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Mitochondrial dysfunction,oxidative stress and apoptotic induction in microglial BV-2 cells treated with sodium arsenate 被引量:5
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作者 Wafa Kharroubi Samia Hai Ahmed +4 位作者 Thomas Nury Pierre Andreoletti Rachid Sakly Mohamed Hammami Gerard Lizard 《Journal of Environmental Sciences》 SCIE EI CAS CSCD 2017年第1期44-51,共8页
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
关键词 Sodium arsenate Microglial BV-2 cells Mitochondrial dysfunction Oxidative phosphorylation complexes Superoxide anions Apoptosis
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