of the enzymes beta-hydroxyacyl-CoA dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase [EC 1.1.1.211-1.1.1.35]. (KEGG).

3-ketodecanoyl-coa
3-ketodecanoyl-coenzyme a
3-oxodecanoyl-coenzyme a


(S)-Hydroxydecanoyl-CoA has a role in the synthesis and oxidation of fatty acids. It is involved in fatty acid elongation in mitochondria. In this pathway 3-Oxodecanoyl-CoA is acted upon by two enzymes, 3-hydroxyacyl-CoA dehydrogenase and long-chain-3-hydroxyacyl-CoA dehydrogenase to produce (S)-Hydroxydecanoyl-CoA. Since coenzyme A is chemically a thiol, it can react with carboxylic acids to form thioesters, thus functioning as an acyl group carrier. It assists in transferring fatty acids from the cytoplasm to mitochondria. A molecule of coenzyme A carrying an acetyl group is also referred to as acetyl-CoA. When it is not attached to an acyl group it is usually referred to as CoASH or HSCoA.

(s)-3-hydroxydecanoyl-coa
(s)-3-hydroxydecanoyl-coenzyme a
3-hydroxydecanoyl-coa
3-hydroxydecanoyl-coenzyme a
3s-hydroxy-decanoyl-coa
3s-hydroxy-decanoyl-coenzyme a
Dl-b-hydroxydecanoyl coenzyme a
Dl-beta-hydroxydecanoyl coenzyme a
S-(3-hydroxydecanoate
S-(3-hydroxydecanoate) coa
S-(3-hydroxydecanoate) coenzyme a
S-(3-hydroxydecanoate)coa
S-(3-hydroxydecanoate)coenzyme a
S-(3-hydroxydecanoic acid
B-hydroxydecanoyl coenzyme a
Beta-hydroxydecanoyl coenzyme a


(2E)-Decenoyl-CoA is a beta-oxidation intermediate, the substrate of the enzyme peroxisomal acyl-CoA thioesterase 2 (PTE-2, 3.1.2.2), which is localized in the peroxisome. The peroxisomal beta-oxidation system contains two sets of enzymes, one of which is involved in the oxidation of branched chain fatty acids and intermediates in the hepatic bile acid biosynthetic pathway and consists of one or two branched-chain acyl-CoA oxidase(s), a D-specific bifunctional protein and the sterol carrier-like protein x (SCPx). Peroxisomes are cellular organelles present in all eukaryotic cells. They play an indispensable role in the metabolism of a variety of lipids including very long-chain fatty acids, dicarboxylic fatty acids, bile acids, prostaglandins, leukotrienes, thromboxanes, pristanic acid, and xenobiotic fatty acids. (PMID: 11673457).

(e)-s-2-decenoate
(e)-s-2-decenoate coa
(e)-s-2-decenoate coenzyme a
(e)-s-2-decenoic acid
2-trans-decenoyl-coa
2-trans-decenoyl-coenzyme a
S-(2e)-2-decenoate
S-(2e)-2-decenoate coa
S-(2e)-2-decenoate coenzyme a
S-(2e)-2-decenoic acid
Trans-2-decenoylcoenzyme a
Trans-d2,3-decenoyl-coa
Trans-d2,3-decenoyl-coenzyme a
Trans-dec-2-enoyl-coa
Trans-dec-2-enoyl-coenzyme a


decanoyl-CoA

Decanoyl CoA is a human liver acyl-CoA ester. It is selected to determine apparent kinetic constants for human liver acyl-CoA due to its relevance to the human diseases with cellular accumulation of this esters, especially to metabolic defects in the acyl-CoA dehydrogenation steps of the branched-chain amino acids, lysine, 5-hydroxy lysine, tryptophan, and fatty acid oxidation pathways. It is concluded that the substrate concentration is decisive for the glycine conjugate formation and that the occurrence in urine of acylglycines reflects an intramitochondrial accumulation of the corresponding acyl-CoA ester. (PMID: 3707752).

Decanoyl coenzyme a monohydrate
Decanoyl-coa
Decanoyl-coenzyme a
S-decanoate
S-decanoate coenzyme a
S-decanoic acid
CoA(10:0)


