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J. Biol. Chem., Vol. 275, Issue 50, 38957-38960, December 15, 2000
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From the Departments of Previous studies have demonstrated that
metallothionein functions as an antioxidant that protects against
oxidative DNA, protein, and lipid damage induced by superoxide anion,
hydrogen peroxide, hydroxyl radical, and nitric oxide. The present
study was undertaken to test the hypothesis that metallothionein also
protects from DNA and lipoprotein damage induced by peroxynitrite, an
important reactive nitrogen species that causes a diversity of
pathological processes. A cell-free system was used. DNA damage was
detected by the mobility of plasmid DNA in electrophoresis. Oxidation
of low density lipoprotein was measured by a thiobarbituric
acid-reactive substance, which was confirmed by lipid hydroperoxide
assay. Plasmid DNA damage and low density lipoprotein oxidation were
induced by 3-morpholinosydnomine, which produces peroxynitrite through the reaction between nitric oxide and superoxide anion or by
synthesized peroxynitrite directly. DNA damage by 3-morpholinosydnomine
was prevented by both metallothionein and superoxide dismutase, whereas the damage caused by peroxynitrite was prevented by metallothionein only. The oxidation of low density lipoprotein by 3-morpholinosydnomine and peroxynitrite was also significantly inhibited by metallothionein. This study thus demonstrates that metallothionein may react directly with peroxynitrite to prevent DNA and lipoprotein damage induced by
this pathological reactive nitrogen species.
ACCELERATED PUBLICATION
Metallothionein Inhibits Peroxynitrite-induced DNA and
Lipoprotein Damage*
,§, and¶
**
Medicine and
¶ Pharmacology & Toxicology, University of Louisville,
§ Veterans Affairs Medical Center, and Jewish
Hospital Heart and Lung Institute, Louisville, Kentucky 40292
*
This work was supported in part by National Institutes of
Health Grants CA68125 and HL59225, Established Investigator Award 9640091N from the American Heart Association National Center (to Y. J. K.), a research grant from the Department of Veterans Affairs (to J. B. K.), and research grants from the Jewish Hospital
Foundation, Louisville, KY (to Y. J. K. and J. B. K.).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.
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