期刊
CHEMICAL RESEARCH IN TOXICOLOGY
卷 21, 期 1, 页码 206-219出版社
AMER CHEMICAL SOC
DOI: 10.1021/tx700283c
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资金
- NCI NIH HHS [CA116318, CA110261, CA26735, CA103146] Funding Source: Medline
- NIEHS NIH HHS [ES002109] Funding Source: Medline
- NIGMS NIH HHS [GM059790] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA110261, R01CA116318, R01CA103146] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES002109] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM059790] Funding Source: NIH RePORTER
Damage to DNA and RNA caused by oxidative mechanisms has been well-studied for its potential role in the development of human disease. Only recently, though, have we begun to appreciate that oxidation of the 2-deoxyribose moiety in DNA is also a determinant of the genetic toxicology of oxidative stress and inflammation, with involvement in more than just strand breaks, such as complex DNA lesions, protein-DNA cross-links, and protein and DNA adducts. As an update to a 1992 review of 2'-deoxyribose oxidation by bleomycin and the enediynes published in Chemical Research in Toxicology [Dedon, P. C., and Goldberg, I. H. (1992) Chem. Res. Toxicol. 5, 311-332], this review focuses on recent developments in the chemical biology, bioanalytical chemistry, and genetic, toxicology of 2-deoxyribose oxidation products in DNA under biologically relevant conditions.
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