3-Oxododecanoyl-CoA, also known as 3-oxolauroyl-coa, belongs to the class of organic compounds known as 3-oxo-acyl coas. These are organic compounds containing a 3-oxo acylated coenzyme A derivative. 3-Oxododecanoyl-CoA is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). 3-Oxododecanoyl-CoA has been primarily detected in urine. Within the cell, 3-oxododecanoyl-CoA is primarily located in the cytoplasm. 3-Oxododecanoyl-CoA exists in all living organisms, ranging from bacteria to humans. 3-Oxododecanoyl-CoA participates in a number of enzymatic reactions. In particular, 3-Oxododecanoyl-CoA can be biosynthesized from (S)-3-hydroxydodecanoyl-CoA through its interaction with the enzyme enoyl-CoA hydratase. In addition, 3-Oxododecanoyl-CoA can be converted into acetyl-CoA and tetradecanoyl-CoA; which is catalyzed by the enzyme acetyl-CoA C-acyltransferase. In humans, 3-oxododecanoyl-CoA is involved in the fatty acid metabolism pathway. 3-Oxododecanoyl-CoA is also involved in several metabolic disorders, some of which include the glutaric aciduria type I pathway, long chain acyl-CoA dehydrogenase deficiency (lcad), short chain acyl CoA dehydrogenase deficiency (scad deficiency), and carnitine palmitoyl transferase deficiency (I). 3-Oxododecanoyl-CoA is a human metabolite involved in the fatty acid elongation in mitochondria pathway. The enzyme acetyl-CoA C-acyltransferase catalyzes the formation of this metabolite from Acetyl-CoA.


(S)-3-Hydroxydodecanoyl-CoA, also known as (S)-3-hydroxylauroyl-coa, belongs to the class of organic compounds known as (s)-3-hydroxyacyl coas. These are organic compounds containing a (S)-3-hydroxyl acylated coenzyme A derivative (S)-3-Hydroxydodecanoyl-CoA is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa) (S)-3-Hydroxydodecanoyl-CoA has been primarily detected in urine. Within the cell, (S)-3-hydroxydodecanoyl-CoA is primarily located in the cytoplasm (S)-3-Hydroxydodecanoyl-CoA exists in all living organisms, ranging from bacteria to humans. In humans, (S)-3-hydroxydodecanoyl-CoA is involved in the fatty acid metabolism pathway (S)-3-Hydroxydodecanoyl-CoA is also involved in several metabolic disorders, some of which include the fatty acid elongation in mitochondria pathway, long-chain-3-hydroxyacyl-CoA dehydrogenase deficiency (lchad), short chain acyl CoA dehydrogenase deficiency (scad deficiency), and the mitochondrial Beta-oxidation OF medium chain saturated fatty acids pathway. (S)-3-Hydroxydodecanoyl-CoA is a human metabolite involved in the fatty acid elongation in mitochondria pathway. The enzyme long-chain-3-hydroxyacyl-CoA dehydrogenase catalyzes the conversion of 3-Oxododecanoyl-CoA to (S)-3-Hydroxydodecanoyl-CoA.

(s)-3-hydroxydodecanoyl-coenzyme a
(s)-3-hydroxylauroyl-coa
(s)-3-hydroxylauroyl-coenzyme a


(2E)-Dodecenoyl-CoA is an intermediate in fatty acid metabolism, the substrate of the enzyme acyl-CoA oxidase [EC-1.3.3.6], and enzymes acyl-CoA dehydrogenase, long-chain-acyl-CoA dehydrogenase [EC 1.3.99.3-1.3.99.13]; (2E)-Dodecenoyl-CoA is an intermediate in fatty acid elongation in mitochondria, being the substrate of the enzyme enoyl-CoA hydratase and [EC 4.2.1.17]. (KEGG).


Dodecyl-Coa

Lauroyl-CoA, also known as dodecanoyl-CoA or C12:0-CoA, belongs to the class of organic compounds known as 2,3,4-saturated fatty acyl coas. These are acyl-CoAs carrying a 2,3,4-saturated fatty acyl chain. Thus, lauroyl-CoA is considered to be a fatty ester lipid molecule. Lauroyl-CoA is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). Lauroyl-CoA has been primarily detected in urine. Within the cell, lauroyl-CoA is primarily located in the cytoplasm and peroxisome. Lauroyl-CoA exists in all living organisms, ranging from bacteria to humans. Lauroyl-CoA participates in a number of enzymatic reactions. In particular, Acetyl-CoA and lauroyl-CoA can be biosynthesized from 3-oxodecanoyl-CoA; which is mediated by the enzyme acetyl-CoA C-acyltransferase. In addition, Lauroyl-CoA can be biosynthesized from dodecanoic acid through the action of the enzyme short chain acyl-CoA synthetase. In humans, lauroyl-CoA is involved in the Beta oxidation OF very long chain fatty acids pathway, the fatty acid metabolism pathway, and the adrenoleukodystrophy, X-linked pathway. Lauroyl-CoA is also involved in several metabolic disorders, some of which include de novo triacylglycerol biosynthesis TG(i-22:0/12:0/i-17:0) pathway, de novo triacylglycerol biosynthesis TG(i-24:0/i-24:0/12:0) pathway, de novo triacylglycerol biosynthesis TG(i-22:0/13:0/12:0) pathway, and de novo triacylglycerol biosynthesis TG(22:0/a-13:0/12:0) pathway. Lauroyl-CoA is a substrate for Protein FAM34A.

