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Originally published In Press as doi:10.1074/jbc.M005366200 on August 1, 2000

J. Biol. Chem., Vol. 275, Issue 42, 32516-32522, October 20, 2000
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Vanadate Induces p53 Transactivation through Hydrogen Peroxide and Causes Apoptosis*

Chuanshu Huang, Zhuo Zhang, Min Ding, Jingxia Li, Jianping Ye, Stephen S. Leonard, Han-Ming Shen, Leon Butterworth, Yongju Lu, Max CostaDagger , Yongyut Rojanasakul§, Vincent Castranova, Val Vallyathan, and Xianglin Shi

From the Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, the Dagger  Nelson Institute of Environmental Medicine and Kaplan Comprehensive Cancer Center, New York University School of Medicine, New York, New York 10016, and the § Department of Basic Pharmaceutical Science, West Virginia University, Morgantown, West Virginia 26506

Vanadium is a metal widely distributed in the environment. Although vanadate-containing compounds exert potent toxic effects on a wide variety of biological systems, the mechanisms controlling vanadate-induced adverse effects remain to be elucidated. The present study investigated the vanadate-induced p53 activation and involvement of reactive oxygen species (ROS) in p53 activation as well as the role of p53 in apoptosis induction by vanadate. Exposure of mouse epidermal JB6 cells to vanadate led to transactivation of p53 activity in a time- and dose-dependent manner. It also caused mitochondrial damage, apoptosis, and generated ROS. Scavenging of vanadate-induced H2O2 by N-acetyl-L-cysteine (a general antioxidant) or catalase (a specific H2O2 inhibitor), or the chelation of vanadate by deferoxamine, resulted in inhibition of p53 activation and cell mitochondrial damage. In contract, an increase in H2O2 generation in response to superoxide dismutase or NADPH enhanced these effects caused by vanadate. Furthermore, vanadate-induced apoptosis occurred in cells expressing wild-type p53 (p53+/+) but was very weak in p53-deficient (p53-/-) cells. These results demonstrate that vanadate induces p53 activation mainly through H2O2 generation, and this activation is required for vanadate-induced apoptosis.

* 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: Health Effects Laboratory Division, NIOSH, Morgantown, WV 26505. Tel.: 304-285-6158; Fax: 304-285-5938; E-mail: xas0@cdc.gov.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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