A study of cytotoxicity and genotoxicity of particulate matter (PM2.5) in human lung epithelial cells (A549)
Kim Woong, 정승찬, 신찬영, 송미경, 조윤, 임정희, 계명찬, 류재천,
소속 상세정보
( Kim Woong )
Korea Institute of Science and Technology Cellular and Molecular Toxicology Laboratory
정승찬 ( Jeong Seung-Chan )
Korea Institute of Science and Technology Cellular and Molecular Toxicology Laboratory
신찬영 ( Shin Chan-Young )
Korea Institute of Science and Technology Cellular and Molecular Toxicology Laboratory
송미경 ( Song Mi-Kyung )
Korea Institute of Toxicology Jeonbuk Department of Inhalation Research
조윤 ( Cho Yoon )
Korea Institute of Science and Technology Cellular and Molecular Toxicology Laboratory
임정희 ( Lim Jung-Hee )
Korea Institute of Science and Technology Cellular and Molecular Toxicology Laboratory
계명찬 ( Gye Myung-Chan )
Hanyang University College of Natural Sciences Department of Life Science
류재천 ( Ryu Jae-Chun )
Korea Institute of Science and Technology Cellular and Molecular Toxicology Laboratory
Abstract
Backgrounds: Exposure to airborne particulate matter (PM2.5), a PM with an aerodynamic diameter of less than 2.5 μm, 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 PM2.5
Results: Both W-PM2.5 and O-PM2.5 exposures significantly reduced the viability of A549 cells in a dosedependent manner, and expression of 17 cell deathrelated 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.
키워드
Particulate matter 2.5 (PM2.5); DNA damage; Gene expression profiling; ROS
원문 및 링크아웃 정보
등재저널 정보