Bisphenol A (BPA) is a widespread compound associated with the manufacture of many consumer products. The BPA-induced reproductive toxicity was reported to be mainly attributed to oxidative stress. However, the role of antioxidants usage to decrease the injurious effects of BPA, on male reproductive functions, remains to unveil. The present research is established to evaluate the role of selenium (Se) and its nano form (NSe) as protective agents to alleviate BPA-induced testicular toxicity. Ninety mature albino male rats were assigned into six equal groups: negative control; orally BPA 150 mg/kg; Se 3 mg/kg; NSe 2 mg/kg; both BPA 150 mg/kg and Se 3 mg/kg; and BPA 150 mg/kg + NSe 2 mg/kg. The experiment lasted for 70 consecutive days, and then serum was collected for estimation of prostatic acid phosphatase. Testicular tissues were subjected to measurement of antioxidant status, lipid peroxidation, DNA damage, and expression of some apoptotic genes. Our results reported that BPA-induced marked testicular damage evidenced by significant elevations in serum prostatic acid phosphatase activity, malondialdehyde levels, a decrease in testicular catalase activity and reduced glutathione level. Moreover, marked DNA internucleosomal fragmentation pattern as well as upregulation of cyclooxygenase-2 and estrogen receptor-2 NSe genes were detected. Coadministration of Se and NSe attenuated the reproductive toxicity induced by BPA via improvement of the antioxidant activity, genetic changes, and restoration of testicular tissue nearly as control one. These results indicated that both Se and NSe forms could be used as reproductive protective agents against the detrimental effect induced by BPA. However, the NSe surpassed the selenium in modulating the DNA laddering, and the studied gene expression levels, and offered a potent reproductive protection.

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The potential toxicity of copper nanoparticles (CNPs) to the human health and environment remains a critical issue. In the present study, we investigated the protective influence of an aqueous extract of green tea leaves (GTE) against CNPs-induced (20–30 nm) hepatotoxicity. Four different groups of rats were used: group I was the control, group II received CNPs (40 mg/kg BW), group III received CNPs plus GTE, and group IV received GTE alone. We highlighted the hepatoprotective effect of GTE against CNPs toxicity through monitoring the alteration of liver enzyme activity, antioxidant defense mechanism, histopathological alterations, and DNA damage evaluation. The rats that were given CNPs only had a highly significant elevation in liver enzymes, alteration in oxidant-antioxidant balance, and severe pathological changes. In addition, we detected a significant elevation of DNA fragmentation percentage, marked DNA laddering, and significance over expression of both caspase-3 and Bax proteins. The findings for group III clarify the efficacy of GTE as a hepatoprotectant on CNPs through improving the liver enzyme activity, antioxidant status, as well as suppressing DNA fragmentation and the expression of the caspase-3 and Bax proteins. In conclusion, GTE was proved to be a potential hepatoprotective additive as it significantly ameliorates the hepatotoxicity and apoptosis induced by CNPs.