Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells

• Published in: Environmental science and pollution research international 2017-11, Vol.24 (32), p.25071-25081
• Main Authors: Wu, Jing, Shi, Yanfeng, Asweto, Collins Otieno, Feng, Lin, Yang, Xiaozhe, Zhang, Yannan, Hu, Hejing, Duan, Junchao, Sun, Zhiwei
• Format: Article
• Language: English
• Subjects: Activation; Air Pollutants - analysis; Air Pollutants - toxicity; Apoptosis; Aquatic Pollution; Atmospheric Protection/Air Quality Control/Air Pollution; Bronchi - drug effects; c-Myc protein; Cell cycle; Cell Line; Cell Proliferation - drug effects; Cell Survival - drug effects; Damage; Deoxyribonucleic acid; DNA; DNA Damage; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental Health; Environmental science; Epithelial Cells - drug effects; ErbB-2 protein; Exposure; G2 Phase Cell Cycle Checkpoints - drug effects; Growth curves; Humans; Lungs; MAP kinase; Molecular modelling; Myc protein; Particulate emissions; Particulate matter; Particulate Matter - analysis; Particulate Matter - toxicity; Research Article; Tumorigenesis; Waste Water Technology; Water Management; Water Pollution Control
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-017-0090-3

There is compelling evidence that exposure to particulate matter (PM) is linked to lung tumorigenesis. However, there is not enough experimental evidence to support the specific mechanisms of PM 2.5 -induced DNA damage and cell cycle arrest in lung tumorigenesis. In this study, we investigated the toxic effects and molecular mechanisms of PM 2.5 on bronchial epithelial (BEAS-2B) cells. PM 2.5 exposure reduced cell viability and enhanced LDH activity. The cell growth curves of BEAS-2B cells decreased gradually with the increase in PM 2.5 dosage. A significant increase in MDA content and a decrease in GSH-Px activity were observed. The generation of ROS was enhanced obviously, while apoptosis increased in BEAS-2B cells exposed to PM 2.5 for 24 h. DNA damage was found to be more severe in the exposed groups compared with the control. For in-depth study, we have demonstrated that PM 2.5 stimulated the activation of HER2/ErbB2 while significantly upregulating the expression of Ras/GADPH, p-BRAF/BRAF, p-MEK/MEK, p-ERK/ERK, and c-Myc/GADPH in a dose-dependent manner. In summary, we suggested that exposure to PM 2.5 sustained the activation of HER2/ErbB2, which in turn promoted the activation of the Ras/Raf/MAPK pathway and the expression of the downstream target c-Myc. The overexpression of c-Myc may lead to G2/M arrest and aggravate the DNA damage and apoptosis in BEAS-2B after exposure to PM 2.5 .