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Selenium and Lycopene Attenuate Cisplatin-induced Testicular Toxicity Associated With Oxidative Stress in Wistar Rats

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UROLOGY
卷 79, 期 5, 页码 -

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.urology.2011.12.006

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OBJECTIVE To investigate the potential protective effects of selenium and lycopene, either alone or in combination, for cisplatin-induced oxidative stress and testicular dysfunction in male rats. METHODS A total of 50 adult male Wistar rats were divided into 5 groups of 10 animals each, as follows: control group (treated with placebo); cisplatin-alone group; cisplatin + lycopene group; cisplatin + selenium group; and cisplatin + selenium + lycopene group. The weights and dimensions of testes, epididymes, and accessory glands as well as sperm concentration, motility, and proportion of normal morphology were assessed. Testicular tissue malondialdehyde (MDA) and glutathione (GSH) levels, as well as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities, and plasma testosterone were determined. RESULTS Cisplatin treatment caused significant reductions in weights and dimensions of testes, epididymes, and accessory glands, sperm concentration, motility, and proportion of normal morphology, enzymatic and nonenzymatic antioxidants, and plasma testosterone levels. There was significantly increased MDA. The co-administration of selenium and lycopene, either separately or in combination, significantly attenuated the harmful effects of cisplatin-induced lipid peroxidation, oxidative stress, loss of genital organ weight and dimensions, as well as function of reproductive organs collectively in the Wistar rat model. The combination of selenium and lycopene was more effective than supplementation of either agent alone in preventing cisplatin-induced testicular damage. CONCLUSION Selenium and lycopene supplementation reduced cisplatin-induced testicular toxicity, improved testicular function and prevented cisplatin-related injury to the rat testes by suppression of oxidative stress. UROLOGY 79: 1184.e1-1184.e6, 2012. (C) 2012 Elsevier Inc.

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