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Transcription of Thioredoxin was Inhibited in Rotenone-induced Mitochondrial Dysfunctional Cells Exposed to H2O2


Hong-Qun Ding1,2, Zhen Ding1, Yu-Yun Xiong2, Jing Gao1,2*
1School of Life Science, Nanjing University, Nanjing 210093, China; 2School of Pharmacy, Jiangsu University, Zhenjiang 212013, China
Abstract: To study the pathological changes of thioredoxin (Trx) mRNA in cells exposed to H2O2 with mild mitochondrial dysfunction, the human neuroblastoma SH-SY5Y cells were insulted by low dose of rotenone to mimic the partial complex I impairment in PD. On this in vitro model, the changes of ATP and reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) were investigated to compare the differences between the mitochondrial deficiency cells and normal ones. Furthermore, mRNA of intracellular redox protein, thioredoxin (Trx), from both kinds of cells followed by H2O2 exposure were analyzed. The results demonstrated that rotenone could dose dependently decrease cellular ATP level and MMP, increase cellular ROS production. Without affecting the cell viability, 3 nmol/L rotenone exposure do not alter the cell morphology and ATP synthesis but increased the ROS generation, which indicated mitochondria had been insulted slightly. It was found that Trx mRNA levels in mitochondrial dysfunctional SH-SY5Y cells insulted by H2O2 were lower than normal ones. These results, together with our previous study, demonstrated that the increased susceptibility to oxidative stress in mitochondrial dysfunctional SH-SY5Y cells might be at least in part related to the down-regulation of Trx.


CSTR: 32200.14.cjcb.2007.05.0025