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*
Department of Internal Medicine I, Eberhard-Karls University, Tübingen, Germany;
Division of Cellular Immunology, Tumor Immunology Program, German Cancer Research Center, Heidelberg, Germany; and
Tularik Inc., San Francisco, CA 94080
We have shown that an estradiol-dependent activation of human T
cell leukemia virus-I Tax leads to the inhibition of cell proliferation
and to the induction of apoptosis. The present study demonstrates that
a hormone-dependent activation of Tax promotes an enhanced prooxidant
state in stably transfected Jurkat cells as measured by changes in the
intracellular levels of glutathione and H2O2;
these changes are followed by apoptotic cell death. Additional
stimulation of the CD3/TCR pathway enhances the oxidative and apoptotic
effects. Both Tax-mediated apoptosis and oxidative stress can be
potently suppressed by antioxidants, as is seen with the administration
of recombinant thioredoxin (adult T cell leukemia-derived factor) or
pyrrolidine dithiocarbamate. Hormone-induced Tax activation induces a
long-lasting activation of NF-
B, which is a major target of reactive
oxygen intermediates. The long-term exposure of Jurkat cells to hormone
eventually results in a selection of cell clones that have lost Tax
activity. A subsequent transfection of these apparently
"nonresponsive" clones allows the recovery of Tax responses in
these cells. Our observations indicate that changes in the
intracellular redox status may be a determining factor in
Tax-mediated DNA damage, apoptosis, and selection against the long-term
expression of Tax function.
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