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

- BPA increased cytotoxicity in gSCs in a dose- and time-dependent manner.
- BPA resulted in loss of mitochondrial membrane potential (ΔΨm) in gSCs.
- BPA increased reactive oxygen species (ROS) production in gSCs.
- BPA induces apoptotic cell death and cytoprotective autophagy in gSCs.
- Rapamycin inhibits BPA-induced apoptosis by alleviating ROS production.

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 600 μM) decreased the cell viability in a concentration-dependent manner. Exposure of gSCs to 500 μM BPA for 12 h 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 500 μM BPA. Furthermore, treatment with 350 nM 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.

Exposure of goat Sertoli cells to 500 μM BPA in vitro decreased cell viability, triggered loss of mitochondrial membrane potential (ΔYm), increased ROS production, and induced autophagy/apoptosis. Autophagy might act as a transitory survival pathway in gSCs under BPA treatment, but when it occurs excessively or when it is impaired, it may be deleterious and lead to activation of apoptosis mediated cell death.101