Protective role of sodium selenite on cisplatin induced oxidative and renal stress

Cisplatin is one of the most commonly used antineoplastic agents. Free oxygen radicals are known to play a major role in cisplatin induced renal and oxidative stress. Sodium selenite as an exogenous source of selenium is used for endogenous selenoprotein synthesis to scavenge the free radicals. The study was designed to investigate the possible protective role of sodium selenite in cisplatin induced renal stress, by using biochemical approaches. Adult male Albino Wistar rats were randomly divided into four groups. The control group received distilled water; sodium selenite group received only sodium selenite [1 mg / kg]; cisplatin group received only cisplatin [3 mg / kg]; cisplatin+ sodium selenite group received sodium selenite [1 mg / kg] for 5 alternate days before cisplatin [3 mg / kg] administration. The effects of sodium selenite on cisplatin-induced oxidative and renal stress were evaluated by plasma creatinine, urea, malondialdehyde, nitrate; kidney tissue malondialdehyde, superoxide dismutase and catalase activities. Administration of cisplatin induced significant increases in plasma creatinine, urea and nitrate concentrations showing renal stress. Cisplatin also induced oxidative stress, as indicated by increased kidney tissue concentrations of malondialdehyde, and reduced activities of superoxide dismutase and catalase. Furthermore, treatment with cisplatin caused a marked elevation of kidney weight and decreased body weight. Sodium selenite pretreatment markedly reduced elevated plasma creatinine, urea and nitrate levels and counteracted the deleterious effects of cisplatin on oxidative stress markers. These results indicate that the sodium selenite might have a protective effect against cisplatin-induced nephrotoxicity and oxidative stress in rat