Abstract

Although an accumulating body of evidence suggests that fine particulate matter (PM 2.5 ) can cause lung injury and lung cancer, the underlying mechanisms are not yet clear. In this study, multiple endpoints associated with the cellular response to PM 2.5 exposure, including the cell proliferation rate, cell apoptosis , malondialdehyde (MDA) content and DNA damage, were evaluated in human bronchial epithelial Beas-2B cells. The mRNA expression profile in PM 2.5 -treated cells was analyzed by transcriptome sequencing. The DNA repair gene Rad51 was then selected for further analysis. We found that the viability and growth of Beas-2B cells decreased while cell apoptosis increased in a dose-dependent manner after PM 2.5 exposure. The comet assay showed that PM 2.5 exposure induced evident DNA damage in PM 2.5 -treated cells. The MDA content in the treated cells was increased, indicating that PM 2.5 exposure promoted lipid peroxidation. Furthermore, Rad51 expression was downregulated in PM 2.5 -treated cells, which may have contributed to the PM 2.5 -induced DNA damage in Beas-2B cells. Upregulation of Rad51 expression could rescue the negative impact of PM 2.5 exposure in Beas-2B cells. Taken together, our research demonstrates that PM 2.5 exposure induces DNA damage and impairs the DNA repair process by downregulating Rad51 expression in Beas-2B cells. This finding is expected to provide new insight into the genotoxicity of PM 2.5 exposure.