Reaction Process: Plant Reactome:R-ADU-1119528

S-adenosylhomocysteine (SAH)

C14H20N6O5S (384.12158300000004)

S-Adenosyl-L-homocysteine (SAH) is formed by the demethylation of S-adenosyl-L-methionine. S-Adenosylhomocysteine (AdoHcy or SAH) is also the immediate precursor of all of the homocysteine produced in the body. The reaction is catalyzed by S-adenosylhomocysteine hydrolase and is reversible with the equilibrium favoring formation of SAH. In vivo, the reaction is driven in the direction of homocysteine formation by the action of the enzyme adenosine deaminase which converts the second product of the S-adenosylhomocysteine hydrolase reaction, adenosine, to inosine. Except for methyl transfer from betaine and from methylcobalamin in the methionine synthase reaction, SAH is the product of all methylation reactions that involve S-adenosylmethionine (SAM) as the methyl donor. Methylation is significant in epigenetic regulation of protein expression via DNA and histone methylation. The inhibition of these SAM-mediated processes by SAH is a proven mechanism for metabolic alteration. Because the conversion of SAH to homocysteine is reversible, with the equilibrium favoring the formation of SAH, increases in plasma homocysteine are accompanied by an elevation of SAH in most cases. Disturbances in the transmethylation pathway indicated by abnormal SAH, SAM, or their ratio have been reported in many neurodegenerative diseases, such as dementia, depression, and Parkinsons disease (PMID:18065573, 17892439). Therefore, when present in sufficiently high levels, S-adenosylhomocysteine can act as an immunotoxin and a metabotoxin. An immunotoxin disrupts, limits the function, or destroys immune cells. A metabotoxin is an endogenous metabolite that causes adverse health effects at chronically high levels. Chronically high levels of S-adenosylhomocysteine are associated with S-adenosylhomocysteine (SAH) hydrolase deficiency and adenosine deaminase deficiency. S-Adenosylhomocysteine forms when there are elevated levels of homocysteine and adenosine. S-Adenosyl-L-homocysteine is a potent inhibitor of S-adenosyl-L-methionine-dependent methylation reactions. It is toxic to immature lymphocytes and can lead to immunosuppression (PMID:221926). S-adenosylhomocysteine, also known as adohcy or sah, is a member of the class of compounds known as 5-deoxy-5-thionucleosides. 5-deoxy-5-thionucleosides are 5-deoxyribonucleosides in which the ribose is thio-substituted at the 5position by a S-alkyl group. S-adenosylhomocysteine is slightly soluble (in water) and a moderately acidic compound (based on its pKa). S-adenosylhomocysteine can be found in a number of food items such as rapini, european plum, rambutan, and pepper (c. pubescens), which makes S-adenosylhomocysteine a potential biomarker for the consumption of these food products. S-adenosylhomocysteine can be found primarily in blood, cerebrospinal fluid (CSF), feces, and urine, as well as throughout most human tissues. S-adenosylhomocysteine exists in all living species, ranging from bacteria to humans. In humans, S-adenosylhomocysteine is involved in several metabolic pathways, some of which include phosphatidylcholine biosynthesis PC(14:0/18:3(9Z,12Z,15Z)), phosphatidylcholine biosynthesis PC(22:4(7Z,10Z,13Z,16Z)/22:0), phosphatidylcholine biosynthesis PC(20:3(5Z,8Z,11Z)/22:2(13Z,16Z)), and phosphatidylcholine biosynthesis PC(18:3(6Z,9Z,12Z)/22:5(7Z,10Z,13Z,16Z,19Z)). S-adenosylhomocysteine is also involved in several metabolic disorders, some of which include 3-phosphoglycerate dehydrogenase deficiency, hawkinsinuria, non ketotic hyperglycinemia, and tyrosine hydroxylase deficiency. Moreover, S-adenosylhomocysteine is found to be associated with neurodegenerative disease and parkinsons disease. S-adenosylhomocysteine is a non-carcinogenic (not listed by IARC) potentially toxic compound. S-Adenosyl-L-homocysteine (SAH) is an amino acid derivative used in several metabolic pathways in most organisms. It is an intermediate in the synthesis of cysteine and adenosine . [Spectral] S-Adenosyl-L-homocysteine (exact mass = 384.12159) and Adenosine (exact mass = 267.09675) were not completely separated on HPLC under the present analytical conditions as described in AC$XXX. Additionally some of the peaks in this data contains dimers and other unidentified ions. [Spectral] S-Adenosyl-L-homocysteine (exact mass = 384.12159) and Cytidine (exact mass = 243.08552) were not completely separated on HPLC under the present analytical conditions as described in AC$XXX. Additionally some of the peaks in this data contains dimers and other unidentified ions. Acquisition and generation of the data is financially supported in part by CREST/JST. COVID info from PDB, Protein Data Bank, WikiPathways Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS SAH (S-Adenosylhomocysteine) is an amino acid derivative and a modulartor in several metabolic pathways. It is an intermediate in the synthesis of cysteine and adenosine[1]. SAH is an inhibitor for METTL3-METTL14 heterodimer complex (METTL3-14) with an IC50 of 0.9 μM[2]. SAH (S-Adenosylhomocysteine) is an amino acid derivative and a modulartor in several metabolic pathways. It is an intermediate in the synthesis of cysteine and adenosine[1]. SAH is an inhibitor for METTL3-METTL14 heterodimer complex (METTL3-14) with an IC50 of 0.9 μM[2].

