Homocysteine

From Free net encyclopedia

{{NatOrganicBox | image= Image:Homocysteine.PNG | name=(2S)-2-amino-4-sulfanyl-butanoic acid | abbreviations=Hcy | C=4 | H=9 | N=1 | O=2 | S=1 | charge= | mass=135.186 | melt_point= | density= | isoelectric_point= | dissoc_constant= | CAS= | EINECS= | PubChem=Template:PubChemLink (L) | SMILES=C(CS)C(C(=O)O)N }}

Homocysteine is a variant of the amino acid cysteine, differing in that its side-chain contains an additional methylene (-CH₂-) group before the thiol (-SH) group.

1 Chemistry
2 Elevated homocysteine
3 Cardiovascular risks
4 Bone weakness
5 References
6 Footnotes

[edit]

Chemistry

Homocysteine's extra methylene group brings the thiol group closer to the carboxyl group, allowing it to chemically react to form a five-membered ring. This occurs at the point where the amino acids normally join to their neighbours in a peptide bond. Homocysteine is therefore unsuitable for incorporating into proteins, because a protein containing homocysteine would cleave itself.

Homocysteine is formed from S-adenosyl methionine by a two step reaction pathway. It can be converted back to methionine, or converted to cysteine or taurine via the transsulfuration pathway. Although homocysteine can be converted back to methionine, there is no indication that dietary homocysteine contributes any methionine nutritionally to humans.<ref name="AnRvNutrition1999-Selhub">Template:Cite journal</ref>

[edit]

Elevated homocysteine

As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of the vitamins folic acid, pyridoxine (B₆), or B₁₂ can lead to high homocysteine levels.<ref name="AmJClinNutrition1994-Miller">Template:Cite journal</ref> Supplementation with pyridoxine, folic acid, B₁₂ or trimethylglycine (betaine) reduces the concentration of homocysteine in the bloodstream.<ref name="ExpertOpPharm2001-Coen">Template:Cite journal</ref> <ref name="NYT2006-Chrichton">Legal note: Metabolite Laboratories is defending a patent as of March 2006 that may cover the mere mention or consideration of the relationship of vitamin B12 and homocysteine levels. See Template:Cite news</ref>. Increased levels of homocysteine are linked to high concentrations of endothelial asymmetric dimethylarginine.

Elevations of homocysteine also occur in the rare hereditary disease homocystinuria and in methyl-tetrahydrofolate-reductase deficiency. The latter is quite common and usually goes unnoticed, although there are reports that thrombosis and cardiovascular disease occurs more often in people with elevated homocysteine.

[edit]

Cardiovascular risks

A high level of blood serum homocysteine is considered to be a marker of potential cardiovascular (risk factor for heart attack and stroke) disease. A current area of research is whether high serum homocysteine itself is a problem or merely an indicator of extant problems.<ref name="BBC2005-NewsBvit">Template:Cite news</ref>

Studies reported in 2006 have shown that giving folic acid to reduce homocysteine levels does not give any benefit and suggested that if given with B₁₂ might instead increase some cardiovascular risks.<ref name="JAmCollCardiol2006-Zoungas">Template:Cite journal</ref><ref name="NEJM2006a">Template:Cite journal</ref><ref name="NEJM2006-Bonna">Template:Cite journal</ref>

[edit]

Bone weakness

Elevated levels of homocysteine have been linked to increased fractures in elderly persons.<ref name="NEJM2004-McLean">Template:Cite journal Free text after free regitration</ref><ref name="NEJM2004-vanMeurs">Template:Cite journal Free text after free regitration</ref> Homocysteine does not appear to have any effect on bone density. Instead, it appears that homocysteine affects collagen by interfering with the cross-linking between collagen fibers and the tissues they reinforce.

Vitamin supplements could counter the effects of homocysteine on collagen. As B₁₂ is inefficiently absorbed from food by elderly persons they could gain a greater benefit from taking vitamin supplements.

[edit]