Homocysteine asymmetric dimethylarginine

Homocysteine decreases the bioavailability of nitrous oxide (NO) via a mechanism involving glutathione peroxidase (37). Tawakol et al. (38) reported that hyperhomocysteinemia is associated with impaired endothelium-dependent vasodilation in humans. Homocysteine impairs the NO synthase pathway both in cell culture (39) and in monkeys with hyperhomocysteinemia, by increasing the levels of asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhibitor (40). Elevation of ADMA may mediate endothelial dysfunction during experimental hyperhomocysteinemia in humans (41). However, Jonasson et al. (42) did not find increased ADMA levels in patients with coronary heart disease and hyperhomocysteinemia, nor did vitamin supplementation have any effect on ADMA levels in spite of substantial plasma tHcy reduction,... 

Stuhlinger MC, et al. Homocysteine impairs the nitric oxide synthase pathway role of asymmetric dimethylarginine, Circulation 2001 104(21 ) 2569-2575. 

Homocysteine metabolism is involved both in the synthesis and degradation of asymmetric dimethylarginine (ADMA), a potent endogenous NO-synthase inhibitor, which is thought to be an independent predictor of cardiovascular mortality in end-stage renal disease. 

Stuhlinger, M.C., Tsao, P.S., Her, J.H., Kimoto, M., Balint, R.F., and Cooke, J.P., 2001. Homocysteine impairs the nitric oxide synthase pathway role of asymmetric dimethylarginine. Circulation. 104 2569-2575. 

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