5. Lipid Peroxidation–Derived DNA Adducts and the Role in Inflammation-Related Carcinogenesis

  1. Yusuke Hiraku1,
  2. Shosuke Kawanishi2 and
  3. Hiroshi Ohshima3
  1. Helmut Bartsch and
  2. Urmila Jagadeesan Nair

Published Online: 4 APR 2014

DOI: 10.1002/9781118826621.ch5

Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects

Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects

How to Cite

Bartsch, H. and Nair, U. J. (2014) Lipid Peroxidation–Derived DNA Adducts and the Role in Inflammation-Related Carcinogenesis, in Cancer and Inflammation Mechanisms: Chemical, Biological, and Clinical Aspects (eds Y. Hiraku, S. Kawanishi and H. Ohshima), John Wiley & Sons, Inc., Hoboken, NJ, USA. doi: 10.1002/9781118826621.ch5

Editor Information

  1. 1

    Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Tsu, Mie, Japan

  2. 2

    Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Suzuka, Mie, Japan

  3. 3

    Department of Nutritional and Environmental Sciences, Graduate School of Integrated Pharmaceutical and Nutritional Sciences, University of Shizuoka, Shizuoka, Japan

Publication History

  1. Published Online: 4 APR 2014
  2. Published Print: 4 APR 2014

ISBN Information

Print ISBN: 9781118160305

Online ISBN: 9781118826621

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Keywords:

  • carcinogenesis;
  • DNA adducts;
  • DNA damage;
  • inflammation-related malignancies;
  • lipid peroxidation (LPO);
  • oxidative/nitrative stress

Summary

Chronic infection and persistent inflammation are now recognized as important risk factors in many human cancers. Emerging evidence suggests that cancer-related inflammatory processes cause tissue damage and genetic instability involved in the initiation, promotion, and progression of carcinogenesis. Reactive oxygen (ROS) and nitrogen (RNS) species and lipid peroxidation (LPO)–mediated tissue damage play a major role in inflammation-related malignancies. This chapter provides information on methods for quantifying some representative lipid peroxidation (LPO)-derived DNA adducts in human biomonitoring studies. It summarizes results from biomarker applications that have provided insights intomechanisms of cancer causation and possibilities of preventive measures in human at risk subjects. Data compiled in this chapter provide evidence that persistent oxidative/nitrative stress and excess LPO are induced by chronic inflammatory processes and infections, causing massive DNA damage from endogenous sources.