Base excision repair of oxidative DNA damage and association with cancer and aging
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Base excision repair of oxidative DNA damage and association with cancer and aging. / Maynard, Scott; Schurman, Shepherd H; Harboe, Charlotte; de Souza-Pinto, Nadja C; Bohr, Vilhelm A.
In: Carcinogenesis, Vol. 30, No. 1, 01.01.2009, p. 2-10.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Base excision repair of oxidative DNA damage and association with cancer and aging
AU - Maynard, Scott
AU - Schurman, Shepherd H
AU - Harboe, Charlotte
AU - de Souza-Pinto, Nadja C
AU - Bohr, Vilhelm A
PY - 2009/1/1
Y1 - 2009/1/1
N2 - 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.
AB - 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.
KW - Aging
KW - Animals
KW - Base Pairing
KW - DNA Damage
KW - DNA Repair
KW - Humans
KW - Neoplasms
KW - Oxidative Stress
KW - Reactive Oxygen Species
KW - Subcellular Fractions
U2 - 10.1093/carcin/bgn250
DO - 10.1093/carcin/bgn250
M3 - Journal article
C2 - 18978338
VL - 30
SP - 2
EP - 10
JO - Carcinogenesis
JF - Carcinogenesis
SN - 0143-3334
IS - 1
ER -
ID: 33566532