Oxidative DNA Damage and Carcinogenesis

  • Ryszard Olinski
  • Marek Foksinski
  • Barbara Tudek
Part of the Molecular Biology Intelligence Unit book series (MBIU)


In living cells, there is a steady formation of DNA lesions. A substantial number of these lesions are formed by endogenous factors such as reactive oxygen species (ROS) that damage DNA on a continuous basis. Therefore, it is likely that ROS are the most important human carcinogens.

An involvement of oxidative DNA damage, particularly 8-hydroxy-7, 8-dihydroguanine (8-OHGua) in the origin and/or progression of cancer is reviewed. It is concluded that severe oxidative stress manifested as an altered level of 8-OHGua in cellular DNA as well as in urine of cancer patients may be a consequence of development of many types of cancer. Although at present it is impossible to answer directly the question concerning involvement of oxidative DNA damage in cancer etiology it is very likely that oxidative DNA base modifications may serve as a source of mutations that initiate carcinogenesis (i.e., they may be causal factors responsible for the process).

It should also be remembered that DNA damage, altered gene expression and mutations are required participants in the process of carcinogenesis. Although these events may be derived by different mechanisms a commonality is the involvement of oxidants in all these phenomena.


Lung Cancer Patient Repair Capacity Uterine Myoma Maximum Life Span Severe Oxidative Stress 


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Copyright information

© Landes Bioscience and Springer Science+Business Media 2007

Authors and Affiliations

  • Ryszard Olinski
    • 1
  • Marek Foksinski
    • 1
  • Barbara Tudek
    • 2
  1. 1.Department of Clinical BiochemistryCollegium Medicum Nicolaus Copernicus UniversityBydgoszczPoland
  2. 2.Department of Molecular Biology Institute of Biochemistry and BiophysicsPolish Academy of SciencesWarsawPoland

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