DNA damaging and apoptotic potentials of Bisphenol A and Bisphenol S in human bronchial epithelial cells

DNA damage caused by environmental agents often lead to many chronic diseases, including cancer. The present study aimed to understand the relative toxicity possessed by Bisphenol A (BPA) and Bisphenol S (BPS) on human bronchial epithelial cells (BEAS-2B). The cells were exposed to either BPA or BPS and evaluated for its cytotoxicity, reactive oxygen species (ROS), DNA fragmentation, phosphorylated histone protein (gamma-H2AX) and DNA tail damage levels. Further, we also studied DNA damage response (DDR) and caspase-3 mechanisms, to evaluate its mechanism of cell death processes. Exposure with 200 mu M of BPA, significantly (p < 0.05) induces caspase-3-mediated cell death by inducing cytotoxicity, ROS, and DNA fragmentation. Higher levels of gamma-H2AX and DNA tail damage indicated BPA's DNA damaging potential through an ATM/ATR/Chkl/p53-dependent pathway in BEAS-2B cells. Overall, in vitro data exhibited moderate toxicity for BPS in comparison with BPA suggesting the need for a thorough clinical investigation over its safety profile.