Dodecanoyl-coa
Dodecanoyl-coenzyme a
Lauroyl coenzyme a
C12:0-coa
Coenzyme a, s-dodecanoate
Lauroyl-coenzyme a
CoA(12:0)


3-Oxotetradecanoyl-CoA is a product of the peroxisomal beta oxidation of hexadenoic acid by the enzyme acyl-CoA oxidase which results in long-chain 3-oxoacyl-CoA-esters. (PMID: 7548202). Myristoyl-CoA:protein N-myristoyltransferase (E.C. 2.3.1.97) is a eukaryotic enzyme that catalyzes the transfer of myristate (C14:O) from myristoyl-CoA to the amino nitrogen of glycine. This covalent protein modification occurs cotranslationally, is apparently irreversible, and affects proteins with diverse functions. (PMID: 2818568).


(S)-3-Hydroxytetradecanoyl-CoA is an intermediate in Fatty acid elongation in mitochondria. (S)-3-Hydroxytetradecanoyl-CoA is the 7th to last step in the synthesis of Hexadecanoic acid and is converted from 3-Oxotetradecanoyl-CoA via the enzyme long-chain 3-hydroxyacyl-CoA dehydrogenase (EC 1.1.1.211). It is then converted to trans-Tetradec-2-enoyl-CoA via the enzyme enoyl-CoA hydratase (EC 4.2.1.17).


(2E)-Tetradecenoyl-CoA is an intermediate in fatty acid metabolism, the substrate of the enzymes acyl-CoA oxidase and Oxidoreductases [EC 1.3.3.6-1.3.99.-] and enzymes acyl-CoA dehydrogenase, long-chain-acyl-CoA dehydrogenase [EC 1.3.99.3-1.3.99.13]; (2E)-Tetradecenoyl-CoA is an intermediate in fatty acid elongation in mitochondria, being the substrate of the enzyme trans-2-enoyl-CoA reductase (NADPH) [EC 1.3.1.38]. (KEGG).


Myristoyl-Coa

Tetradecanoyl-CoA (or myristoyl-CoA) is an intermediate in fatty acid biosynthesis, fatty acid elongation and the beta oxidation of fatty acids. It is also used in the myristoylation of proteins. The first pass through the beta-oxidation process starts with the saturated fatty acid palmitoyl-CoA and produces myristoyl-CoA. A total of four enzymatic steps are required, starting with VLCAD CoA dehydrogenase (Very Long Chain) activity, followed by three enzymatic steps catalyzed by enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and ketoacyl-CoA thiolase, all present in the mitochondria. Myristoylation of proteins is also catalyzed by the presence of myristoyl-CoA along with Myristoyl-CoA:protein N-myristoyltransferase (NMT). Myristoylation is an irreversible, co-translational (during translation) protein modification found in animals, plants, fungi and viruses. In this protein modification a myristoyl group (derived from myristioyl CoA) is covalently attached via an amide bond to the alpha-amino group of an N-terminal amino acid of a nascent polypeptide. It is more common on glycine residues but also occurs on other amino acids. Myristoylation also occurs post-translationally, for example when previously internal glycine residues become exposed by caspase cleavage during apoptosis. Myristoylation plays a vital role in membrane targeting and signal transduction in plant responses to environmental stress. Compared to other species that possess a single functional myristoyl-CoA: protein N-myristoyltransferase (NMT) gene copy, human, mouse and cow possess 2 NMT genes, and more than 2 protein isoforms.

Myristoyl-coa
Myristoyl-coenzyme a
N-c14:0coa
N-c14:0coenzyme a
S-tetradecanoyl-coenzyme a
Tetradecanoyl coa
Tetradecanoyl coenzyme a
Tetradecanoyl-coenzyme a
CoA(14:0)


3-Oxohexadecanoyl-CoA has a role in the synthesis and oxidation of fatty acid. It is involved in the pathway, fatty acid elongation in mitochondria. In this pathway Acetyl-CoA is acted upon by the enzyme, acetyl-CoA C-acyltransferase to produce 3-Oxohexadecanoyl-CoA. Since coenzyme A is chemically a thiol, it can react with carboxylic acids to form thioesters, thus functioning as an acyl group carrier. It assists in transferring fatty acids from the cytoplasm to the mitochondria. A molecule of coenzyme A carrying an acetyl group is also referred to as acetyl-CoA. When it is not attached to an acyl group it is usually referred to as 'CoASH' or 'HSCoA'.


(S)-3-Hydroxyhexadecanoyl-CoA is a beta-oxidation intermediate derivative of palmitoyl-CoA and the substrate of the enzyme peroxisomal acyl-CoA thioesterase 2 (PTE-2, EC 3.1.2.2), which is localized in the peroxisome. The peroxisomal beta-oxidation system contains two sets of enzymes, one of which is involved in the oxidation of branched chain fatty acids and intermediates in the hepatic bile acid biosynthetic pathway and consists of one or two branched-chain acyl-CoA oxidase(s), a D-specific bifunctional protein and the sterol carrier-like protein x (SCPx). Peroxisomes are cellular organelles present in all eukaryotic cells. They play an indispensable role in the metabolism of a variety of lipids including very long-chain fatty acids, dicarboxylic fatty acids, bile acids, prostaglandins, leukotrienes, thromboxanes, pristanic acid, and xenobiotic fatty acids. (S)-3-Hydroxyhexadecanoyl-CoA may accumulate intracellularly in certain long-chain fatty acid/j-oxidation deficiencies. Succinate-driven synthesis of ATP from ADP and phosphate is progressively inhibited by increasing concentrations of (S)-3-Hydroxyhexadecanoyl-CoA. (PMID: 11673457, 8739955, 7662716).

