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

Abstract

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 (γ-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 μM of BPA, significantly (p < 0.05) induces caspase-3-mediated cell death by inducing cytotoxicity, ROS, and DNA fragmentation. Higher levels of γ-H2AX and DNA tail damage indicated BPA’s DNA damaging potential through an ATM/ATR/Chk1/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.