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