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

• DOI: 10.3390/ijerph17134874
• Publication Date: 2020-07-06T15:07:42Z
• Authors: Bing-Yu Niu; Wen-Ke Li; Jiang-Shuai Li; Qi-Hao Hong; Sara Khodahemmati; Jing-Feng Gao; Zhi-Xiang Zhou
• Keywords: Comet Assay; XRCC1; Viability assay; Malondialdehyde

Epidemiological studies have corroborated that respiratory diseases, including lung cancer, are related to fine particulate matter (<2.5 μm) (PM2.5) exposure. The toxic responses of PM2.5 greatly influenced by the source PM2.5. However, effects from Beijing on bronchial genotoxicity scarce. In present study, was sampled and applied in vitro investigate its mechanisms behind it. Human epithelial cells 16HBE were used as a model for Low (67.5 μg/mL), medium (116.9 high (202.5 μg/mL) doses cell After exposure, viability, oxidative stress markers, DNA (deoxyribonucleic acid) strand breaks, 8-OH-dG levels, micronuclei formation, repair gene expression measured. results showed significantly induced cytotoxicity 16HBE. Moreover, levels reactive oxygen species (ROS), malondialdehyde (MDA), cellular heme oxygenase (HO-1) increased, level glutathione (GSH) decreased, which represented occurrence severe micronucleus rate elevated, damage occurred indicators comet assay, γ-H2AX 8-OH-dG, markedly enhanced PM2.5, accompanied influence 8-oxoguanine glycosylase (OGG1), X-ray cross-complementing 1 (XRCC1), poly (ADP-ribose) polymerase-1 (PARP1) expression. These support significant role cells, may occur through combined effect genes.