(s)-3-hydroxyhexadecanoyl-coenzyme a
(s)-3-hydroxypalmitoyl-coenzyme a
Dl-3-hydroxyhexadecanoyl-s-coenzyme a
Dl-3-hydroxyhexadecanoyl-scoa
Dl-3-hydroxyhexadecanoyl-scoenzyme a
S-(3-hydroxyhexadecanoate
S-(3-hydroxyhexadecanoate)coenzyme a
S-(3-hydroxyhexadecanoic acid
S-dl-3-hydroxyhexadecanoate
S-dl-3-hydroxyhexadecanoic acid
B-hydroxypalmitoyl-coa
B-hydroxypalmitoyl-coenzyme a
Beta-hydroxypalmitoyl-coa
Beta-hydroxypalmitoyl-coenzyme a


(2E)-Hexadecenoyl-CoA is an intermediate in fatty acid metabolism, the substrate of the enzyme enoyl-CoA hydratase [EC:4.2.1.17]; (2E)-Hexadecenoyl-CoA is also the substrate of the enzyme trans-2-enoyl-CoA reductase [EC:1.3.1.38], in the fatty acid elongation pathway in mitochondria. (PMID: 1278159, KEGG).


palmitoyl-CoA

Palmityl-CoA, also known as palmitoyl CoA or CoA, palmitoyl, belongs to the class of organic compounds known as long-chain fatty acyl coas. These are acyl CoAs where the group acylated to the coenzyme A moiety is a long aliphatic chain of 13 to 21 carbon atoms. Palmityl-CoA is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). Palmityl-CoA has been found throughout most human tissues, and has also been primarily detected in urine. Within the cell, palmityl-CoA is primarily located in the cytoplasm and mitochondria. In humans, palmityl-CoA is involved in cardiolipin biosynthesis CL(16:0/18:2(9Z,12Z)/22:6(4Z,7Z,10Z,13Z,16Z,19Z)/16:0) pathway, cardiolipin biosynthesis CL(16:0/22:5(4Z,7Z,10Z,13Z,16Z)/16:1(9Z)/22:5(4Z,7Z,10Z,13Z,16Z)) pathway, cardiolipin biosynthesis CL(16:0/18:0/16:0/22:5(4Z,7Z,10Z,13Z,16Z)) pathway, and cardiolipin biosynthesis CL(22:5(7Z,10Z,13Z,16Z,19Z)/16:0/22:5(7Z,10Z,13Z,16Z,19Z)/16:1(9Z)) pathway. Palmityl-CoA is also involved in several metabolic disorders, some of which include de novo triacylglycerol biosynthesis TG(14:1(9Z)/16:0/14:1(9Z)) pathway, de novo triacylglycerol biosynthesis TG(16:0/14:1(9Z)/14:1(9Z)) pathway, de novo triacylglycerol biosynthesis TG(a-25:0/i-14:0/16:0) pathway, and de novo triacylglycerol biosynthesis TG(20:3(5Z,8Z,11Z)/16:0/22:5(7Z,10Z,13Z,16Z,19Z)) pathway. Palmityl-CoA is a fatty acid coenzyme derivative which plays a key role in fatty acid oxidation and biosynthesis.

Hexadecanoyl coa
Hexadecanoyl coenzyme a
Palmitoyl coa
Palmitoyl coenzyme a
Palmitoyl-coa
Palmitoyl-coenzyme a
Palmityl-coa
Palmityl-coenzyme a
S-hexadecanoate
S-hexadecanoate coa
S-hexadecanoate coenzyme a
S-hexadecanoic acid
S-palmitoylcoenzyme a
CoA(16:0)


Palmitic Acid

Palmitic acid, or hexadecanoic acid, is one of the most common saturated fatty acids found in animals, plants, and microorganisms. As its name indicates, it is a major component of the oil from the fruit of oil palms (palm oil). Excess carbohydrates in the body are converted to palmitic acid. Palmitic acid is the first fatty acid produced during fatty acid synthesis and is the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to make up 21–30% (molar) of human depot fat (PMID: 13756126), and it is a major, but highly variable, lipid component of human breast milk (PMID: 352132). Palmitic acid is used to produce soaps, cosmetics, and industrial mould release agents. These applications use sodium palmitate, which is commonly obtained by saponification of palm oil. To this end, palm oil, rendered from palm tree (species Elaeis guineensis), is treated with sodium hydroxide (in the form of caustic soda or lye), which causes hydrolysis of the ester groups, yielding glycerol and sodium palmitate. Aluminium salts of palmitic acid and naphthenic acid were combined during World War II to produce napalm. The word "napalm" is derived from the words naphthenic acid and palmitic acid (Wikipedia). Palmitic acid is also used in the determination of water hardness and is a surfactant of Levovist, an intravenous ultrasonic contrast agent.

