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The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice kidney.

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Affiliations

  • 1. Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, 818 East Tianyuan Road, Nanjing 211166, China.
      Authors
    • Wang Y 1
    (1 author)

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, 16 Apr 2013, 58:61-67
https://doi.org/10.1016/j.fct.2013.04.013 PMID: 23603105 

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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Read article at publisher's site: https://doi.org/10.1016/j.fct.2013.04.013

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