title: PM2.5-induced oxidative stress triggers autophagy in human lung epithelial A549 cells.
abstract: Exposure to higher levels of air pollution particulate matter (PM) with an aerodynamic diameter of less than 2.5 μm (PM2.5) links with an increased risk of cardiovascular and respiratory deaths and hospital admission as well as lung cancer. Although the mechanism underlying the correlation between PM2.5 exposure and adverse effects has not fully elucidated, PM2.5-induced oxidative stress has been considered as an important molecular mechanism of PM2.5-mediated toxicity. In this work, human lung epithelial A549 cells were used to further investigate the biological effects of PM2.5 on autophagy. The cell viability showed both time- and concentration-dependent decrease when exposure to PM2.5, which can be attributed to increase of the levels of extracellular lactate dehydrogenase (LDH) release and intracellular reactive oxygen species (ROS) generation in A549 cells. Moreover, PM2.5-induced oxidative damage in A549 cells was observed through the alteration of superoxide dismutase (SOD) and catalase (CAT) activities compared to the unexposed control cells. PM2.5-induced autophagy was indicated by an increase in microtubule-associated protein light chain-3 (LC3) puncta, and accumulation of LC3 in both time- and concentration-dependent manner. PM2.5-induced mRNA expression of autophagy-related protein Atg5 and Beclin1 was also observed compared with those of the unexposed control cells. These results suggest the possibility that PM2.5-induced oxidative stress probably plays a key role in autophagy in A549 cells, which may contribute to PM2.5-induced impairment of pulmonary function.
authors.affiliation: Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, No. 19A Yuquan Road, Beijing 100049, China.
authors.forename: Xiaobei
authors.initials: X
authors.lastname: Deng
authors.forename: Fang
authors.initials: F
authors.lastname: Zhang
authors.forename: Wei
authors.initials: W
authors.lastname: Rui
authors.forename: Fang
authors.initials: F
authors.lastname: Long
authors.forename: Lijuan
authors.initials: L
authors.lastname: Wang
authors.forename: Zhaohan
authors.initials: Z
authors.lastname: Feng
authors.forename: Deliang
authors.initials: D
authors.lastname: Chen
authors.forename: Wenjun
authors.initials: W
authors.lastname: Ding
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D001343:Autophagy; D002374:Catalase / Q000378:metabolism; D045744:Cell Line, Tumor; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008168:Lung / Q000166:cytology; D018384:Oxidative Stress; D052638:Particulate Matter / Q000633:toxicity*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D013482:Superoxide Dismutase
keywords: 2′,7′-dichlorodihydrofluorescein diacetate; 2′,7′-dichlorofluorescein; 4,6-diamido-2-phenylindole hydrochloride; Autophagy; DAPI; DCF; DCFH-DA; EC; LC3; LDH; Lung epithelial A549 cells; N-acetylcysteine; NAC; OC; OH(); Oxidative stress; PAHs; PM; PM(2.5); ROS; SEM; TEM; ambient airborne particulate matter; elemental carbon; hydroxyl radical; lactate dehydrogenase; microtubule-associated proteins light chain 3; organic carbon; polycyclic aromatic hydrocarbons; reactive oxygen species; scanning electron microscopy; superoxide anion; transmission electron microscopy