1-hexyldecanoate
1-hexyldecanoic acid
1-pentadecanecarboxylic acid
C16 fatty acid
Cetylic acid
Edenor c16
Emersol 140
Emersol 143
Glycon p-45
Hexadecanoate
Hexadecanoic acid
Hexadecanoic acid palmitic acid
Hexadecoate
Hexadecoic acid
Hexadecylic acid
Hexaectylic acid
Hydrofol
Hydrofol acid 1690
Hystrene 8016
Hystrene 9016
Industrene 4516
Kortacid 1698
Loxiol ep 278
Lunac p 95
Lunac p 95kc
Lunac p 98
N-hexadecanoate
N-hexadecanoic acid
N-hexadecoate
N-hexadecoic acid
Pam
Plm
Palmitate
Palmitic acid
Palmitinate
Palmitinic acid
Palmitinsaeure
Palmitoate
Palmitoic acid
Pentadecanecarboxylate
Pentadecanecarboxylic acid
Prifac 2960
Prifrac 2960
Pristerene 4934
Univol u332
C16:0
Ch3-[ch2]14-cooh
1-pentadecanecarboxylate
Cetylate
Hexadecylate
Hexaectylate
Hexadecanoate (n-c16:0)
FA(16:0)


O-palmitoyl-L-carnitine

L-Palmitoylcarnitine is a long-chain acyl fatty acid derivative ester of carnitine which facilitates the transfer of long-chain fatty acids from cytoplasm into mitochondria during the oxidation of fatty acids. L-palmitoylcarnitine, due to its amphipatic character is, like detergents, a surface-active molecule and by changing the membrane fluidity and surface charge can change activity of several enzymes and transporters localized in the membrane. L-palmitoylcarnitine has been also reported to change the activity of certain proteins. On the contrary to carnitine, palmitoylcarnitine was shown to stimulate the activity of caspases 3, 7 and 8 and the level of this long-chain acylcarnitine increased during apoptosis. Palmitoylcarnitine was also reported to diminish completely binding of phorbol esters, the protein kinase C activators and to decrease the autophosphorylation of the enzyme. Apart from these isoform nonspecific phenomena, palmitoylcarnitine was also shown to be responsible for retardation in cytoplasm of protein kinase C isoforms β and δ and, in the case of the latter one, to decrease its interaction with GAP-43. Some of the physico-chemical properties of palmitoylcarnitine may help to explain the need for coenzyme A-carnitine-coenzyme A acyl exchange during mitochondrial fatty acid import. The amphiphilic character of palmitoylcarnitine may also explain its proposed involvement in the pathogenesis of myocardial ischemia. L-Palmitoylcarnitine accumulates in ischemic myocardium and potentially contribute to myocardial damage through alterations in membrane molecular dynamics , one mechanism through which could play an important role in ischemic injury. Palmitoylcarnitine is characteristically elevated in carnitine palmitoyltransferase II deficiency, late-onset (OMIM 255110). (PMID 2540838, 15363641, 8706815).


glutaryl-CoA

Glutaryl-CoA is a substrate for 2-oxoglutarate dehydrogenase E1 component (mitochondrial), Dihydrolipoyllysine-residue succinyltransferase component of 2- oxoglutarate dehydrogenase complex (mitochondrial) and Glutaryl-CoA dehydrogenase (mitochondrial).


dihydrofolate

Dihydrofolic acid is a folic acid derivative acted upon by dihydrofolate reductase to produce tetrahydrofolic acid. It interacts with bacteria during cell division. It can be targeted with drug analogs to prevent nucleic acid synthesis. Dihydrofolic acid is also known by the name Dihydrofolate - more commonly Vitamin B9.


Folic acid

Folic acid is a member of the vitamin B family that stimulates the hematopoietic system. It is present in the liver and kidney and is found in mushrooms, spinach, yeast, green leaves, and grasses (poaceae). Folic acid, being biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase. These folic acid congeners are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylated tRNA, and generate and use formate. Folic acid is used in the treatment and prevention of folate deficiencies and megaloblastic anemia.


