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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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Exposure to organomercurials has been associated with harmful effects on the central nervous system (CNS). However, the mechanisms underlying organomercurial-mediated neurotoxic effects need to be elucidated. Exposure to toxic elements may promote cellular modifications such as alterations in protein synthesis in an attempt to protect tissues and organs from damage. In this context, the use of a "proteomic profile" is an important tool to identify potential early biomarkers or targets indicative of neurotoxicity. The aim of this study was to investigate potential modifications in rat cerebral cell proteome following exposure to methylmercury (MeHg) or ethylmercury (EtHg). For MeHg exposure, animals were administered by gavage daily 140 µg/kg/d of Hg (as MeHg) for 60 d and sacrificed 24 h after the last treatment. For EtHg exposure, 800 µg/kg/d of Hg (as EtHg) was given intramuscularly (im) in a single dose and rats were sacrificed after 4 h. Control groups received saline either by gavage or im. After extraction of proteins from whole brain samples and separation by two-dimensional electrophoresis (2-DE), 26 differentially expressed proteins were identified from exposed animals by matrix-assisted laser desorption ionization-time of flight (MALDI-TOF/TOF). Both MeHg and EtHg exposure induced an overexpression of calbindin, a protein that acts as a neuroprotective agent by (1) adjusting the concentration of Ca(2+) within cells and preventing neurodegenerative diseases and (2) decreasing expression of glutamine synthetase, a crucial protein involved in regulation of glutamate concentration in synaptic cleft. In contrast, expression of superoxide dismutase (SOD), a protein involved in antioxidant defense, was elevated in brain of MeHg-exposed animals. Taken together, our data provide new valuable information on the possible molecular mechanisms associated with MeHg- and EtHg-mediated toxicity in cerebral tissue. These observed protein alterations may be considered as biomarkers candidates for biological monitoring of organomercurial poisoning.