Three groups of female rats （n=6 per group） were exposed to 1 and 10 mg/L of sodium arsenate for 90 days. The antioxidant and peroxidation parameters in kidney and liver tissues were evaluated, also the fatty acid c...Three groups of female rats （n=6 per group） were exposed to 1 and 10 mg/L of sodium arsenate for 90 days. The antioxidant and peroxidation parameters in kidney and liver tissues were evaluated, also the fatty acid composition were determined. In liver the synthesis pathway of n-3 polyunsaturated fatty acids （PUFA） seemed to be more affected than the n-6 PUFA, while in kidney the n-6 pathway was more affected.展开更多
The treatment of microglial BV-2 cells with sodium arsenate（As（V）：0.1-400 μmol/L — 48 hr）induces a dose-dependent response.The neurotoxic effects of high concentrations of As（V）（100,200 and 400 μmol/L） are...The treatment of microglial BV-2 cells with sodium arsenate（As（V）：0.1-400 μmol/L — 48 hr）induces a dose-dependent response.The neurotoxic effects of high concentrations of As（V）（100,200 and 400 μmol/L） are characterized by increased levels of mitochondrial complexesⅠ,Ⅱ,and Ⅳ followed by increased superoxide anion generation.Moreover,As（V） triggers an apoptotic mode of cell death,demonstrated by an apoptotic SubG1 peak,associated with an alteration of plasma membrane integrity.There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP.It is therefore tempting to speculate that As（V） triggers mitochondrial dysfunction,which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage,which in turn induces an apoptotic mode of cell death.展开更多
基金supported by the Tunisian Ministry of Higher Education and Scientific Research through the Research Laboratory of‘Nutrition-Functional Food and Vascular Health’LRNAFS LR12ES05Faculty of Medicine,Monastir
文摘Three groups of female rats （n=6 per group） were exposed to 1 and 10 mg/L of sodium arsenate for 90 days. The antioxidant and peroxidation parameters in kidney and liver tissues were evaluated, also the fatty acid composition were determined. In liver the synthesis pathway of n-3 polyunsaturated fatty acids （PUFA） seemed to be more affected than the n-6 PUFA, while in kidney the n-6 pathway was more affected.
基金supported by grants from the University of Bourgogne(Dijon,France)the University of Monastir(Monastir,Tunisia)
文摘The treatment of microglial BV-2 cells with sodium arsenate（As（V）：0.1-400 μmol/L — 48 hr）induces a dose-dependent response.The neurotoxic effects of high concentrations of As（V）（100,200 and 400 μmol/L） are characterized by increased levels of mitochondrial complexesⅠ,Ⅱ,and Ⅳ followed by increased superoxide anion generation.Moreover,As（V） triggers an apoptotic mode of cell death,demonstrated by an apoptotic SubG1 peak,associated with an alteration of plasma membrane integrity.There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP.It is therefore tempting to speculate that As（V） triggers mitochondrial dysfunction,which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage,which in turn induces an apoptotic mode of cell death.
