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The chemical toxicology of 2-deoxyribose oxidation in DNA

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

  1. NCI NIH HHS [CA116318, CA110261, CA26735, CA103146] Funding Source: Medline
  2. NIEHS NIH HHS [ES002109] Funding Source: Medline
  3. NIGMS NIH HHS [GM059790] Funding Source: Medline
  4. NATIONAL CANCER INSTITUTE [R01CA110261, R01CA116318, R01CA103146] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES002109] Funding Source: NIH RePORTER
  6. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM059790] Funding Source: NIH RePORTER

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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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