DNA polymerase beta is involved in the protection against the cytotoxicity and genotoxicity of cigarette smoke.

Reactive oxygen species (ROS) and oxidative DNA damage have been implicated in the cigarette smoke-induced cytotoxicity and genotoxicity. DNA polymerase β (polβ), a key base excision repair (BER) enzyme in repairing oxidative DNA damage, may play a crucial role in fighting against the cytotoxicity and genotoxicity of cigarette smoke. In this study, we applied a novel approach to collect cigarette smoke extract (CSE) and investigated the cytotoxic and genotoxic effects of CSE by using the mouse embryo fibroblasts that express wild-type of polβ (polβ(+/+)), null of polβ (polβ(-/-)) and overexpression of polβ (polβ(oe)). Our results showed that polβ(-/-) cells treated with CSE exhibited a higher ROS level and more DNA single-strand breaks and chromosomal aberrations than that of polβ(+/+) and polβ(oe) cells. These data suggested that polβ mediated-BER may involve in repairing the CSE-induced DNA damage and protection against the cytotoxicity and genotoxicity of CSE.