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

Research output: Contribution to journalJournal articleResearchpeer-review

Scott Maynard, Shepherd H Schurman, Charlotte Harboe, Nadja C de Souza-Pinto, Vilhelm A Bohr

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.
Original languageEnglish
JournalCarcinogenesis
Volume30
Issue number1
Pages (from-to)2-10
Number of pages9
ISSN0143-3334
DOIs
Publication statusPublished - 1 Jan 2009

    Research areas

  • Aging, Animals, Base Pairing, DNA Damage, DNA Repair, Humans, Neoplasms, Oxidative Stress, Reactive Oxygen Species, Subcellular Fractions

ID: 33566532