Beta-Alanine

C3H7NO2 (89.0476762)

beta-Alanine is the only naturally occurring beta-amino acid - an amino acid in which the amino group is at the beta-position from the carboxylate group. It is formed in vivo by the degradation of dihydrouracil and carnosine. It is a component of the naturally occurring peptides carnosine and anserine and also of pantothenic acid (vitamin B-5), which itself is a component of coenzyme A. Under normal conditions, beta-alanine is metabolized into acetic acid. beta-Alanine can undergo a transanimation reaction with pyruvate to form malonate-semialdehyde and L-alanine. The malonate semialdehyde can then be converted into malonate via malonate-semialdehyde dehydrogenase. Malonate is then converted into malonyl-CoA and enter fatty acid biosynthesis. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, beta-alanine may act as a false transmitter replacing gamma-aminobutyric acid. When present in sufficiently high levels, beta-alanine can act as a neurotoxin, a mitochondrial toxin, and a metabotoxin. A neurotoxin is a compound that damages the brain or nerve tissue. A mitochondrial toxin is a compound that damages mitochondria and reduces cellular respiration as well as oxidative phosphorylation. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of beta-alanine are associated with at least three inborn errors of metabolism, including GABA-transaminase deficiency, hyper-beta-alaninemia, and methylmalonate semialdehyde dehydrogenase deficiency. beta-Alanine is a central nervous system (CNS) depressant and is an inhibitor of GABA transaminase. The associated inhibition of GABA transaminase and displacement of GABA from CNS binding sites can also lead to GABAuria (high levels of GABA in the urine) and convulsions. In addition to its neurotoxicity, beta-alanine reduces cellular levels of taurine, which are required for normal respiratory chain function. Cellular taurine depletion is known to reduce respiratory function and elevate mitochondrial superoxide generation, which damages mitochondria and increases oxidative stress (PMID: 27023909). Individuals suffering from mitochondrial defects or mitochondrial toxicity typically develop neurotoxicity, hypotonia, respiratory distress, and cardiac failure. beta-Alanine is a biomarker for the consumption of meat, especially red meat. Widely distributed in plants including algae, fungi and many higher plants. Flavouring ingredient β-Alanine. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=107-95-9 (retrieved 2024-07-01) (CAS RN: 107-95-9). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0). β-Alanine is a non-essential amino acid that is shown to be metabolized into carnosine, which functions as an intracellular buffer. β-Alanine is a non-essential amino acid that is shown to be metabolized into carnosine, which functions as an intracellular buffer. β-Alanine is a non-essential amino acid that is shown to be metabolized into carnosine, which functions as an intracellular buffer.

