Microcystin-LR induced oxidative stress, inflammation, and apoptosis in alveolar type II epithelial cells of ICR mice in vitro

Abstract Previous studies have shown that microcystin-LR (MC-LR) produced by toxic cyanobacterial blooms could inflict damage to the lung. However, the mechanisms underlying MC-induced pulmonary toxicity are not fully described. In this study, the primary' fetal alveolar type II epithelial cells (AEC II) from ICR mice, which are involved in formation of bioactive component of pulmonary epithelium and secretion of pulmonary surfactants, were exposed to MC-LR at different concentrations (0, 0.625, 1.25, 2.5, 5, 10, 20 μg/mL) for different time (12, 24, 36 h). Results showed that the viabilities of AEC II exposed to 10 and 20 μg MC-LR/mL were significantly decreased compared with the control group. Furthermore, MC-LR exposure resulted in overproduction of reactive oxygen species (ROS) and induced a significant reduction in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Expressions of apoptosis-related proteins including bax, cyt-c, and caspase-9 were significantly up-regulated by exposure to 2.5, 5, 10, or 20 μg MC-LR/mL. When exposed to 5, 10, or 20 μg MC-LR/mL, expressions of proteins involved in inflammatory, p-65 and iNOS were significantly greater than those of the controls. In conclusion, inflammation and apoptosis might be responsible for MC-LR-induced pulmonary injury.