Bisphenol A affects cell viability involved in autophagy and apoptosis in goat testis sertoli cell.

Bisphenol A (BPA) is shown to be the endocrine disruptor that induces reproductive dysfunction in male animals. In this study, we aim to probe the effects of BPA exposure on induction of autophagy in goat Sertoli Cells (gSCs), as well as the relationship between autophagy and apoptosis. Results indicated that exposure to BPA (100, 200, 300, 400, 500 and 600μM) decreased the cell viability in a concentration-dependent manner. Exposure of gSCs to 500μM BPA for 12h resulted in in vitro triggered loss of mitochondrial membrane potential (ΔΨm) and increased reactive oxygen species (ROS) production. Apoptosis with an increase in Bax:Bcl-2 ratio and higher rates of autophagy, such as autophagosome formation and increased expression of autophagy-related markers were also induced in gSCs exposed to 500μM BPA. Furthermore, treatment with 350nM Rapamycin (Rap, autophagy activator) alleviated a decrease in cell viability, intracellular ROS production, and reduction of ΔΨm, as well as decreasing apoptosis. Collectively, our results indicated that gSCs viability was disrupted after BPA treatment through affecting ROS production, mitochondrial membrane potential and inducing autophagy/apoptosis.