Prophylaxis of oxidative DNA damage by formamidopyrimidine-DNA glycosylase

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Lying at the gas-exchange interface, lung epithelia may be at risk of oxidation-induced mutagenesis. Further, inflammation processes possibly consequent on smoking liberate reactive oxygen species that multiply the carcinogenic effects of tobacco. DNA repair mechanisms play a major role in counteracting the deleterious effects of oxidative DNA damage. Some studies find positive associations between lung cancer and variations in the human 8-oxoguanine DNA glycosylase (hOGG1) gene that encodes a major DNA glycosylase for oxidized lesions with sluggish kinetics properties. The bacterial homologue formamidopyrimidine-DNA glycosylase (FPG) is 80-fold faster than hOGG1 in repairing mutagenic oxidative lesions. Cell-culture studies have shown that FPG can be expressed in mammalian cells, where it accelerates DNA repair and abates mutagenicity of a wide range of DNA-damaging agents. Prophylaxis of oxidative DNA damage and mutation could be achieved in lung epithelia and other tissues of at-risk individuals by expression of the FPG protein. Currently available vehicles for this peculiar type of gene therapy are briefly surveyed.

Original languageEnglish
Pages (from-to)1-7
Number of pages7
JournalInternational Journal of Cancer
Issue number1
Publication statusPublished - Jul 1 2006


  • 8-oxoguanine
  • DNA base excision repair
  • Gene therapy
  • Glycosylase
  • Lung cancer
  • Mutation
  • Oxidative DNA damage

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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