Urinary 8-oxo-2′-deoxyguanosine: Redox regulation of DNA repair in vivo?

Joseph Lunec*, Karen A. Holloway, Marcus S. Cooke, Steve Faux, Helen R. Griffiths, Mark D. Evans

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


DNA is susceptible to damage by reactive oxygen species (ROS). ROS are produced during normal and pathophysiological processes in addition to ionizing radiation, environmental mutagens, and carcinogens. 8-oxo-2′-deoxyguanosine (8-oxodG) is probably one of the most abundant DNA lesion formed during oxidative stress. This potentially mutagenic lesion causes G → T transversions and is therefore an important candidate lesion for repair, particularly in mammalian cells. Several pathways exist for the removal, or repair, of this lesion from mammalian DNA. The most established is via the base excision repair enzyme, human 8-oxoguanine glycosylase (hOgg1), which acts in combination with the human apurinic endonuclease (hApe). The latter is known to respond to regulation by redox reactions and may act in combination with hOgg1. We discuss evidence in this review article concerning alternative pathways in humans, such as nucleotide excision repair (NER), which could possibly remove the 8-oxodG lesion. We also propose that redox-active components of the diet, such as vitamin C, may promote such repair, affecting NER specifically. © 2002 Elsevier Science Inc.

Original languageEnglish
Pages (from-to)875-885
Number of pages11
JournalFree Radical Biology and Medicine
Issue number7
Publication statusPublished - Oct 2002


  • antioxidants
  • ascorbic acid
  • cell signaling
  • DNA damage
  • DNA repair
  • free radicals
  • oxidative stress


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