PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells

摘要: Exposure to higher levels of air pollution particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM2.5) links increased risk cardiovascular and respiratory deaths hospital admission as well lung cancer. Although the mechanism underlying correlation between PM2.5 exposure adverse effects has not fully elucidated, PM2.5-induced oxidative stress been considered important molecular PM2.5-mediated toxicity. In this work, human epithelial A549 cells were used further investigate biological on autophagy. The cell viability showed both time- concentration-dependent decrease when PM2.5, which can be attributed increase extracellular lactate dehydrogenase (LDH) release intracellular reactive oxygen species (ROS) generation in cells. Moreover, damage was observed through alteration superoxide dismutase (SOD) catalase (CAT) activities compared unexposed control autophagy indicated by microtubule-associated protein light chain-3 (LC3) puncta, accumulation LC3 manner. mRNA expression autophagy-related Atg5 Beclin1 also those These results suggest possibility that probably plays a key role cells, may contribute impairment pulmonary function.