Yanhong Chen

Inorganic arsenic primarily originates from geological processes and human activities. Exposure to high concentrations of inorganic arsenic can cause diverse health problems, with lung injury being one of the main hazards. The present study sought to elucidate the cytotoxicity and underlying mechanisms of inorganic arsenic in BEAS-2B cells. The results showed that exposure of BEAS-2B cells to arsenic trioxide (As₂O₃) for 24 h resulted in a dose-dependent decline in viability. As₂O₃ triggered reactive oxygen species (ROS) production in BEAS-2B cells, and ROS contributed to increased p-IRE1α and p-eIF2α abundance relative to β-actin, along with GRP78 protein expression. The autophagy-associated and apoptotic responses induced by As₂O₃ in BEAS-2B cells were likewise associated with ROS. Further analysis revealed that increased p-IRE1α abundance relative to β-actin is involved in As₂O₃-triggered autophagy-associated responses and apoptosis in BEAS-2B cells. The antioxidant N-acetylcysteine (NAC) markedly attenuated As₂O₃-induced apoptosis and autophagy-associated responses and reduced p-IRE1α abundance relative to β-actin. Collectively, these findings indicate that the ROS/IRE1α pathway contributes to As₂O₃-triggered autophagy-associated responses and apoptosis in BEAS-2B cells.