期刊
ENVIRONMENTAL POLLUTION
卷 226, 期 -, 页码 412-425出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2017.04.010
关键词
PM2.5; Exposure scenario; Toxic effects; Cellular responses; Autophagy
资金
- National Key Basic Research Program of China (973 Program) [2011CB503803]
- National Natural Science Foundation of China [81430090]
- Beijing Key Laboratory of Environmental Toxicology [2016HJDL04]
Worsening air pollution is a serious threat to public health in many urban and heavily industrialized areas. Particle size and chemical composition are well known determinants of the pathological response to air pollution. In addition, pathological responses may depend on the exposure profile (or scenario) of air pollution. For instance, we previously demonstrated that repeated exposure to low levels of fine airborne particulate matter (PM2.5) induced distinct epigenetic changes compared to acute high-doses exposure. In the present study, we evaluated the differential pathological responses of BEAS-2B human bronchial epithelial cells to two distinct PM2.5 exposure scenarios: 24-h exposure to high-doses PM2.5 (0, 6, 12, 24, 48, 96 mu g/cm(2)) and 10 days' repeated exposure to low levels of PM2.5 (0, 1.5, 3, 6 mu g/cm(2)). Acute exposure to high concentrations of PM2.5 caused ROS burst, marked DNA damage, dysfunction of the endoplasmic reticulum (ER) stress response, autophagy and necrotic cell death. In contrast, repeated low levels of PM2.5 led to sustained low-grade ROS accumulation, milder DNA damage, ER stress/unfolded protein response (UPR), S-phase arrest, apoptosis, and autophagy. Notably, most cells surviving repeated low-level exposure showed a series of abnormal adaptive responses, such as inhibition of mitochondria biogenesis and epigenetic dysregulation. These results indicate that different PM2.5 exposure scenarios induce distinct forms cytotoxicity and adaptive response. In addition to particle size and chemical composition, exposure scenario may be a critical factor determining the toxic health effects of PM2.5. (C)2017 Elsevier Ltd. All rights reserved.
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