Abstract

Based on prospective and experimental data, mild to moderate elevation of homocysteine is a stabilized and independent risk factor for cardiovascular disease. The hyperhomocystenemia is a consequence of inhibition of transsulphuration pathway or inhibition of remethylation pathway of homocysteine metabolism, transsulphuration is mediated by CBS and remethylation is mediated directly by MS and indirectly by MTHFR. The SNPs in these genes alter the activity of corresponding proteins hence it may or may not be responsible for mild to moderate hyperhomocysteinemia. The consequences of hyperhomocysteinemia arise in the form of endothelial cell injury by increased oxidative stress and reduced bioavailability of nitric oxide, increased platelet adhesiveness, enhanced LDL deposition on arterial wall and activation of coagulation cascade. Some environmental factors are also known to contribute in progression toward disease.

Key words: Homocysteine, oxidative stress, inflammation.

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