Lipid Peroxidation and Oxidative Stress Induced Etheno- DNA Adducts in Humans and Rodents

  • J. Nair
  • H. Bartsch
Conference paper
Part of the NATO Science Series book series (NAII, volume 129)


Oxidative processes are involved in aging as well as the pathogenesis of different degenerative diseases. Oxidative stress enhances lipid peroxidation (LPO), implicated in promotion and progression stages of carcinogenesis, in particular in chronic inflammation and infection. Oxidative stress and LPO are also entailed in the development of artherosclerosis and coronary heart disease. In the last decade it has become evident that reactive aldehydes such as trans-4-hydroxy-2-nonenal and malondialdehyde generated during LPO can react with nucleic acid bases to form exocyclic DNA adducts. Formation of DNA-adducts from exogeneous and endogenous carcinogens or its metabolites is one of the earliest damage to the genome in the cells. If not repaired, DNA adducts once formed in surviving cells, will lead to mutations upon cell division and disrupt genomic integrity and lead to cancer. Using an ultrasensitive immunoaffinity-32P-postlabelling method, we have demonstrated that exocyclic 1,N 6 -ethenodeoxyadenosine (sdA) 3,N 4 -ethenodeoxycytidine (εdC) are present in DNA of non-exposed rodent and asymptomatic human tissues, reflecting the physiological LPO processes. The etheno-DNA adduct levels were significantly increased by cancer risk factors that contribute to oxidative stress/LPO, such as chronic infections, inflammatory conditions and metal storage diseases in humans and rodents.


Nitric Oxide Reactive Nitrogen Species Cancer Risk Factor Copper Accumulation Menkes Disease 
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Copyright information

© Springer Science+Business Media Dordrecht 2003

Authors and Affiliations

  • J. Nair
    • 1
  • H. Bartsch
    • 1
  1. 1.Division of Toxicology and Cancer Risk FactorsGerman Cancer Research Center (DKFZ)HeidelbergGermany

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