Effects of Decabromodiphenyl Ether (BDE209) Exposure on Toxicity and Oxidative Stress of Beas-2B Cells

Decabromodiphenyl ether (BDE209) has been widely used because of its excellent flame-retardant properties and ability. On the one hand, many studies have shown that the presence of BDE209 can potentially threaten human health and the environment. The production and processing of products containing BDE209 is prohibited except for special applications in China. On the other hand, the study of BDE209 on respiratory cells is not yet fully understood. Consequently, this study aims to investigate the mechanisms of toxic damage and oxidative stress induced by BDE209 exposure in lung epithelial Beas-2B cells. The proliferation of Beas-2B cells under BDE209 exposure was first analyzed by using a real-time label-free cell analyzer (RTCA). Then the cells’ morphological changes were observed using laser confocal microscopy. Subsequently, the effects of BDE209 exposure alone, combined exposure to N-acetylcysteine (NAC) and BDE209, on reactive oxygen species (ROS) levels and antioxidant defense-related factors in Beas-2B cells were analyzed separately. The results show that BDE209 exposure induces the proliferation of Beas-2B cells with a dose-dependent increase in inhibition. Microscopic observation of Beas-2B cells reveals significant damage and death. The levels of ROS are significantly increased (p < 0.01), the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) are increased, the contents of catalase (CAT) are decreased, and the activities of glutathione peroxidase (GPX) are first decreased and then increased. However, under the co-exposure of NAC and BDE209, ROS levels are significantly reduced (p < 0.01), MDA contents decrease, and SOD activities increase. In summary, BDE209 exposure leads to inhibition of Beas-2B cell proliferation, cellular morphology damage, increased ROS levels, and disturbances in antioxidant defense-related factors. The cells showed toxic damage and oxidative stress. In contrast, NAC can suppress ROS levels, enhance SOD activity, and inhibit GPX activity, thereby alleviating BDE209-induced cellular damage.