线粒体
氧化应激
细胞凋亡
膜电位
氧化磷酸化
砷酸钠
砷酸盐
三磷酸腺苷
程序性细胞死亡
活性氧
细胞生物学
化学
超氧化物
线粒体内膜
分子生物学
生物
生物化学
砷
酶
有机化学
作者
Wafa Kharroubi,Samia Haj Ahmed,Thomas Nury,Pierre Andreoletti,R Sakly,Mohamed Hammami,Gérard Lizard
标识
DOI:10.1016/j.jes.2016.08.028
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 complexes I, 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.
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