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A study of cytotoxicity and genotoxicity of particulate matter (PM2.5) in human lung epithelial cells (A549)

Title
A study of cytotoxicity and genotoxicity of particulate matter (PM2.5) in human lung epithelial cells (A549)
Author
계명찬
Keywords
Particulate matter 2.5 (PM2.5); DNA damage; Gene expression profiling; ROS
Issue Date
2018-04
Publisher
KOREAN SOCIETY TOXICOGENOMICS & TOXICOPROTEOMICS-KSTT
Citation
MOLECULAR & CELLULAR TOXICOLOGY, v. 14, no. 2, page. 163-172
Abstract
Backgrounds: Exposure to airborne particulate matter (PM2.5), a PM with an aerodynamic diameter of less than 2.5 mu m, is known to be associated with a variety of adverse health effects, particularly related to the respiratory system. However, the molecular mechanisms involved in fine PM toxicity are still not well-characterized. In this study, we estimate pulmonary toxic mechanism using two types (water soluble extract, WPM2.5, and organic soluble extract, O-PM2.5) of PM2.5 on human lung epithelial cells (A549).Methods: Samples were collected using a high-volume air sampler. Each sample was divided into two groups by its own types (water soluble extract, W-PM2.5, and organic soluble extract, O-PM2.5). In the present study, two types of PM2.5-induced cytotoxic and genotoxic effects and expression of toxicity-related genes were evaluated using human lung epithelial cells (A549). Also, the production of intracellular reactive oxygen species was measured to investigate the mechanism of cell death induced by PM2.5Results: Both W-PM2.5 and O-PM2.5 exposures significantly reduced the viability of A549 cells in a dose-dependent manner, and expression of 17 cell death-related genes were significantly regulated in the PM2.5 exposure group. Exposure of PM2.5 significantly induced the production of ROS. Further, data obtained from the Comet assay indicated that two extracts of PM2.5 caused DNA damage in A549 cells in a dose-dependent manner.Conclusion: Our study suggests that ROS-mediated DNA damage may play a major role in PM2.5-induced cell death. This finding represents the basis for further studies addressing the pathophysiological mechanisms of PM2.5 exposure.
URI
https://link.springer.com/article/10.1007%2Fs13273-018-0018-0http://repository.hanyang.ac.kr/handle/20.500.11754/118140
ISSN
1738-642X; 2092-8467
DOI
10.1007/s13273-018-0018-0
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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