Reactive oxygen species and antioxidant mechanisms in human tissues and their relation to malignancies

APMIS. 2007 Feb;115(2):81-103. doi: 10.1111/j.1600-0463.2007.apm_514.x.


Reactive oxygen species (ROS) are formed in mammalian cells as a consequence of aerobic respiration. Despite multiple conserved redox modulating systems, a given proportion of ROS continuously escape from the mitochondrial respiratory chain, being sufficiently potent to damage cells in various ways, including numerous carcinogenic DNA mutations. Oxidative stress resulting from an imbalanced ratio between ROS production and detoxification may also disturb physiological signal transduction, lead to chain reactions in lipid layers, and damage DNA repair enzymes. The significance of ROS and antioxidant systems in carcinogenesis is still complicated and in many ways contradictory. Enhanced antioxidant mechanisms in tumor cells in vivo have been implicated in chemoresistance and lead to poor prognosis, whereas most in vitro studies have reported tumor-suppressing properties of antioxidant enzymes. The present review aims to clarify the significance of oxidative stress and the role of cell redox state modulating systems in human malignancies in light of the current literature.

Publication types

  • Review

MeSH terms

  • Antioxidants / metabolism*
  • Cell Transformation, Neoplastic
  • DNA Repair
  • Glutathione / metabolism
  • Glutathione Disulfide / metabolism
  • Humans
  • Lipid Peroxidation
  • Models, Biological
  • Mutation
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Neoplasms / physiopathology*
  • Nitric Oxide / physiology
  • Oxidation-Reduction
  • Reactive Oxygen Species / metabolism*
  • Transcription Factors / metabolism


  • Antioxidants
  • Reactive Oxygen Species
  • Transcription Factors
  • Nitric Oxide
  • Glutathione
  • Glutathione Disulfide