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

Wafa Kharroubi , Samia Haj Ahmed , Thomas Nury , Pierre Andreoletti , Rachid Sakly , Mohamed Hammami , Gérard Lizard


Received April 22, 2016,Revised June 15, 2016, Accepted August 19, 2016, Available online November 09, 2016

Volume 29,2017,Pages 44-51

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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