Abstract
We contrasted possible protection against apoptosis afforded by either BCL-2 expression or anti-oxidant inhibitors in the same tumor target challenged by two distinct triggers of apoptosis. Exposure of L929 fibroblasts to tumor necrosis factor (TNF) or etoposide (VP-16) induced apoptotic death with similar kinetics. Enforced expression of BCL-2 significantly protected against apoptosis induced by VP-16 but had no effect against TNF-induced apoptosis. In contrast, the anti-oxidants desferrioxamine, butylated hydroxyanisol and N-acetyl cysteine all inhibited TNF-induced apoptosis in a concentration-dependent fashion. Although exposure to VP-16 resulted in a significant generation of intracellular oxyradicals, the above three anti-oxidant inhibitors had no effect on VP-16-induced apoptotic death. Interestingly, enforced expression of BCL-2 also inhibited the ability of VP-16 to generate oxy-radicals and to depress intracellular glutathione levels. These results indicate that BCL-2 can exert anti-oxidant effects but argue against the hypothesis that these effects are critical to its protection against apoptosis.
Similar content being viewed by others
Article PDF
Author information
Authors and Affiliations
Additional information
Edited by C.J.Thiele
Rights and permissions
About this article
Cite this article
Gardner, A., Xu, FH., Fady, C. et al. Evidence against the hypothesis that BCL-2 inhibits apoptosis through an anti-oxidant effect. Cell Death Differ 4, 487–496 (1997). https://doi.org/10.1038/sj.cdd.4400264
Received:
Revised:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/sj.cdd.4400264
Keywords
This article is cited by
-
Oxidative Stress Parameters of L929 Cells Cultured on Plasma-Modified PDLLA Scaffolds
Applied Biochemistry and Biotechnology (2011)