Showing Metabocard for L-methionine (BASm0003002)

Common NameL-methionine
DescriptionMethionine (Met), also known as L-methionine, is an alpha-amino acid. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon). Amino acids are organic compounds that contain amino (-NH2) and carboxyl (-COOH) functional groups, along with a side chain (R group) specific to each amino acid. Methionine is one of 20 proteinogenic amino acids, i.e., the amino acids used in the biosynthesis of proteins. Methionine is found in all organisms ranging from bacteria to plants to animals. It is classified as an aliphatic, non-polar amino acid. Methionine is an essential amino acid (there are 9 essential amino acids), meaning the body cannot synthesize it, and it must be obtained from the diet. It is required for normal growth and development of humans, other mammals, and avian species. In addition to being a substrate for protein synthesis, methionine is an intermediate in transmethylation reactions, serving as the major methyl group donor in vivo, including the methyl groups for DNA and RNA intermediates. Methionine is a methyl acceptor for 5-methyltetrahydrofolate-homocysteine methyltransferase (methionine synthase), the only reaction that allows for the recycling of this form of folate, and is also a methyl acceptor for the catabolism of betaine. Methionine is the metabolic precursor for cysteine. Only the sulfur atom from methionine is transferred to cysteine; the carbon skeleton of cysteine is donated by serine (PMID: 16702340 ). There is a general consensus concerning normal sulfur amino acid (SAA) requirements. WHO recommendations amount to 13 mg/kg per 24 h in healthy adults. This amount is roughly doubled in artificial nutrition regimens. In disease or after trauma, requirements may be altered for methionine, cysteine, and taurine. Although in specific cases of congenital enzyme deficiency, prematurity, or diminished liver function, hypermethioninemia or hyperhomocysteinemia may occur, SAA supplementation can be considered safe in amounts exceeding 2-3 times the minimum recommended daily intake. Apart from some very specific indications (e.g. acetaminophen poisoning) the usefulness of SAA supplementation is not yet established (PMID: 16702341 ). Methionine is known to exacerbate psychopathological symptoms in schizophrenic patients, but there is no evidence of similar effects in healthy subjects. The role of methionine as a precursor of homocysteine is the most notable cause for concern. Acute doses of methionine can lead to acute increases in plasma homocysteine, which can be used as an index of the susceptibility to cardiovascular disease. Sufficiently high doses of methionine can actually result in death. Longer-term studies in adults have indicated no adverse consequences of moderate fluctuations in dietary methionine intake, but intakes higher than 5 times the normal amount resulted in elevated homocysteine levels. These effects of methionine on homocysteine and vascular function are moderated by supplements of vitamins B-6, B-12, C, and folic acid (PMID: 16702346 ). When present in sufficiently high levels, methionine can act as an atherogen and a metabotoxin. An atherogen is a compound that when present at chronically high levels causes atherosclerosis and cardiovascular disease. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of methionine are associated with at least ten inborn errors of metabolism, including cystathionine beta-synthase deficiency, glycine N-methyltransferase deficiency, homocystinuria, tyrosinemia, galactosemia, homocystinuria-megaloblastic anemia due to defects in cobalamin metabolism, methionine adenosyltransferase deficiency, methylenetetrahydrofolate reductase deficiency, and S-adenosylhomocysteine (SAH) hydrolase deficiency. Chronically elevated levels of methionine in infants can lead to intellectual disability and other neurological problems, delays in motor skills, sluggishness, muscle weakness, and liver problems. Many individuals with these metabolic disorders tend to develop cardiovascular disease later in life. Studies on feeding rodents high levels of methionine have shown that methionine promotes atherosclerotic plaques independently of homocysteine levels (PMID: 26647293 ). A similar study in Finnish men showed the same effect (PMID: 16487911 ).
Structure
Molecular FormulaC5H11NO2S
Average Mass149.21100
Monoisotopic Mass149.05105
IUPAC Name(2S)-2-amino-4-(methylsulfanyl)butanoic acid
Traditional NameL-methionine
CAS Registry Number63-68-3
SMILESCSCC[C@H]([NH3+])C(=O)[O-]
InChI IdentifierInChI=1S/C5H11NO2S/c1-9-3-2-4(6)5(7)8/h4H,2-3,6H2,1H3,(H,7,8)/t4-/m0/s1
InChI KeyFFEARJCKVFRZRR-BYPYZUCNSA-N
CHEBI IDCHEBI:57844
HMDB IDHMDB0000696
Pathways
NameSMPDB/PathBank
Glycine, serine and threonine metabolism
Glycine, serine and threonine metabolism
Transcription/Translation
Methionine Metabolism
Cystathionine Beta-Synthase Deficiency
Dihydropyrimidine Dehydrogenase Deficiency (DHPD)
S-Adenosylhomocysteine (SAH) Hydrolase Deficiency
Methionine Adenosyltransferase Deficiency
Glycine N-methyltransferase Deficiency
Non Ketotic Hyperglycinemia
Dimethylglycine Dehydrogenase Deficiency
Sarcosinemia
Azithromycin Action Pathway
Clarithromycin Action Pathway
Clindamycin Action Pathway
Erythromycin Action Pathway
Roxithromycin Action Pathway
Telithromycin Action Pathway
Amikacin Action Pathway
Gentamicin Action Pathway
Kanamycin Action Pathway
Neomycin Action Pathway
Netilmicin Action Pathway
Spectinomycin Action Pathway
Streptomycin Action Pathway
Clomocycline Action Pathway
Demeclocycline Action Pathway
Doxycycline Action Pathway
Minocycline Action Pathway
Oxytetracycline Action Pathway
Tetracycline Action Pathway
Lymecycline Action Pathway
Methylenetetrahydrofolate Reductase Deficiency (MTHFRD)
Hypermethioninemia
Spermidine and Spermine Biosynthesis
Dimethylglycine Dehydrogenase Deficiency
Hyperglycinemia, non-ketotic
Homocystinuria-megaloblastic anemia due to defect in cobalamin metabolism, cblG complementation type
Tobramycin Action Pathway
Tigecycline Action Pathway
Arbekacin Action Pathway
Paromomycin Action Pathway
3-Phosphoglycerate dehydrogenase deficiency
Rolitetracycline Action Pathway
Methacycline Action Pathway
Lincomycin Action Pathway
Chloramphenicol Action Pathway
Troleandomycin Action Pathway
Josamycin Action Pathway
Sarcosine Oncometabolite Pathway
StateSolid
Water Solubility2.39e+01 g/l
logP-1.85
logS-0.80
pKa (Strongest Acidic)2.53
pKa (Strongest Basic)9.50
Hydrogen Acceptor Count3
Hydrogen Donor Count2
Polar Surface Area63.32 Ų
Rotatable Bond Count4
Physiological Charge0
Formal Charge0
Refractivity37.59 m³·mol⁻¹
Polarizability15.50

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