The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice kidney |
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Affiliation: | 1. College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, People''s Republic of China;2. College of Veterinary Medicine, Northwest A & F University, Yangling 712100, People''s Republic of China;3. National Research Institute for Family Planning, Beijing 100081, People''s Republic of China;4. Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agriculture University, Nanchang 330045, People''s Republic of China.;1. Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, PR China;2. National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, PR China;3. School of Earth Sciences and Resources, China University of Geosciences, Beijing 100083, PR China |
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Abstract: | Selenium, an essential trace element, showed the significant protective effects against kidney damage induced by some heavy metals. Our previous research have found that the protection effects of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium (Cd)-induced LLC-PK1 cells. The present study as a continuation of our earlier one to investigate the protective effects and mechanism of selenium on Cd-induced apoptosis of kidney in vivo. Cadmium exposure increased the production of reactive oxygen species (ROS) and altered the levels of oxidative stress related biomarkers in kidney tissue. A concomitant by the loss of mitochondrial membrane potential, cytochrome c release and regulation of VDAC, Bcl-2 and Bax were observed. Apoptotic nature of cell death is confirmed by activation of caspase-3, which is also supported by histological examination. During the process, selenium played a beneficial role against Cd-induced renal damage. Pretreatment with selenium partially blocked Cd-induced ROS generation, inhibited Cd induced mitochondrial membrane potential collapse, prevented cytochrome c release, inhibited caspase activation and changed the level of VDAC, Bcl-2 and Bax. Combining all, results suggest that selenium has an ability to inhibit mitochondrial apoptotic pathway in oxidative stress mediated kidney dysfunction caused by cadmium. |
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Keywords: | Selenium Cadmium Kidney Oxidative stress Apoptosis |
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