Mitochondrial Respiratory Chain Inhibitors Involved in ROS Production Induced by Acute High Concentrations of Iodide and the Effects of SOD as a Protective Factor

作者：Wang, Lingyan; Duan, Qi; Wang, Tingting; Ahmed, Mohamed; Zhang, Na; Li, Yongmei; Li, Lanying; Yao, Xiaomei^*

来源：Oxidative Medicine and Cellular Longevity, 2015, 2015: 217670.

DOI：10.1155/2015/217670

• OXIDATIVE STRESS
• HYDROGEN-PEROXIDE
• SUPEROXIDE-DISMUTASE
• INDUCED APOPTOSIS
• COMPLEX-I
• ANTIOXIDANT DEFENSE
• ELECTRON-TRANSPORT
• THYROID-DISORDERS
• CANCER-CELLS
• ANTIMYCIN-A

A major source of reactive oxygen species (ROS) generation is the mitochondria. By using flow cytometry of the mitochondrial fluorescent probe, MitoSOX Red, western blot of mitochondrial ROS scavenger Peroxiredoxin (Prx) 3 and fluorescence immunostaining, ELISA of cleaved caspases 3 and 9, and TUNEL staining, we demonstrated that exposure to 100 mu M KI for 2 hours significantly increased mitochondrial superoxide production and Prx 3 protein expression with increased expressions of cleaved caspases 3 and 9. Besides, we indicated that superoxide dismutase (SOD) at 1000 unit/mL attenuated the increase in mitochondrial superoxide production, Prx 3 protein expression, and lactate dehydrogenase (LDH) release and improved the relative cell viability at 100 mu M KI exposure. However, SOD inhibitor diethyldithiocarbamic acid (DETC) (2mM), Rotenone (0.5 mu M), a mitochondrial complex I inhibitor, and Antimycin A (10 mu M), a complex III inhibitor, caused an increase in mitochondrial superoxide production, Prx 3 protein expression, and LDH release and decreased the relative cell viability. We conclude that the inhibitors of mitochondrial respiratory chain complex I or III may be involved in oxidative stress caused by elevated concentrations of iodide, and SOD demonstrates its protective effect on the Fischer rat thyroid cell line (FRTL) cells.

• 出版日期2015
• 单位天津医科大学