Mitochondrial dysfunction,oxidative stress and apoptotic induction in microglial BV-2 cells treated with sodium arsenate

查看全文 作　　者：Wafa [1,2]Kharroubi;Samia Hai [1,2]Ahmed;Thomas [1]Nury;Pierre [1]Andreoletti;Rachid [2]Sakly;Mohamed [2]Hammami;Gerard [1]Lizard

机构地区：[1]Univ.Bourgogne Franche-Comte Laboratory Bio-PeroxIL,Biochemistry of the Peroxisome,Inflammation and Lipid Metabolism EA7270/INSERM,Faculty of Sciences Gabriel,Dijon 21000,France;[2]Laboratory of Nutrition-Functional Foods and Vascular Diseases,Faculty of Medicine,University of Monastir,Monastir 5019,Tunisia

出　　处：《Journal of Environmental Sciences》索引2017年第29卷第1期,共8页

基　　金：supported by grants from the University of Bourgogne(Dijon,France);the University of Monastir(Monastir,Tunisia) 摘　　要：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. 关键词：线粒体膜电位细胞凋亡小胶质细胞功能障碍砷酸钠诱导氧化应激治疗

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Mitochondrial dysfunction,oxidative stress and apoptotic induction in microglial BV-2 cells treated with sodium arsenate

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