Effects of Acute In vivo Cisplatin and Selenium Treatment on Hematological and Oxidative Stress Parameters in Red Blood Cells of Rats

被引:0
作者
Snežana D. Marković
Dragana S. Djačić
Danijela M. Cvetković
Ana D. Obradović
Jovana B. Žižić
Branka I. Ognjanović
Andraš Š. Štajn
机构
[1] University of Kragujevac,Faculty of Science, Department for Biology and Ecology
来源
Biological Trace Element Research | 2011年 / 142卷
关键词
Active substances; Antioxidative defense system; Cisplatin; Glutathione; Hematology; Lipid peroxidation; Reactive oxygen species; Selenium;
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摘要
Although cisplatin (cisPt) is one of the most often used cytotoxic drugs in the treatment of cancer, its clinical application is associated with nephrotoxicity and a cumulative anemia. In this study, we evaluated posible protective effects of selenium (Se) on hematological and oxidative stress parameters in rats, acutely treated with cisPt. Four groups of Wistar albino rats included control rats, cisPt-treated (7.5 mg/kg of body weight of cisPt, i.p.), Se-treated (6 mg/kg of body weight of Na2SeO4, i.p.), and Se and cisPt co-treated rats. The rats were killed 72 h after treatment; hematological and oxidative stress parameters were followed in red blood cells. The results showed depletion in platelet number induced by high acute doses of cisPt and strong utilization of reduced glutathione, resulting in elevation of GSSG/2 GSH ratio. Se treatment was followed by stimulated erythropoiesis, increased lipid peroxidation, and GSH depletion. Se and cisPt co-treatment were followed by stimulated erythropoiesis and significant recovery of reduced glutathione status when compared with cisPt-treated rats. In conclusion, acute doses of Se and cisPt primarily act as pro-oxidants. CisPt influenced antioxidative properties of exogenous Se and their synergistic effects may partially participate in protection against cisPt-induced toxicity.
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页码:660 / 670
页数:10
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  • [1] Taguchi T(2005)Cisplatin-associated nephrotoxicity and pathological events Contrib Nephrol 148 107-121
  • [2] Nazneen A(1998)Cellular and molecular determinants of cisplatin resistance Eur J Cancer 34 1535-1542
  • [3] Abid MR(1999)Cytotoxic drugs and the CD95 pathway Leukemia 13 1854-1858
  • [4] Perez RP(2000)Apoptotic mechanisms in acute renal failue Am J Med 108 403-415
  • [5] Friesen C(2008)Hydroxyl radical scavenger ameliorates cisplatin-induced nephrotoxicity by preventing oxidative stress, redox state unbalance, impairment of energetic metabolism and apoptosis in rat kidney mitochondria Cancer Chemother Pharmacol 61 145-155
  • [6] Fulda S(1990)Reaction of cis- and trans-[PtCl2(NH3)2] with reduced glutatione studied by 1H, 13C, 19Pt, and 15N-{1H}DEPT NMR J Inorg Biochem 38 305-326
  • [7] Debatin KM(2002)Cisplatin induces acute renal failure by impairing antioxidant system in guinea pigs: effects of antioxidant supplementation on the cisplatin nephrotoxicity Drug Chem Toxicol 25 1-8
  • [8] Ueda N(2000)The importance of selenium to human health Lancet 356 233-241
  • [9] Kaushal GP(2009)Selenium and selenium-antagonistic elements in nutritional cancer prevention Crit Rev Biotechnol 29 10-17
  • [10] Shah SV(2002)Metabolic pathway for selenium in the body: speciation by HPLC-ICP MS with enriched Se Food Addit Contam 19 974-983