Lipid Peroxidative Damage on Cisplatin Exposure and Alterations in Antioxidant Defense System in Rat Kidneys: A Possible Protective Effect of Selenium

Abstract

Cisplatin (Cis-diamminedichloroplatinum II, CP) is an important chemotherapeutic agent, useful in the treatment of several cancers, but with several side effects such as nephrotoxicity. The present study investigated the possible protective effect of selenium (Se) against CP-induced oxidative stress in the rat kidneys. Male Wistar albino rats were injected with a single dose of cisplatin (7 mg CP/kg b.m., i.p.) and selenium (6 mg Se/kg b.m, as Na2SeO3, i.p.), alone or in combination. The obtained results showed that CP increased lipid peroxidation (LPO) and decreased reduced glutathione (GSH) concentrations, suggesting the CP-induced oxidative stress, while Se treatment reversed this change to control values. Acute intoxication of rats with CP was followed by statistically significant decreased activity of antioxidant defense enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase (GST). Treatment with Se reversed CP-induced alterations of antioxidant defense enzyme activities and significantly prevented the CP-induced kidney damage.

Effect of Antioxidants and Mesenchymal Stem Cells on Cisplatin Induced Renal Fibrosis in Rats

“…Owing to the reports by Ognjanovic et al [37] and Ohnishi et al [38] they addressed the same findings as in our study [36,37,39].…”

Protective effect of CV247 against cisplatin nephrotoxicity in rats

“…Two groups were intraperitoneally injected with a single dose of cisplatin (CDDP) at 6.5 mg/kg body weight. 41 CDDP was suspended in 10 ml/kg 1% methyl cellulose. One of the groups injected with CDDP was subsequently treated with vehicle (C) or CV at 3 ml/kg body weight, p.o.…”

Ascorbic Acid (Vitamin C)-Mediated Protection on Mutagenic Potentials of Cisplatin in Mice Bearing Ascites Dalton ’s Lymphoma

“…Elevation of GSH levels has been shown to increase the resistance of cancer cells to cisplatin (Meijer et al, 1990;Kartalou and Essigmann, 2001), while depletion of GSH levels could potentiate the cytotoxicity of a variety of antitumor agents (Arrick and Nathan, 1984). Several investigators have demonstrated that cisplatin induces ROS primarily by decreasing the activity of antioxidant enzymes and by depleting intracellular concentrations of GSH (Husain et al, 1998;Ognjanovic et al, 2012). Depletion in the renal GSH level in rats has also been reported in response to oxidative stress caused by cisplatin treatment (Silva et al, 2001).…”