Oxidation of low density lipoprotein by thiols: superoxide-dependent and -independent mechanisms.

Plasma aminothiol oxidation in chronic hemodialysis patients

“…It also has been demonstrated that cyste-and the presence of diabetes, cardiovascular mortality is 10-to 20-fold higher than in the general population ine, and not homocysteine, leads to increased reactive oxygen species production by vascular smooth muscle [45]. Furthermore, risk factors such as hypertension and hypercholesterolemia, which are predictive of cardiovas-cells [30,51]. The potential synergistic toxicity of hyperhomocysteinemia and hypercysteinemia in patients with cular morbidity and mortality in the general population, are not as predictive of cardiovascular complications in chronic kidney disease has not been well explored and likely will be a subject for further investigation.…”

Impairment of Endothelial Functions by Acute Hyperhomocysteinemia and Reversal by Antioxidant Vitamins

“…Homocysteine may promote atherogenesis by various mechanisms. [12][13][14][15]35,36 In vitro studies show that exposure of endothelial cells to homocysteine results in oxidative effects, including generation of superoxide anion radicals and hydrogen peroxide, 37 which leads to inactivation of nitric oxide and endothelial damage. The various mechanisms proposed to explain the toxic effects of homocysteine, including endothelial dysfunction, lipoprotein oxidation, increased monocyte adhesion, and smooth muscle cell proliferation, are to a large extent mediated by nitric oxide availability.…”

“…Methionine taken orally is converted to homocysteine by demethylation, and the effect of an oral load can be used as a diagnostic test to identify individuals with enzyme defects or poor vitamin status who show an exaggerated rise in homocysteine levels. 10,11 Several mechanisms are likely to be involved in the induction of vascular damage by homocysteine, including endothelial cell desquamation, 12 oxidation of lowdensity lipoprotein, 13 increased mono-Interventions Subjects were given each of 3 loads in random order at 1-week intervals: oral methionine, 100 mg/kg in fruit juice; the same methionine load immediately following ingestion of antioxidant vitamin E, 800 IU, and ascorbic acid, 1000 mg; and methionine-free fruit juice (placebo). Ten of the 20 subjects also ingested a placebo load with vitamins.…”

Plasma homocysteine level is unrelated to long-term cardiovascular events in patients with previous percutaneous coronary intervention

“…Homocysteine (Hcy) is a sulfhydryl-containing amino acid derived from the demethylation of has been paid much attention [3]. Experimental studies have suggested that Hcy may promote atherosclerosis through several mechanisms including endothelial dysfunction [4], oxidation of low-density lipoprotein [5,6], the activation of inflammatory pathways [7], smooth muscle cell proliferation [4,7], and the activation of coagulation factors and platelets [4,7].…”