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J. Biol. Chem., Vol. 276, Issue 46, 43004-43009, November 16, 2001
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From the Oxidative injuries including apoptosis can be
induced by reactive oxygen species (ROS) and reactive nitrogen species
(RNS) in aerobic metabolism. We determined impacts of a
selenium-dependent glutathione peroxidase-1 (GPX1) on
apoptosis induced by diquat (DQ), a ROS (superoxide) generator, and
peroxynitrite (PN), a potent RNS. Hepatocytes were isolated from GPX1
knockout (GPX1
Opposite Roles of Selenium-dependent Glutathione
Peroxidase-1 in Superoxide Generator Diquat- and Peroxynitrite-induced
Apoptosis and Signaling*
,
Department of Animal Science, Cornell
University, Ithaca, New York 14853 and the § Institute of
Physiological Chemistry I, Heinrich Heine University, Postfach 101007, 40001 Dusseldorf, Germany
/) or wild-type (WT) mice, and treated with 0.5 mM DQ or 0.1-0.8 mM PN for up to 12 h. Loss of cell viability, high levels of apoptotic cells, and severe
DNA fragmentation were produced by DQ in only GPX1/ cells and by PN
in only WT cells. These two groups of cells shared similar cytochrome
c release, caspase-3 activation, and
p21WAF1/CIP1 cleavage. Higher levels of protein
nitration were induced by PN in WT than GPX1/ cells. Much less
and/or slower cellular GSH depletion was caused by DQ or PN in
GPX1/ than in WT cells, and corresponding GSSG accumulation
occurred only in the latter. In conclusion, it is most striking that,
although GPX1 protects against apoptosis induced by
superoxide-generator DQ, the enzyme actually promotes apoptosis induced
by PN in murine hepatocytes. Indeed, GSH is a physiological
substrate for GPX1 in coping with ROS in these cells.
*
This work was supported in part by a National Institutes of
Health Grant DK53018 (to X. G. L.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.:
607-254-4703; Fax: 607-255-9829; E-mail:
xl20@cornell.edu.
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