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. 2012;13(2):1790-1803.
doi: 10.3390/ijms13021790. Epub 2012 Feb 8.

Lipid peroxidative damage on Cisplatin exposure and alterations in antioxidant defense system in rat kidneys: a possible protective effect of selenium

Branka I Ognjanović  1 , Nataša Z Djordjević  1 , Miloš M Matić  1 , Jasmina M Obradović  1 , Jelena M Mladenović  1 , Andraš Š Štajn  1 , Zorica S Saičić  2
Affiliations

Lipid peroxidative damage on Cisplatin exposure and alterations in antioxidant defense system in rat kidneys: a possible protective effect of selenium

Branka I Ognjanović et al. Int J Mol Sci. 2012.

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 Na(2)SeO(3), 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.

Keywords: antioxidant defense system; cisplatin; lipid peroxidation; nephrotoxicity; selenium.

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Figures

Figure 1
Figure 1
Effect of Se treatment on superoxide dismutase (SOD) activity in kidney of CP-treated rats. Values are expressed as means ± SD; n = 6 for each treatment group; CP: Cisplatin; Se: selenium; * p < 0.05 compared with control group, # p < 0.05 compared with CP group.
Figure 2
Figure 2
Effect of Se treatment on catalase (CAT) activity in kidney of CP-treated rats. Values are expressed as means ± SD; n = 6 for each treatment group; CP: Cisplatin; Se: selenium; * p < 0.05 compared with control group, # p < 0.05 compared with CP group.
Figure 3
Figure 3
Effect of Se treatment on glutathione peroxidase (GSH-Px) activity in kidney of CP-treated rats. Values are expressed as means ± SD; n = 6 for each treatment group; CP :Cisplatin; Se: selenium; * p < 0.05 compared with control group, # p < 0.05 compared with CP group.
Figure 4
Figure 4
Effect of Se treatment on glutathione reductase (GR) activity in kidney of CP-treated rats. Values are expressed as means ± SD; n = 6 for each treatment group; CP: Cisplatin; Se: selenium; * p < 0.05 compared with control group, # p < 0.05 compared with CP group.
Figure 5
Figure 5
Effect of Se treatment on glutathione-S-transferase (GST) activity in kidney of CP-treated rats. Values are expressed as means ± SD; n = 6 for each treatment group; CP: Cisplatin; Se: selenium; * p < 0.05 compared with control group, # p < 0.05 compared with CP group.
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References

    1. Baek S.M., Kwon C.H., Kim J.H., Woo J.S., Jung J.S., Kim Y.K. Differential roles of hydrogen peroxide and hydroxyl radical in cisplatin-induced cell death in renal proximal tubular epithelial cells. J. Lab. Clin. Med. 2003;142:178–186. - PubMed
    1. Hanigan M.H., Devarajan P. Cisplatin nephrotoxicity: Molecular mechanisms. Cancer Ther. 2003;1:47–61. - PMC - PubMed
    1. Jordan P., Carmo-Fonseca M. Molecular mechanisms involved in cisplatin cytotoxicity. Cell Mol. Life Sci. 2000;57:1229–1235. - PMC - PubMed
    1. Kroning R., Lichestenstein A.K., Nagami G.T. Sulfur-containing amino acids decrease cisplatin cytotoxicity and uptake in renal tubular epithelial cell lines. Cancer Chemother. Pharmacol. 2000;45:43–49. - PubMed
    1. Cohen S.M., Lippard S.J. Cisplatin: From DNA damage to cancer chemotherapy. Prog. Nucleic Acis. Res. Mol. Biol. 2001;67:93–130. - PubMed

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