Homocysteine is an aminoacid with that a sulfur-containing metabolite of methionine. Human plasma contains
both reduced with sulfhydryl (homocysteine) and oxidized with disulphide (homocystine) forms of homocysteine.
Oxidized forms of homocystein account for 98-99% of total homocysteine (tHcy). In the homocysteine
metabolism, there are two major pathways. The first is remethylation back to methionine using vitamin B12 as
cofactor. The second pathway is transsulfuration to cysteine using vitamin B6 as cofactor. These reactions reduce
total homocysteine (tHcy) concentrations in cells and blood. Median fasting total homocysteine levels in adult
males and pediatric populations are between 5-15 and 3.7-10.3 micromol/L, respectively. Increased plasma tHcy
concentrations are found with methionine-rich diets, low vitamin B intake, male gender, increasing age, impaired
renal function, and genetically determined defects of the enzymes involving in homocysteine metabolism. An
inverse relation exists between plasma tHcy and circulating folate or vitamin B6 concentrations. Folic acid
supplements of 0.5 mg/d can reduce tHcy levels by approximately 25%. In recent years, a number of casecontrol
studies have established that hyperhomocysteinemia are a causal factor for coronary, cerebral, and
peripheral vascular diseases. In this review, we analysed the inter relation between homocysteine and
cardiovascular disease.
Key words: Homocysteine, Vascular Disease, Homocysteinemia, Homocystinuria
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