Effects of DNA Damage and Oxidative Stress in Human Bronchial Epithelial Cells Exposed to PM2.5 from Beijing, China, in Winter

Bibliographic Data

ID15473148
AuthorsBingyu Niu (0000-0002-5395-409X, Beijing University of Technology), Bing-Yu Niu (Beijing University of Technology), Wenke Li (0000-0003-0984-9468, Beijing University of Technology), Wen-Ke Li (Beijing University of Technology), Jiangshuai Li (0000-0001-6710-7329, Beijing University of Technology), Jiang-Shuai Li (Beijing University of Technology), Qihao Hong (Beijing University of Technology), Qi-Hao Hong (Beijing University of Technology), Sara Khodahemmati (Beijing University of Technology), Jingfeng Gao (0000-0002-5430-7812, Beijing University of Technology), Jing-Feng Gao (Beijing University of Technology), Zhixiang Zhou (0000-0001-7326-550X, Beijing University of Technology, corresponding author), Zhi-Xiang Zhou (Beijing University of Technology)
Year2020
Volume17
Issue13
Pages4874-4874
Publication date2020-07-06
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueInternational Journal of Environmental Research and Public Health (JOURNAL)
Journal identifiersISSN: 1661-7827 • E-ISSN: 1660-4601
PublisherMultidisciplinary Digital Publishing Institute (PUBLISHER • CH)
DOI10.3390/ijerph17134874
PMID32640694
OpenAlexW3038904669
LanguageEN
References cited52

Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter ( 2.5 ) exposure. The toxic responses of PM 2.5 are greatly influenced by the source of PM 2.5 . However, the effects of PM 2.5 from Beijing on bronchial genotoxicity are scarce. In the present study, PM 2.5 from Beijing was sampled and applied in vitro to investigate its genotoxicity and the mechanisms behind it. Human bronchial epithelial cells 16HBE were used as a model for exposure. Low (67.5 μg/mL), medium (116.9 μg/mL), and high (202.5 μg/mL) doses of PM 2.5 were used for cell exposure. After PM 2.5 exposure, cell viability, oxidative stress markers, DNA (deoxyribonucleic acid) strand breaks, 8-OH-dG levels, micronuclei formation, and DNA repair gene expression were measured. The results showed that PM 2.5 significantly induced cytotoxicity in 16HBE. Moreover, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and cellular heme oxygenase (HO-1) were increased, and the level of glutathione (GSH) was decreased, which represented the occurrence of severe oxidative stress in 16HBE. The micronucleus rate was elevated, and DNA damage occurred as indicators of the comet assay, γ-H2AX and 8-OH-dG, were markedly enhanced by PM 2.5 , accompanied by the influence of 8-oxoguanine DNA glycosylase (OGG1), X-ray repair cross-complementing gene 1 (XRCC1), and poly (ADP-ribose) polymerase-1 (PARP1) expression. These results support the significant role of PM 2.5 genotoxicity in 16HBE cells, which may occur through the combined effect on oxidative stress and the influence of DNA repair genes

Biology · Cell · Comet Assay · DNA · DNA damage · DNA repair · Gene · Genotoxicity · Genotype · Lipid peroxidation · Malondialdehyde · Micronucleus test · Oxidative stress · Reactive oxygen species · Superoxide dismutase · Toxicity · Viability assay · XRCC1 · Air Quality and Health Impacts · Carcinogens and Genotoxicity Assessment · Chemistry · Energy and Environment Impacts · Biochemistry · Molecular Biology

Tools

Open DOIOpen Access