Formic acid

Formic acid is the simplest carboxylic acid. Formate is an intermediate in normal metabolism. It takes part in the metabolism of one-carbon compounds and its carbon may appear in methyl groups undergoing transmethylation. It is eventually oxidized to carbon dioxide. Formate is typically produced as a byproduct in the production of acetate. It is responsible for both metabolic acidosis and disrupting mitochondrial electron transport and energy production by inhibiting cytochrome oxidase activity, the terminal electron acceptor of the electron transport chain. Cell death from cytochrome oxidase inhibition by formate is believed to result partly from depletion of ATP, reducing energy concentrations so that essential cell functions cannot be maintained. Furthermore, inhibition of cytochrome oxidase by formate may also cause cell death by increased production of cytotoxic reactive oxygen species (ROS) secondary to the blockade of the electron transport chain. In nature, formic acid is found in the stings and bites of many insects of the order Hymenoptera, including bees and ants. The principal use of formic acid is as a preservative and antibacterial agent in livestock feed. When sprayed on fresh hay or other silage, it arrests certain decay processes and causes the feed to retain its nutritive value longer.

Add-f
Ameisensaure
Aminate
Aminic acid
Bilorin
Collo-bueglatt
Collo-didax
Formate
Formira
Formisoton
Formylate
Formylic acid
Hydrogen carboxylate
Hydrogen carboxylic acid
Methanoate
Methanoic acid
Methanoic acid monomer
Myrmicyl
Sodium formate
Sybest
Wonderbond hardener m 600l


10-formyltetrahydrofolic acid

10-Formyltetrahydrofolate (10-CHO-THF) is form of tetrahydrofolate that acts as a donor of formyl groups in anabolism. In particular, 10-CHO-THF is used as a substrate in a number of formyltransferase reactions. It plays an important role in purine biosynthesis, where 10-CHO-THF is a substrate for phosphoribosylaminoimidazolecarboxamide formyltransferase, as well as in the formylation of the methionyl initiator tRNA (fMet-tRNA), when 10-CHO-THF is a substrate for methionyl-tRNA formyltransferase. 10-Formyltetrahydrofolate is a substrate for Trifunctional purine biosynthetic protein adenosine-3, Bifunctional methylenetetrahydrofolate dehydrogenase/cyclohydrolase (mitochondrial), 10-formyltetrahydrofolate dehydrogenase, Folylpolyglutamate synthase (mitochondrial), Bifunctional purine biosynthesis protein PURH and C-1-tetrahydrofolate synthase (cytoplasmic).


Oxisterigmatocystin D

N5-Formyl-THF, also known as leucovorin or folinate, calcium, belongs to the class of organic compounds known as tetrahydrofolic acids. These are heterocyclic compounds based on the 5,6,7,8-tetrahydropteroic acid skeleton conjugated with at least one L-glutamic acid unit. N5-Formyl-THF exists as a solid and is considered to be practically insoluble (in water) and relatively neutral. N5-Formyl-THF has been found in human bladder, testicle and pancreas tissues, and has also been primarily detected in blood. Within the cell, N5-formyl-THF is primarily located in the mitochondria and cytoplasm. N5-Formyl-THF exists in all living organisms, ranging from bacteria to humans. In humans, N5-formyl-THF is involved in the methotrexate action pathway, the folate metabolism pathway, and the folate malabsorption, hereditary pathway. N5-Formyl-THF is also involved in the metabolic disorder called methylenetetrahydrofolate reductase deficiency (MTHFRD). The active metabolite of folic acid. Leucovorin is used principally as its calcium salt as an antidote to folic acid antagonists which block the conversion of folic acid to folinic acid.


N-formyl-L-glutamic acid

N-Formyl-L-glutamate is an intermediate in the histidine metabolism, in a reaction mediated by the enzyme formiminotransferase cyclodeaminase [EC:2.1.2.5 4.3.1.4], a bifunctional enzyme that channels 1-carbon units from formiminoglutamate to the folate pool.(KEGG).

(2s)-2-(formylamino)pentanedioate
(2s)-2-(formylamino)pentanedioic acid
(2s)-2-formamidopentanedioate
(2s)-2-formamidopentanedioic acid
N-formyl-l-glutamate
N-formyl-l-glutamic acid


5-formimidoyltetrahydrofolic acid

5-Formiminotetrahydrofolic acid belongs to the class of organic compounds known as tetrahydrofolic acids. These are heterocyclic compounds based on the 5,6,7,8-tetrahydropteroic acid skeleton conjugated with at least one L-glutamic acid unit. 5-Formiminotetrahydrofolic acid is considered to be a practically insoluble (in water) and relatively neutral molecule. Within the cell, 5-formiminotetrahydrofolic acid is primarily located in the cytoplasm. In humans, 5-formiminotetrahydrofolic acid is involved in the folate metabolism pathway, the folate malabsorption, hereditary pathway, the histidine metabolism pathway, and the methotrexate action pathway. 5-Formiminotetrahydrofolic acid is also involved in a couple of metabolic disorders, which include the histidinemia pathway and methylenetetrahydrofolate reductase deficiency (MTHFRD). 5-Formiminotetrahydrofolic acid is a substrate for Formimidoyltransferase-cyclodeaminase.


