title: The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice kidney.
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.
authors.affiliation: Department of Nutrition and Food Hygiene, School of Public Health, Nanjing Medical University, 818 East Tianyuan Road, Nanjing 211166, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Yuchen
authors.initials: Y
authors.lastname: Wu
authors.forename: Kang
authors.initials: K
authors.lastname: Luo
authors.forename: Yuxin
authors.initials: Y
authors.lastname: Liu
authors.forename: Ming
authors.initials: M
authors.lastname: Zhou
authors.forename: Shu
authors.initials: S
authors.lastname: Yan
authors.forename: Hui
authors.initials: H
authors.lastname: Shi
authors.forename: Yunqing
authors.initials: Y
authors.lastname: Cai
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002104:Cadmium / Q000633:toxicity*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D051379:Mice; D008813:Mice, Inbred ICR; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D012643:Selenium / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D051028:bcl-2-Associated X Protein; D002104:Cadmium; D012643:Selenium
keywords: Apoptosis; Cadmium; Kidney; Oxidative stress; Selenium