Homocysteine

Not to be confused with homocystine.
Homocysteine
Skeletal formula
Ball-and-stick model
Names
IUPAC name
2-Amino-4-sulfanylbutanoic acid
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.006.567 Edit this at Wikidata
EC Number
  • 207-222-9
KEGG
UNII
  • InChI=1S/C4H9NO2S/c5-3(1-2-8)4(6)7/h3,8H,1-2,5H2,(H,6,7) checkY
    Key: FFFHZYDWPBMWHY-UHFFFAOYSA-N checkY
  • InChI=1/C4H9NO2S/c5-3(1-2-8)4(6)7/h3,8H,1-2,5H2,(H,6,7)
    Key: FFFHZYDWPBMWHY-UHFFFAOYAS
  • C(CS)C(C(=O)O)N
Properties
C4H9NO2S
Molar mass 135.18 g/mol
Appearance White crystalline powder
Melting point 234–235 °C (453–455 °F; 507–508 K)[2] (decomposes)
soluble
log P -2.56 [1]
Acidity (pKa) 2.25 [1]
Hazards
GHS labelling:
GHS07: Exclamation mark
Warning
H302
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Homocysteine (/ˌhoʊmoʊˈsɪstiːn/) or Hcy: is a non-proteinogenic α-amino acid. It is a homologue of the amino acid cysteine, differing by an additional methylene bridge (-CH2-). It is biosynthesized from methionine by the removal of its terminal Cε methyl group. In the body, homocysteine can be recycled into methionine or converted into cysteine with the aid of vitamin B6, B9, and B12.[3]

High levels of homocysteine in the blood (hyperhomocysteinemia) is regarded as a marker of cardiovascular disease, likely working through atherogenesis, which can result in ischemic injury. Therefore, hyperhomocysteinemia is a possible risk factor for coronary artery disease. Coronary artery disease occurs when an atherosclerotic plaque blocks blood flow to the coronary arteries, which supply the heart with oxygenated blood.[4][5]

Hyperhomocysteinemia has been correlated with the occurrence of blood clots, heart attacks, and strokes, although it is unclear whether hyperhomocysteinemia is an independent risk factor for these conditions.[6] Hyperhomocysteinemia also has been associated with early-term spontaneous abortions[7] and with neural tube defects.[8]

  1. ^ a b Chalcraft, Kenneth R.; Lee, Richard; Mills, Casandra; Britz-McKibbin, Philip (2009). "Virtual Quantification of Metabolites by Capillary Electrophoresis-Electrospray Ionization-Mass Spectrometry: Predicting Ionization Efficiency Without Chemical Standards". Analytical Chemistry. 81 (7): 2506–2515. doi:10.1021/ac802272u. PMID 19275147.
  2. ^ Allen, Milton J.; Steinman, Harry G. (1952). "The Electrolytic Reduction of Homocystine at a Controlled Reference Potential". Journal of the American Chemical Society. 74 (15): 3932–3933. doi:10.1021/ja01135a502.
  3. ^ "Homocysteine" (PDF). moh.gov.vn. Retrieved 5 April 2023.
  4. ^ Kim J, Kim H, Roh H, Kwon Y (2018). "Causes of hyperhomocysteinemia and its pathological significance". Arch Pharm Res. 41 (4): 372–383. doi:10.1007/s12272-018-1016-4. PMID 29552692. S2CID 3986295.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Boudi, Brian F. "Noncoronary Atherosclerosis". Medscape. Archived from the original on 2013-05-11.
  6. ^ Homocysteine: The Facts, Tufts Health and Nutrition Letter, July 31, 2020 update
  7. ^ Nelen WL, Blom HJ, Steegers EA, den Heijer M, Thomas CM, Eskes TK (2000). "Homocysteine and folate levels as risk factors for recurrent early pregnancy loss". Obstet Gynecol. 95 (4): 519–24. doi:10.1016/s0029-7844(99)00610-9. PMID 10725483. S2CID 26125655.
  8. ^ van der Put NJ et al Folate, Homocysteine and Neural Tube Defects: An Overview Archived 2015-09-16 at the Wayback Machine Exp Biol Med (Maywood) April 2001 vol. 226 no. 4 243-270