Tetrahydrofolyl-[Glu](n) is involved in the folate biosynthesis pathway. Tetrahydrofolyl-[Glu](n) can be reversibly converted into Tetrahydrofolyl-[Glu](2) by folylpolyglutamate synthase [EC:6.3.2.17]. Tetrahydrofolyl-[Glu](n) can be irreversibly converted into tetrahydrofolate by gamma-glutamyl hydrolase [EC:3.4.19.9].


5,6,7,8-tetrahydrofolyl-L-glutamic acid

Tetrahydrofolyl-[Glu](n) is involved in the folate biosynthesis pathway. Tetrahydrofolyl-[Glu](n) can be reversibly converted into Tetrahydrofolyl-[Glu](2) by folylpolyglutamate synthase [EC:6.3.2.17]. Tetrahydrofolyl-[Glu](n) can be irreversibly converted into tetrahydrofolate by gamma-glutamyl hydrolase [EC:3.4.19.9]. Sample structure image shows the case when n=3.


Sorbitol

Sorbitol is a polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications. Ascorbic acid fermentation; in solution form for moisture-conditioning of cosmetic creams and lotions, toothpaste, tobacco, gelatin; bodying agent for paper, textiles, and liquid pharmaceuticals; softener for candy; sugar crystallization inhibitor; surfactants; urethane resins and rigid foams; plasticizer, stabilizer for vinyl resins; food additive (sweetener, humectant, emulsifier, thickener, anticaking agent); dietary supplement. (Hawley's Condensed Chemical Dictionary) Biological Source: Occurs widely in plants ranging from algae to the higher orders. Fruits of the plant family Rosaceae, which include apples, pears, cherries, apricots, contain appreciable amounts. Rich sources are the fruits of the Sorbus and Crataegus species Use/Importance: Used for manufacturing of sorbose, propylene glycol, ascorbic acid, resins, plasticizers and as antifreeze mixtures with glycerol or glycol. Tablet diluent, sweetening agent and humectant, other food uses. Sorbitol is used in photometric determination of Ru(VI) and Ru(VIII); in acid-base titration of borate (Dictionary of Organic Compounds).

(-)-sorbitol
D-glucitol
D-sorbitol
D-sorbol
Diakarmon
Esasorb
Foodol d 70
Glucarine
Glucitol
Karion
Karion instant
Kyowa powder 50m
L-gulitol
Multitol
Neosorb
Neosorb 20/60dc
Neosorb 70/02
Neosorb 70/70
Neosorb p 20/60
Neosorb p 60
Neosorb p 60w
Nivitin
Resulax
Sionit
Sionit k
Sionite
Sionon
Siosan
Sorbex m
Sorbex r
Sorbex rp
Sorbex s
Sorbex x
Sorbilande
Sorbilax
Sorbit
Sorbit d 70
Sorbit d-powder
Sorbit dp
Sorbit dp 50
Sorbit kyowa powder 50m
Sorbit l 70
Sorbit s
Sorbit t 70
Sorbit w 70
Sorbit w-powder
Sorbit w-powder 50
Sorbit wp
Sorbite
Sorbitol f
Sorbitol fk
Sorbitol fp
Sorbitol s
Sorbitol syrup c
Sorbitur
Sorbo
Sorbogem 712
Sorbol
Sorbostyl
(2r,3r,4r,5s)-hexane-1,2,3,4,5,6-hexol
D-(-)-sorbitol
D-sorbit
E 420
E-420
E420
G-ol
Glc-ol


alpha-D-glucose

Alpha-D-Glucose, also known as alpha-dextrose or alpha-D-GLC, belongs to the class of organic compounds known as hexoses. These are monosaccharides in which the sugar unit is a is a six-carbon containing moeity. Alpha-D-Glucose exists as a solid, soluble (in water), and a very weakly acidic compound (based on its pKa). Alpha-D-Glucose has been found in human epidermis and intestine tissues, and has also been detected in multiple biofluids, such as feces and saliva. Within the cell, Alpha-D-glucose is primarily located in the cytoplasm. Alpha-D-Glucose exists in all living organisms, ranging from bacteria to humans. Alpha-D-Glucose participates in a number of enzymatic reactions. In particular, Alpha-D-Glucose and Beta-D-glucose can be biosynthesized from α,α-trehalose; which is mediated by the enzyme cytoplasmic trehalase. Furthermore, Beta-D-Glucose and Alpha-D-glucose can be biosynthesized from α,α-trehalose; which is catalyzed by the enzyme periplasmic trehalase. Furthermore, Alpha-D-Glucose can be converted into α-D-glucose 6-phosphate through its interaction with the enzyme glucose PTS permease. Finally, Alpha-D-Glucose can be converted into α-D-glucose 6-phosphate; which is catalyzed by the enzyme glucose PTS permease. In humans, Alpha-D-glucose is involved in the nucleotide sugars metabolism pathway, the starch and sucrose metabolism pathway, the fructose intolerance, hereditary pathway, and the fructose and mannose degradation pathway. Alpha-D-Glucose is also involved in several metabolic disorders, some of which include the glycogenosis, type ia. von gierke disease pathway, sucrase-isomaltase deficiency, fructose-1,6-diphosphatase deficiency, and the mucopolysaccharidosis vi. sly syndrome pathway. Outside of the human body, Alpha-D-glucose can be found in a number of food items such as naranjilla, shallot, apple, and peach (var.). This makes Alpha-D-glucose a potential biomarker for the consumption of these food products. Alpha-D-Glucose is a primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.

