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The aim of this study was to investigate the possible protective role of lycopene on cisplatin (CP)-induced spermiotoxicity using quantitative, biochemical and histopathological approaches. Adult male Sprague-Dawley rats were randomly divided into four groups. The control group received physiological saline; animals in cisplatin group received only cisplatin; pre-treatment group received a 10-day of lycopene before administration of cisplatin while animals in post-treatment group received a 5-day of lycopene following administration of cisplatin. Cisplatin (7 mg kg(-1)) was intraperitoneally (i.p.) injected as a single dose and lycopene (4 mg kg(-1)) was administered by gavage in corn oil. Traits of reproductive organs; sperm characteristics, testicular histological findings, plasma testosterone levels and the testicular tissue oxidative status were determined. Administration of cisplatin to rats decreased sperm concentration (p < 0.05) and sperm motility (p < 0.001), increased total abnormal sperm rates (p < 0.05) as compared with the control group. While a marked normalization was achieved only in sperm concentration with lycopene in pre-treatment group, significant normalizations were achieved in the sperm concentration, sperm motility, total abnormal sperm rates in post-treatment group. No significant differences in levels of testosterone were observed among all groups. An increase in testes malondialdehyde concentrations (p < 0.05) and glutathione peroxidase activities (p < 0.001) were detected while significant decreases in glutathione levels (p < 0.001) in cisplatin alone group when compared to control group. While pre-treatment with lycopene restoring only malondialdehyde concentrations, its post-treatment caused normalization in both malondialdehyde and glutathione levels when compared with the cisplatin alone group. On the other hand, significant increases were determined in GSH-Px activities in all experimental groups when compared with the control group. Although the mechanism is not clear, the results from this experimental study suggest that the lycopene have a possible protective effect against cisplatin-induced spermiotoxicity, effect of giving lycopene after cisplatin being superior to the giving it before cisplatin.

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In this study, we investigated the effect of melatonin on cisplatin-induced spermiotoxicity using quantitative, biochemical and histopathological approaches. Cisplatin (CP, 7 mg/kg) and melatonin (10 mg/kg) were intraperitoneally injected. The rats were decapitated on 5th (short-term group) or 50th day (long-term group) after CP injection. Traits of reproductive organs, sperm characteristics, testicular histological findings, and the lipid peroxidation in the testicular tissue were determined. Melatonin mitigated CP-induced reductions in testes, epididymis and accessory gland weights in rats decapitated on day 5. Both short- and long-term CP treatment decreased sperm concentration, sperm motility and increased abnormal sperm rates compared with the control. But the reduction of sperm concentration in long-term CP treatment was insignificant. Although treatment with melatonin provided moderately normalization with respect to sperm concentration in short-term treatment group, melatonin caused a marked normalization of sperm motility in both CP + melatonin groups. Both groups treated with the melatonin showed decreases in abnormal sperm rates compared with alone CP. While testicular malondialdehyde levels were elevated after CP treatment, glutathione peroxidase activity decreased significantly in both groups. Glutathione levels reduced after long-term treatment, but not in short-term group by CP administration. Treatment with CP plus melatonin provided significant amelioration of oxidative stress parameters. Histopathological findings of testes in both short- and long-term treatment groups paralleled the biochemical and spermatogenic results. This study clearly indicates that CP-treatment impaired markedly testicular function and combined treatment with melatonin prevented much of the toxicity in rats.