Propiobetaine

C6H13NO2 (131.0946238)

S-Adenosylmethionine

C15H23N6O5S+ (399.1450568)

S-adenosylmethionine, also known as sam or adomet, is a member of the class of compounds known as 5-deoxy-5-thionucleosides. 5-deoxy-5-thionucleosides are 5-deoxyribonucleosides in which the ribose is thio-substituted at the 5position by a S-alkyl group. S-adenosylmethionine is slightly soluble (in water) and a moderately acidic compound (based on its pKa). S-adenosylmethionine can be found in a number of food items such as common grape, half-highbush blueberry, jerusalem artichoke, and thistle, which makes S-adenosylmethionine a potential biomarker for the consumption of these food products. S-adenosylmethionine can be found primarily in blood, cerebrospinal fluid (CSF), feces, and urine, as well as throughout most human tissues. S-adenosylmethionine exists in all eukaryotes, ranging from yeast to humans. In humans, S-adenosylmethionine is involved in several metabolic pathways, some of which include phosphatidylcholine biosynthesis PC(22:1(13Z)/22:6(4Z,7Z,10Z,13Z,16Z,19Z)), phosphatidylcholine biosynthesis PC(22:0/18:3(9Z,12Z,15Z)), phosphatidylcholine biosynthesis PC(24:0/24:0), and phosphatidylcholine biosynthesis PC(20:5(5Z,8Z,11Z,14Z,17Z)/20:0). S-adenosylmethionine is also involved in several metabolic disorders, some of which include methylenetetrahydrofolate reductase deficiency (MTHFRD), 3-phosphoglycerate dehydrogenase deficiency, monoamine oxidase-a deficiency (MAO-A), and aromatic l-aminoacid decarboxylase deficiency. Moreover, S-adenosylmethionine is found to be associated with diabetes mellitus type 2 and neurodegenerative disease. S-adenosylmethionine is a non-carcinogenic (not listed by IARC) potentially toxic compound. S-Adenosyl methionine is a common cosubstrate involved in methyl group transfers, transsulfuration, and aminopropylation. Although these anabolic reactions occur throughout the body, most SAM-e is produced and consumed in the liver. More than 40 methyl transfers from SAM-e are known, to various substrates such as nucleic acids, proteins, lipids and secondary metabolites. It is made from adenosine triphosphate (ATP) and methionine by methionine adenosyltransferase (EC 2.5.1.6). SAM was first discovered by Giulio Cantoni in 1952 . Significant first-pass metabolism in the liver. Approximately 50\\\% of S-Adenosylmethionine (SAMe) is metabolized in the liver. SAMe is metabolized to S-adenosylhomocysteine, which is then metabolized to homocysteine. Homocysteine can either be metabolized to cystathionine and then cysteine or to methionine. The cofactor in the metabolism of homocysteine to cysteine is vitamin B6. Cofactors for the metabolism of homocysteine to methionine are folic acid, vitamin B12 and betaine (T3DB). S-Adenosylmethionine (CAS: 29908-03-0), also known as SAM or AdoMet, is a physiologic methyl radical donor involved in enzymatic transmethylation reactions and present in all living organisms. It possesses anti-inflammatory activity and has been used in the treatment of chronic liver disease (From Merck, 11th ed). S-Adenosylmethionine is a natural substance present in the cells of the body. It plays a crucial biochemical role by donating a one-carbon methyl group in a process called transmethylation. S-Adenosylmethionine, formed from the reaction of L-methionine and adenosine triphosphate catalyzed by the enzyme S-adenosylmethionine synthetase, is the methyl-group donor in the biosynthesis of both DNA and RNA nucleic acids, phospholipids, proteins, epinephrine, melatonin, creatine, and other molecules.