Carcinogenesis, Teratogenesis & Mutagenesis ›› 2015, Vol. 27 ›› Issue (2): 95-100.doi: 10.3969/j.issn.1004-616x.2015.02.004

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The protective effects and underlying mechanisms of selenium administration on hepatic oxidative injury in rats with cadmium exposure

FU Han, LIU Ying, LIU Jiangzheng, YU Weihua, PENG Jie, HAI Chunxu   

  1. Department of Toxicology, School of Military Preventive Medicine, Shaanxi Provincial Key Lab of Free Radical Biology and Medicine, the Fourth Military Medical University, Xi'an 710032, Shaanxi, China
  • Received:2015-01-12 Revised:2015-03-08 Online:2015-03-31 Published:2015-03-31
  • About author:10.3969/j.issn.1004-616x.2015.02.004

Abstract:

OBJECTIVE:This study was designed to investigate the protective effects and underlying mechanisms of selenium pre-administration on hepatic oxidative injury in rats exposed to cadmium. METHODS:Rats were exposed to cadmium pre-administrated with selenium, then the inhibitory effects of selenium on liver injury, apoptosis and oxidative stress were studied. The measurements of the serum ALT and AST activities were conducted to evaluate liver function. The Bax and Bcl-2 protein levels were measured by Western Blotting and the values of Bax/Bcl-2 were obtained to evaluate hepatic apoptosis. The measurements of hepatic ROS accumulation by DHE stain and hepatic MDA level were conducted to evaluate hepatic oxidative stress. The measurements of hepatic antioxidase SOD, SOD-1, GPx activities in liver and the protein levels of SOD-1, CAT, GPx-1 and Nrf-2 were obtained to evaluate hepatic antioxidative defense ability. RESULTS:The selenium pre-administration exerted effectively protective effects on cadmium-induced liver injury, supported by the inhibition of increased ALT and AST activity. Secondly, the selenium pre-administration effectively alleviated the liver apoptosis in rats exposed to cadmium, evidenced by the decrease of Bax/Bcl-2 ratio. Thirdly, the selenium pre-administration significantly inhibited the hepatic oxidative stress in rats exposed to cadmium, illustrated by the decrease of hepatic ROS accumulation and MDA level. Finally, the enhancement of antioxidative defense ability might be the key mechanism involved in the protective effects of selenium against cadmium-induced liver injury, supported by the increase of hepatic SOD, GPx activities, and the protein expressions of SOD-1, CAT, and GPx-1 via Nrf-2 activation. CONCLUSION:Selenium pre-administration had a protective effect against hepatic oxidative injury induced by cadmium exposure and the strengthening of antioxidant defense ability via Nrf-2 activation might contribute to this protective effect.

Key words: oxidative stress, selenium pre-administration, cadmium exposure, liver injury, antioxidation

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