Oxidative stress and cell cycle checkpoint function

Free Radic Biol Med. 2000 May 1;28(9):1387-404. doi: 10.1016/s0891-5849(00)00224-0.


Oxidative stress and the damage that results from it have been implicated in a wide number of disease processes including atherosclerosis, autoimmune disorders, neuronal degeneration, and cancer. Reactive oxygen species (ROS) are ubiquitous and occur naturally in all aerobic species, coming from both exogenous and endogenous sources. ROS are quite reactive and readily damage biological molecules, including DNA. While the damaging effects of ROS on DNA have been intensively studied, the effects of oxidative damage on cell cycle checkpoint function have not. Here will we review several biologically important ROS and their sources, the cell cycle, checkpoints, and current knowledge about the effects of ROS on initiating checkpoint responses.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Aerobiosis
  • Animals
  • Apoptosis / physiology
  • Cell Cycle / physiology*
  • Cell Cycle Proteins / physiology
  • Cells / radiation effects
  • Cyclins / physiology
  • DNA Damage
  • DNA Repair
  • DNA Replication
  • Electron Transport
  • Gene Expression Regulation / physiology
  • Humans
  • Hydrogen Peroxide / metabolism
  • Hydroxyl Radical / metabolism
  • Inflammation / metabolism
  • Models, Biological
  • Nitric Oxide / metabolism
  • Oxidation-Reduction
  • Oxidative Stress / physiology*
  • Reactive Oxygen Species*
  • Superoxides / metabolism


  • Cell Cycle Proteins
  • Cyclins
  • Reactive Oxygen Species
  • Superoxides
  • Nitric Oxide
  • Hydroxyl Radical
  • Hydrogen Peroxide