Fine particulate matter exposure induces DNA damage by downregulating Rad51 expression in human bronchial epithelial...

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.