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.
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PM2.5-induced oxidative stress could trigger autophagy in various cell types.
“It has been reported that PM2.5-induced oxidative stress could trigger autophagy in various cell types (Deng et al. 2013, Su et al. 2017; Zhou et al. 2017).”
From Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis (2018) · cites this paper as Deng et al. 2013
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- Authors
- Deng, X., Zhang, F., Rui, W., Long, F., Wang, L., Feng, Z., Chen, D., & Ding, W.
- Affiliations
- University of Chinese Academy of Sciences (CN)
- Chinese Academy of Sciences (CN)
- China-Japan Friendship Hospital (CN)
- Corresponding author
- Feng, Zhaohan
- Ding, Wenjun
- Venue
- Toxicology in Vitro
- Publisher
- Elsevier BV
- Published
- 2013-09
- Volume
- 27
- Issue
- 6
- Pages
- 1762-1770
- ISSN
- 0887-2333 (ISSN-L)
- OpenAlex
- W1981790437
- Cited by
- 400
- References
- 41
- Citations by year
- 2026: 18 · 2025: 16 · 2024: 20 · 2023: 26 · 2022: 38 · 2021: 50 · 2020: 57 · 2019: 35 · 2018: 44 · 2017: 35 · 2016: 21 · 2015: 24 · 2014: 15 · 2013: 1
- FWCI
- 14.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Toxicology in Vitro (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Gong-Yi Program of China Ministry of Environmental Protection (200909016)
- National Natural Science Foundation of China (10875170)
- the National Science and Technology Ministry of China (2007BAC27B02-2)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Indoor Air Quality and Microbial Exposure
- Keywords
- PM2.5, particulate matter, oxidative stress, autophagy, A549 cells, lung epithelial cells, reactive oxygen species, superoxide dismutase, catalase, LC3, Beclin-1, ATG5, air pollution toxicity, lung function
- MeSH terms
- Air Pollutants, Autophagy, Catalase, Epithelial Cells, Humans, L-Lactate Dehydrogenase, Lung, Superoxide Dismutase, Reactive Oxygen Species, Oxidative Stress, Cell Line, Tumor, Particulate Matter
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