期刊
DOSE-RESPONSE
卷 11, 期 2, 页码 270-280出版社
INT DOSE-RESPONSE SOC
DOI: 10.2203/dose-response.12-005.Gao
关键词
mitohormesis; rotenone; mitochondria; PGC1-alpha
资金
- Natural Science Foundation of Jiangsu Province [BK2008249]
- National Natural Science Foundation of China [31171143, 30971197]
- National Key Projects of Fundamental R/D of China (973 Project) [2011CB510004]
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. coactivator a (PGC1-alpha) 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.
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