title: Mitochondrial Respiratory Chain Inhibitors Involved in ROS Production Induced by Acute High Concentrations of Iodide and the Effects of SOD as a Protective Factor.
abstract: 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 μM 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 μM KI exposure. However, SOD inhibitor diethyldithiocarbamic acid (DETC) (2 mM), Rotenone (0.5 μM), a mitochondrial complex I inhibitor, and Antimycin A (10 μM), 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.
authors: Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors: Lingyan
authors: L
authors: Wang
authors: Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors: Qi
authors: Q
authors: Duan
authors: Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors: Tingting
authors: T
authors: Wang
authors: Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors: Mohamed
authors: M
authors: Ahmed
authors: Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors: Na
authors: N
authors: Zhang
authors: Key Lab of Hormones and Development Ministry of Health, Institute of Endocrinology, Metabolic Disease Hospital, Tianjin Medical University, Tianjin 300070, China.
authors: Yongmei
authors: Y
authors: Li
authors: Key Lab of Hormones and Development Ministry of Health, Institute of Endocrinology, Metabolic Disease Hospital, Tianjin Medical University, Tianjin 300070, China.
authors: Lanying
authors: L
authors: Li
authors: Department of Pathophysiology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.
authors: Xiaomei
authors: X
authors: Yao
mesh_terms: D042967:Electron Transport Complex I / Q000378:metabolism*; D007454:Iodides / Q000737:chemistry*; D051336:Mitochondrial Membranes / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism*
chemical_list: D007454:Iodides; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D042967:Electron Transport Complex I