Evidence of hormesis on human neuronal SK-N-BE cells treated with sodium arsenate: impact at the mitochondrial level
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Exposure 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.
KeywordsSodium arsenate Human neuronal SK-NB-E Mitochondrial dysfunctions OXPHOS complexes
Dulbecco’s Modified Eagle Medium
Mitochondrial transmembrane potential
This work was supported by grants from the Université de Bourgogne (Dijon, France), and the Université de Monastir (Monastir, Tunisia).
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