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.

Despite all the studies performed to date, therapy choices for liver injuries are very few. Therefore, the search for a new treatment that could safely and effectively block or reverse liver injuries remains a challenge. Quercetin (QR) and ellagic acid (EA) had potent antioxidant and anti-inflammatory activities. The current study aimed at evaluating the potential hepatoprotective influence of QR and EA against thioacetamide (TAA)-induced liver toxicity in rats and the underlying mechanism using silymarin as a reference drug. Fifty mature male rats were orally treated daily with EA and QR in separate groups for 45 consecutive days, and then were injected with TAA twice with 24 h intervals in the last 2 days of the experiment. Administration of TAA resulted in marked elevation of liver indices, alteration in oxidative stress parameters, and significant elevation in expression level of fibrosis-related genes (MMP9 and MMP2). Administration of QR and EA significantly attenuated the hepatic toxicity through reduction of liver biomarkers, improving the redox status of the tissue, as well as hampering the expression level of fibrosis-related genes. In this study, QR and EA were proved to attenuate the hepatotoxicity through their antioxidant, metal-chelating capacity, and anti-inflammatory effects.

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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.

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BackgroundThe safety of Deltamethrin (DM) has been raised as a point of concern. The current investigation was envisaged to explore the responsiveness of oxidative stress parameters, DNA fragmentation and expression levels of TP53, cycloxygenase 2 (COX2) and cytochrome p4502E1 (CYP2E1) as toxicological endpoint in rats treated with DM. as well as attention was provided to the neuroprotective effect of vitamin E (VE).MethodsFour different groups of rats were used in this study, group I served as control, group II received DM (0.6 mg/kg BW), group III received both DM plus VE and finally group IV received VE only (200 mg/kg BW). The treatment regimen was extending for one month for all groups and the brain tissues were collected for further analysis.ResultsThe obtained results showed a highly statistically significant increase in lipid peroxidation (LPO) content, nitric oxide concentration, and DNA fragmentation percentage and expression level of CYP2E1, TP53 and COX2 genes, in addition statistical significant reduction in total antioxidant capacity in DM treated group as compared to control were detected. Oral administration of VE attenuated the neurotoxic effects of DM through improvement of oxidative status, DNA fragmentation percentage and suppressing the expression level of CYP2E1, TP53 and COX2 genes.ConclusionFrom this study we concluded that VE supplementation has beneficial impacts on DM neurotoxicity in rats through its antioxidant and antiapoptotic properties.

Hexavelant chromium (Cr (V1)) is a widely distributed environmental pollutant inducing damage in different organs of human and animals. The current study was designed to investigate the mechanistic role of rosmarinic acid (RA) to diminish chromium‐induced hepatorenal oxidative damage and preneoplastic lesions in rats. Plant material was collected, identified, and extracted. The isolated RA was elucidated relying on the nuclear magnetic resonance spectroscopic data. Twenty‐eight male Wistar rats received the following materials daily via oral gavage for 60 days; (Gp1): normal saline, (Gp2) 25 mg/kg.bwt RA, (Gp3) 10 mg/kg.bwt potassium dichromate (K2Cr2O7), (Gp4) K2Cr2O7 + RA. All rats were euthanized at the end of the experiment by cervical dislocation and the liver and kidney were collected. Prolonged continuous exposure of rats to chromium‐induced oxidant/antioxidant imbalance manifested by significant elevation of malondialdehyde with reduction in reduced glutathione levels. Remarkable histopathological alterations in the liver and kidney tissue sections were recorded and confirmed by overexpression of the immunohistochemical staining of caspase‐3, placental glutathione‐S transferase, proliferating cell nuclear antigen together with a significant downregulation of nuclear factor erythroid‐2 related factor 2 (Nrf2) gene and upregulation of nibrin gene. Observable improvements in the entire toxicopathological parameters were recorded in group cotreated with RA. Our findings revealed that Cr‐induced preneoplastic lesions on the liver and kidney tissues of rats when exposed daily for long period of time, as well as confirmed the ability of RA to alleviate this toxicity through upregulation of Nrf2 pathway and its powerful antioxidant effects.