Inhibition of receptor-mediated apoptosis upon Bcl-2 overexpression is not associated with increased antioxidant status

Biochem Biophys Res Commun. 2008 Oct 10;375(1):145-50. doi: 10.1016/j.bbrc.2008.07.133. Epub 2008 Aug 5.

Abstract

Bcl-2 is reported to augment the antioxidant capacity of cells and this is hypothesized to contribute to the anti-apoptotic activity of this oncoprotein. We generated a number of stable Jurkat cell lines expressing varying levels of Bcl-2, and showed a strong correlation between Bcl-2 levels and resistance to Fas-mediated apoptosis. While individual differences could be detected, there was no overall correlation between Bcl-2 and the expression and activity of superoxide dismutases, catalase, glutathione peroxidases, thioredoxin, thioredoxin reductases, and peroxiredoxins. Cells transfected with Bcl-2 averaged 70% more glutathione than parental cells, but there was no correlation between glutathione and resistance to apoptosis. This challenges the hypothesis that the anti-apoptotic properties of Bcl-2 are linked to a global increase in antioxidant status.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antioxidants / metabolism*
  • Apoptosis*
  • Glutathione / metabolism
  • Humans
  • Hydrogen Peroxide / toxicity
  • Jurkat Cells
  • Oxidoreductases / metabolism*
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis*
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Transfection
  • fas Receptor / metabolism

Substances

  • Antioxidants
  • Proto-Oncogene Proteins c-bcl-2
  • fas Receptor
  • Hydrogen Peroxide
  • Oxidoreductases
  • Glutathione