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 journalArticle

Abstract

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
Volume33
Issue number7
DOIs
Publication statusPublished - Oct 2002

Fingerprint

DNA Repair
Oxidation-Reduction
Repair
Reactive Oxygen Species
DNA
DNA-(Apurinic or Apyrimidinic Site) Lyase
Environmental Carcinogens
Mutagens
Ionizing Radiation
Ascorbic Acid
Oxidative Stress
Nucleotides
Diet
Oxidative stress
Redox reactions
Ionizing radiation
Enzymes
Nutrition
Carcinogens
8-oxo-7-hydrodeoxyguanosine

Keywords

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

Cite this

Lunec, J., Holloway, K. A., Cooke, M. S., Faux, S., Griffiths, H. R., & Evans, M. D. (2002). Urinary 8-oxo-2′-deoxyguanosine: Redox regulation of DNA repair in vivo? Free Radical Biology and Medicine, 33(7), 875-885. https://doi.org/10.1016/S0891-5849(02)00882-1
Lunec, Joseph ; Holloway, Karen A. ; Cooke, Marcus S. ; Faux, Steve ; Griffiths, Helen R. ; Evans, Mark D. / Urinary 8-oxo-2′-deoxyguanosine : Redox regulation of DNA repair in vivo?. In: Free Radical Biology and Medicine. 2002 ; Vol. 33, No. 7. pp. 875-885.
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Lunec, J, Holloway, KA, Cooke, MS, Faux, S, Griffiths, HR & Evans, MD 2002, 'Urinary 8-oxo-2′-deoxyguanosine: Redox regulation of DNA repair in vivo?', Free Radical Biology and Medicine, vol. 33, no. 7, pp. 875-885. https://doi.org/10.1016/S0891-5849(02)00882-1

Urinary 8-oxo-2′-deoxyguanosine : Redox regulation of DNA repair in vivo? / Lunec, Joseph; Holloway, Karen A.; Cooke, Marcus S.; Faux, Steve; Griffiths, Helen R.; Evans, Mark D.

In: Free Radical Biology and Medicine, Vol. 33, No. 7, 10.2002, p. 875-885.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Urinary 8-oxo-2′-deoxyguanosine

T2 - Redox regulation of DNA repair in vivo?

AU - Lunec, Joseph

AU - Holloway, Karen A.

AU - Cooke, Marcus S.

AU - Faux, Steve

AU - Griffiths, Helen R.

AU - Evans, Mark D.

PY - 2002/10

Y1 - 2002/10

N2 - 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.

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KW - antioxidants

KW - ascorbic acid

KW - cell signaling

KW - DNA damage

KW - DNA repair

KW - free radicals

KW - oxidative stress

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