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

Environ Toxicol Pharmacol. 2012 Sep;34(2):370-380. doi: 10.1016/j.etap.2012.05.012. Epub 2012 Jun 2.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Survival / drug effects
  • Comet Assay
  • Complex Mixtures / toxicity*
  • Cytotoxins / toxicity*
  • DNA Damage
  • DNA Polymerase beta / genetics
  • DNA Polymerase beta / metabolism*
  • DNA Repair
  • Embryo, Mammalian
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Mice
  • Micronucleus Tests
  • Mutagens / toxicity*
  • Nicotiana
  • Reactive Oxygen Species / metabolism
  • Smoke*
  • Smoking / adverse effects


  • Complex Mixtures
  • Cytotoxins
  • Mutagens
  • Reactive Oxygen Species
  • Smoke
  • DNA Polymerase beta