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Effects of Low Concentrations of Rotenone upon Mitohormesis in SH-SY5Y Cells.
|Title||Effects of Low Concentrations of Rotenone upon Mitohormesis in SH-SY5Y Cells.|
|Publication Type||Journal Article|
|Year of Publication||2013|
|Authors||Yuyun X, Jinjun Q, Minfang X, Jing Q, Juan X, Rui M, Li Z, Jing G|
|Journal||Dose-response : a publication of International Hormesis Society|
The mitochondrial toxin rotenone exerts cytotoxicity via overproduction of reactive oxygen species (ROS) and depolarization of the mitochondrial membrane. We investigated the effects of rotenone (12.5, 25, 50, 100 nmol/L) on mitochondrial biogenesis and the potential roles of ROS production in SH-SY5Y cells. Mitochondrial biogenesis was assessed by counting the number of mitochondria, determining protein expression of peroxisome proliferator-activated receptor γ coactivator α (PGC1-α) and its regulator, SIRT1, and oxygen consumption. ROS production and levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) were also determined. Compared with controls, rotenone (12.5 nmol/L) significantly increased the quantity of mitochondria and amount of oxygen consumption, whereas rotenone at >12.5 nmol/L decreased the quantity of mitochondria and amount of oxygen consumption. GSH contents and GSH/GSSG were also significantly enhanced by rotenone at 12.5 nmol/L and decreased by rotenone at >12.5 nmol/L. Except for ROS production and SIRT1 protein expression, all concentration-response relationships showed a typical inverted-U shape. ROS production was continually increased in cells treated with rotenone. These data indicate that low concentrations of rotenone can induce mitohormesis, which may be attributed to ROS production.
|Alternate Journal||Dose Response|