Effects of the Retraining in Endurance on Anthropometric and Metabolic Profiles' Evolution of the Tunisian Obese Pubescent Boys

Abstract: 96.4 ± 13.2 kg, 1.71 ± 0.

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

International audienceThe 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

Evidence of hormesis on human neuronal SK-N-BE cells treated with sodium arsenate: impact at the mitochondrial level.

International audienceExposure of human neuronal SK-N-BE cells to sodium arsenate (AsV 0.1-400 μM; 48 h) induced a biphasic toxic effect evoking hormesis. Indeed, at low concentrations, AsV stimulates cell proliferation visualized by phase contrast microscopy, whereas at high concentrations, an induction of cell death associated with a loss of cell adhesion was observed. These side effects were confirmed with crystal violet test, cell cycle analysis, evaluation of the percentage of Ki67 positive cells, and staining with propidium iodide. The impact of AsV on mitochondrial functions, which was determined by the MTT assay, the measurement of mitochondrial transmembrane potential with DiOC6(3), and the rate of mitochondrial ATP, also support an hormesis process. In addition, in the presence of high concentrations of AsV, a significant decrease of the protein expression of OXPHOS complexes of the respiratory chain was observed by western blot supporting that AsV-induced cell death is associated with mitochondrial alterations. Therefore, there are some evidences of hormesis on AsV-treated SK-N-BE cells, and at high concentrations, the mitochondria are a target of toxicity induced by AsV