Prevention of Hypoxia-Induced Cell Death by Bcl-2 and Bcl-xL

Nature. 1995 Apr 27;374(6525):811-3. doi: 10.1038/374811a0.

Abstract

The proto-oncogene bcl-2, isolated from the t(14;18) chromosomal breakpoint in follicular B-lymphoma, and a bcl-2-related gene bcl-x (ref. 4) prevent apoptotic cell death induced by various treatments. Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS), expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia), which drastically decreases the net formation of oxygen free radicals and does not increase oxidized lipid, protein or DNA. Furthermore, neither ROS scavenger nor inhibitor of ROS scavenger affects cell death, regardless of the expression of Bcl-2 or Bcl-xL. Thus our data suggest that Bcl-2 and Bcl-xL exert an anti-cell death function by a mechanism other than regulation of ROS activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Death*
  • Cell Hypoxia
  • Cell Line
  • Chickens
  • Free Radical Scavengers
  • Humans
  • Oxygen / metabolism
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-bcl-2
  • Rats
  • Reactive Oxygen Species / metabolism*
  • Tumor Cells, Cultured
  • bcl-X Protein

Substances

  • BCL2L1 protein, human
  • Bcl2l1 protein, rat
  • Free Radical Scavengers
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Reactive Oxygen Species
  • bcl-X Protein
  • Oxygen