Oxidants in receptor tyrosine kinase signal transduction pathways

Antioxid Redox Signal. 2003 Dec;5(6):781-8. doi: 10.1089/152308603770380089.

Abstract

The accumulation of oxygen in the atmosphere created an evolutionary stress for organisms to survive because oxygen, while the by-product of photosynthesis and an important substrate in oxidative metabolism, can also be partially reduced to form toxic products. These forms of oxygen, reduced by one electron or two electrons, yield superoxide anion (O(2).-) and hydrogen peroxide (H(2)O(2)), respectively. Recent studies suggest that reactive oxygen species (ROS) such as O(2).- and H(2)O(2) function as mitogenic mediators of activated growth-factor receptor signaling. Reported data imply that growth factor-stimulated ROS generation can mediate intracellular signaling pathways by activating protein tyrosine kinases, inhibiting protein tyrosine phosphatase, and regulating redox-sensitive gene expression. This review examines the mechanisms of growth factor-induced generation of ROS and their roles in specific receptor tyrosine kinase signaling pathways.

Publication types

  • Review

MeSH terms

  • Animals
  • Epidermal Growth Factor / metabolism
  • Fibroblast Growth Factors / metabolism
  • Gene Expression Regulation
  • Growth Substances
  • Humans
  • Hydrogen Peroxide
  • Models, Biological
  • Oxidants / physiology*
  • Oxidation-Reduction
  • Oxidative Stress
  • Oxygen / metabolism
  • Platelet-Derived Growth Factor / metabolism
  • Reactive Oxygen Species
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Signal Transduction*
  • Superoxides
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Growth Substances
  • Oxidants
  • Platelet-Derived Growth Factor
  • Reactive Oxygen Species
  • Vascular Endothelial Growth Factor A
  • Superoxides
  • Fibroblast Growth Factors
  • Epidermal Growth Factor
  • Hydrogen Peroxide
  • Receptor Protein-Tyrosine Kinases
  • Oxygen