Protective Potential of Adiponectin and Quercetin on Alleviating Bisphenol-A-Induced Toxicity in Muscle Cells Through the KEAP1/NRF2 Pathway

Background: Bisphenol A (BPA) is a toxic environmental estrogenic compound which exerts its detrimental effects by increasing oxidative stress and decreasing levels of antioxidants. This study aimed to evaluate beneficial effect of adiponectin and quercetin in reducing BPA-induced oxidative stress by assessing the Prooxidant-antioxidant balance (PAB) assay, catalase activity and KEAP1/NRF2 expression in muscle cells.Methods and Results: L6 rat muscle cells were exposed to BPA (50 an100 μM) with and without treatment with different concentrations of adiponectin (10 and 100 ng/ml) and quercetin (10 and 25 ng/ml) for 24 and 48 hours. Cell viability was assessed using MTT assay, and the PAB was evaluated with the ELISA at 540 nm. Catalase level was also evaluated in all groups. Furtheremore, the expression of KEAP1/Nrf2 genes was assessed using qRT-PCR. The results showed a significant reduction in L6 cells survival after being treated with 100 μM BPA. Adiponectin and quercetin treatment also increased cell survival compared to BPA-treated cells. It was also found that PAB increased with BPA exposure, and quercetin treatment significantly reduced it compared to BPA treatment. The catalase activity was reduced in BPA-treated cells, which was significantly increased by treatment with adiponectin and quercetin. A significant decrease in Nrf2 gene expression was observed in BPA-treated cells compared to the control group. It was further found that cell treatment with quercetin and adiponectin significantly increased the expression of Nrf2 gene compared to the control group.Conclusions: Taking together, our results implied that adiponectin and quercetin could modulate BPA-induced oxidative stress in muscle cells through KEAP1/Nrf2 pathway. Accordingly, it can be concluded that adiponectin in low dose and quercetin, may have significant impact in reducing toxicity due to BPA.

Apigenin induces oxidative stress in mouse Sertoli TM4 cells

Background and Aim: Apigenin (API) is an estrogenic compound found in many plants. Sertoli cells reside in the testis and are a key target of environmental toxicants. This study aimed to examine the cytotoxicity, especially oxidative stress of API in mouse Sertoli TM4 cells. Materials and Methods: Mouse Sertoli TM4 cells were treated with 50 and 100 μM API for 48 h. Cell viability, lactate dehydrogenase (LDH) activities, glutathione reductase (GR) activities, production of reactive oxygen species (ROS), and malondialdehyde (MDA) levels were evaluated using various assays. Results: Treatment with API at both 50 and 100 μM decreased viability and GR activity but increased LDH activity, ROS production, and MDA levels in mouse Sertoli TM4 cells. Conclusion: Exposure to API induced oxidative stress in mouse Sertoli TM4 cells.