Hexopyranose A-d-glucopyranose A-d-glucose A-dextrose A-glucose Alpha-d-glucopyranose Alpha-d-glucose Alpha-dextrose Alpha-glucose Alpha-delta-glucopyranose Alpha-delta-glucose Alpha-d-glc A-d-glc α-d-glc α-d-glucose α-dextrose


beta-D-fructofuranose 2-phosphate

Beta-D-Fructose 2-phosphate, also known as 2-O-phosphono-b-D-fructofuranose or b-D-fructofuranose 2-phosphate, belongs to the class of organic compounds known as c-glycosyl compounds. These are glycoside in which a sugar group is bonded through one carbon to another group via a C-glycosidic bond. Beta-D-Fructose 2-phosphate is soluble (in water) and an extremely strong acidic compound (based on its pKa). Beta-D-Fructose 2-phosphate exists in all living organisms, ranging from bacteria to humans. In humans, Beta-D-fructose 2-phosphate is involved in the fructose and mannose degradation pathway and the fructose intolerance, hereditary pathway. Beta-D-Fructose 2-phosphate is also involved in the metabolic disorder called the fructosuria pathway. beta-D-Fructose 2-phosphate is involved in the fructose eand mannose system. beta-D-Fructose 2-phosphate is produced from beta-D-Fructose 2,6-bisphosphate by the enzyme fructose-2,6-bisphosphate 6-phosphatase [EC 3.1.3.54].

Beta-d-fructofuranose 2-phosphate
Beta-d-fructose 2-phosphate
2-o-phosphono-beta-d-fructofuranose
2-phospho-beta-d-fructofuranose
2-o-phosphono-b-d-fructofuranose
2-o-phosphono-β-d-fructofuranose
B-d-fructofuranose 2-phosphate
B-d-fructofuranose 2-phosphoric acid
Beta-d-fructofuranose 2-phosphoric acid
β-d-fructofuranose 2-phosphate
β-d-fructofuranose 2-phosphoric acid
2-phospho-b-d-fructofuranose
2-phospho-β-d-fructofuranose
B-d-fructose 2-phosphate
B-d-fructose 2-phosphoric acid
Beta-d-fructose 2-phosphoric acid
β-d-fructose 2-phosphate
β-d-fructose 2-phosphoric acid


beta-D-mannose 6-phosphate

Mannose 6-phosphate, also known as alpha-D-mannose-6-p or man-6-p, belongs to the class of organic compounds known as hexose phosphates. These are carbohydrate derivatives containing a hexose substituted by one or more phosphate groups. Mannose 6-phosphate is soluble (in water) and a moderately acidic compound (based on its pKa). Mannose 6-phosphate has been found throughout most human tissues. Within the cell, mannose 6-phosphate is primarily located in the cytoplasm. In humans, mannose 6-phosphate is involved in the fructose and mannose degradation pathway and the fructose intolerance, hereditary pathway. Mannose 6-phosphate is also involved in the metabolic disorder called the fructosuria pathway. Mannose-6-phosphate is a potent competitive inhibitor of pinocytosis of human platelet beta-glucuronidase and it is a necessary component of the recognition marker on the enzyme for pinocytosis by human fibroblasts as well (PMID 908752).


D-mannopyranose

D-Mannose is a carbohydrate. High-mannose-type oligosaccharides have been shown to play important roles in protein quality control. Several intracellular proteins, such as lectins, chaperones and glycan-processing enzymes, are involved in this process. These include calnexin/calreticulin, UDP-glucose:glycoprotein glucosyltransferase (UGGT), cargo receptors (such as VIP36 and ERGIC-53), mannosidase-like proteins (e.g. EDEM and Htm1p) and ubiquitin ligase (Fbs). They are thought to recognize high-mannose-type glycans with subtly different structures. Mannose-binding lectin (MBL) is an important constituent of the innate immune system. This protein binds through multiple lectin domains to the repeating sugar arrays that decorate many microbial surfaces, and is then able to activate the complement system through a specific protease called MBL-associated protease-2. The primary pathway for the formation of L-fucose in procaryotic and eucaryotic cells is from D-mannose via an internal oxidation reduction and then epimerization of GDP-D-mannose to produce GDP-L-fucose. (PMID: 9488699, 16154739, 11414367).

(+)-mannose (+-)-mannose Carubinose D(+)-mannose D-mannopyranose D-mannose Dl-mannose Mannose Seminose Mannopyranose