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08:35

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Published on: October 5, 2012

Evidence against the hypothesis that BCL-2 inhibits apoptosis through an anti-oxidant effect

A Gardner1, F H Xu, C Fady

  • 1Department of Medicine, VA West Los Angeles Hospital-UCLA Medical Center, Los Angeles, California, USA.

Cell Death and Differentiation
|August 1, 1997
PubMed

Insights

BCL-2 protein protects against etoposide-induced apoptosis, while antioxidants block tumor necrosis factor (TNF)-induced apoptosis. BCL-2 shows antioxidant effects, but this is not key to its anti-apoptotic function.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Apoptosis, or programmed cell death, is a critical cellular process.
  • The BCL-2 protein family plays a key role in regulating apoptosis.
  • Oxidative stress, indicated by intracellular oxyradicals, is implicated in apoptosis.

Purpose of the Study:

  • To investigate the protective mechanisms of BCL-2 expression versus antioxidant inhibitors against apoptosis.
  • To determine if BCL-2's anti-apoptotic function is mediated by its antioxidant effects.

Main Methods:

  • L929 fibroblasts were exposed to two apoptosis inducers: tumor necrosis factor (TNF) and etoposide (VP-16).
  • Protection was assessed using enforced BCL-2 expression and various antioxidant inhibitors (desferrioxamine, butylated hydroxyanisole, N-acetyl cysteine).
  • Intracellular oxyradical generation and glutathione levels were measured.

Main Results:

  • BCL-2 expression protected against VP-16-induced apoptosis but not TNF-induced apoptosis.
  • Antioxidants inhibited TNF-induced apoptosis in a dose-dependent manner but did not affect VP-16-induced apoptosis.
  • VP-16 induced oxyradical generation, which was inhibited by BCL-2 expression; BCL-2 also prevented glutathione depletion.

Conclusions:

  • BCL-2 exhibits antioxidant properties, interfering with VP-16-induced oxidative stress.
  • Despite its antioxidant effects, these are not the primary mechanism for BCL-2's protection against VP-16-induced apoptosis.
  • Distinct pathways mediate apoptosis triggered by TNF and VP-16, with differential sensitivity to BCL-2 and antioxidants.

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