Carcinogenesis Advance Access published online on October 31, 2008
Carcinogenesis, doi:10.1093/carcin/bgn250
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Published by Oxford University Press 2008.
Base excision repair of oxidative DNA damage and association with cancer and aging
1 Laboratory of Molecular Gerontology, National Institute on Aging, NIH, Baltimore, MD 21224
2 Dept. of Biochemistry, Chemistry Institute, University of São Paulo, Brazil
* To whom correspondence should be addressed. Fax: +1 410 558 8157; Email: bohrv{at}grc.nia.nih.gov
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 which 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, such as 8-hydroxyguanine (8-oxoG), formamidopyrimidines, 5-hydroxyuracil and thymine glycol, 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.
Received September 16, 2008; revised October 25, 2008; accepted October 27, 2008.
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