Nitric oxide (NO) is a potent vasodilator with multiple protective effects involved in the regulation of cardiovascular functions. Endothelial NO synthase (eNOS) gene polymorphisms and environmental factors, such as mercury (Hg) exposure, may influence NO levels and increase the risk of cardiovascular damage. The aim of this study was to determine the role of the T-786C and Glu298Asp polymorphisms of the eNOS gene on nitrite concentrations following Hg exposure in humans. It was postulated that Hg exposure might decrease circulating nitrite concentrations and that variants in the eNOS gene might enhance the adverse effects of Hg resulting in increased risk of cardiovascular disease. Blood samples were collected from 202 volunteers exposed to methylmercury (MeHg) following fish consumption. Blood Hg concentrations (BHg) were determined by inductively coupled plasma-mass spectrometry and nitrite plasma concentration by a chemiluminescent method. The mean Hg concentration was 50.5 ± 35.4 μg/L and mean nitrite concentration was 251.4 ± 106.3 nM. There were no significant differences in age, arterial blood pressure, body mass index, heart rate, and concentrations of Hg and nitrite concentrations between the genotype groups . When data were grouped together (TC + CC and TT group), there were still no marked differences. A multiple regression model indicated that decreased NO production was predominantly due to Hg, age, and gender. Polymorphisms did not seem to influence this effect. Our findings suggest that eNOS gene polymorphisms (T-786C and Glu298Asp) are not associated with an increased risk for cardiovascular diseases in MeHg-exposed subjects.
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