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Bcl-2 does not protect Burkitt's lymphoma cells from oxidant-induced cell
death
Y Lee and E Shacter
Laboratory of Immunology, Food and Drug Administration, Center for
Biologics Evaluation and Research, Bethesda, MD 20892-4555, USA.
Bcl-2 is an oncogene that confers deregulated growth potential to B
lymphocytes through its ability to inhibit apoptotic cell death. A specific
molecular activity for the Bcl-2 protein has not been identified, but
several lines of evidence have supported a role in protection of cells from
oxidative stress. We investigated whether there is a correlation between
expression of high levels of Bcl-2 and susceptibility of human Burkitt's
lymphoma cell lines to H2O2-induced killing. The amount of H2O2 required to
kill 50% of cells in 24 hours varied widely in the seven different lymphoma
cell lines that were tested, ranging from 35 to 500 micromol/L H2O2.
However, expression of high levels of endogenous Bcl-2 did not protect the
cells from H2O2- induced killing, even though it was effective in
protecting the cells from apoptosis induced by agents such as A23187. Thus,
Bcl-2 was functional in preventing apoptosis but did not act in an
antioxidant capacity. The results were confirmed using a Burkitt's lymphoma
cell line overexpressing transfected bcl-2. The results may be explained by
the observation that H2O2 was inefficient at inducing apoptosis in these
mature B-cell lines. Nonapoptotic death induced by H2O2 was not prevented
by Bcl-2.
Volume 89,
Issue 12,
pp. 4480-4492,
06/15/1997
Copyright © 1997 by The American Society of Hematology
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