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

Date publication

janvier 2017

Journal

Journal of environmental sciences (China)

Auteurs

Membres identifiés du Cancéropôle Est :
Dr LIZARD Gérard

Tous les auteurs :
Kharroubi W, Haj Ahmed S, Nury T, Andreoletti P, Sakly R, Hammami M, Lizard G

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/28115150

Résumé

The treatment of microglial BV-2 cells with sodium arsenate (As(V): 0.1-400μmol/L - 48hr) induces a dose-dependent response. The neurotoxic effects of high concentrations of As(V) (100, 200 and 400μmol/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.

Mots clés

Adenosine Triphosphate, Animals, Apoptosis, Arsenates, toxicity, Cell Line, Hazardous Substances, toxicity, Membrane Potential, Mitochondrial, drug effects, Mice, Mitochondria, drug effects, Oxidation-Reduction, Oxidative Stress, drug effects

Référence

J Environ Sci (China). 2017 Jan;51:44-51