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PMID: 18978338 Published · ppublish English Journal Article Research Support, N.I.H., Intramural Review

Base excision repair of oxidative DNA damage and association with cancer and aging.

Carcinogenesis ·Vol. 30 ·No. 1 ·2009-01-00 ·Pages 2-10

Maynard S, Schurman SH, Harboe C, de Souza-Pinto NC, Bohr VA

Abstract

Aging has been associated with damage accumulation in the genome and with increased cancer incidence. Reactive oxygen species (ROS) are produced from endogenous sources, most notably the oxidative metabolism in the mitochondria, and from exogenous sources, such as ionizing radiation. ROS attack DNA readily, generating a variety of DNA lesions, such as oxidized bases and strand breaks. If not properly removed, DNA damage can be potentially devastating to normal cell physiology, leading to mutagenesis and/or cell death, especially in the case of cytotoxic lesions that block the progression of DNA/RNA polymerases. Damage-induced mutagenesis has been linked to various malignancies. The major mechanism that cells use to repair oxidative damage lesions, such as 8-hydroxyguanine, formamidopyrimidines, and 5-hydroxyuracil, is base excision repair (BER). The BER pathway in the nucleus is well elucidated. More recently, BER was shown to also exist in the mitochondria. Here, we review the association of BER of oxidative DNA damage with aging, cancer and other diseases.

MeSH Terms
Aging/genetics Animals Base Pairing DNA Damage DNA Repair Humans Neoplasms/genetics Oxidative Stress Reactive Oxygen Species/metabolism Subcellular Fractions/metabolism
Chemicals
Reactive Oxygen Species
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Maynard Scott
Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA.
Schurman Shepherd H
Harboe Charlotte
de Souza-Pinto Nadja C
Bohr Vilhelm A
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Article Info
Journal
Carcinogenesis
Abbr.
Carcinogenesis
ISSN
1460-2180
Published
2009-01-00
Epub
2008-00-31
Pages
2-10
Language
English
Region
England
NLM ID
8008055
PMCID
PMC2639036
Subset
IM
Grants
Intramural NIH HHS · United States
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