Toxicological Sciences 56, 255-261 (2000)
Copyright © 2000 by the Society of Toxicology
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Metals and Disorders of Cell Accumulation: Modulation of Apoptosis and Cell Proliferation
* Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, National Cancer Institute at National Institute of Environmental Health Sciences, 111 Alexander Drive, P.O. Box 12233, MD F0-09, Research Triangle Park, North Carolina;
College of Optometry and Department of Biology and Biochemistry, University of Houston, Houston, Texas;
Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky;
§ Department of Pharmacology, Molecular and Cellular Oncology Program, The George Washington University Medical Center, Washington, D.C.; and
¶ Institute of Chemical Toxicology, Wayne State University, Detroit, Michigan
Received March 7, 2000; accepted April 20, 2000
Key Words: arsenic; apoptosis; cell proliferation; chromium; lead; mercury.
Introduction
As a class of agents, toxic metals are a concern of the highest priority for human exposure. The metals have a vast array of remarkably adverse effects, including those of carcinogenicity, neurotoxicity, and immunotoxicity. Metals are also non-biodegradable and persist in the environment. Anthropogenic use has led to global dispersion of metals in the environment. Because of their wide distribution and extensive use in modern society, some human exposure to toxic metals is inevitable. Defining the mechanisms of metal toxicity has been problematic because of the intricate nature of the interactions of metals with living systems. Additionally, many metals, like zinc, copper, calcium, trivalent chromium and iron, are essential to life and complex mechanisms have evolved for their safe transport and usage, including transport and storage proteins. Essential metals are involved in a variety of critical functions including control of gene transcription, nerve conductance, oxygen carrying and delivery, and as
Mitochondria Coordinate the Upstream and Downstream Events in Lead-Induced Rod Photoreceptor-Selective Apoptosis (D. A. Fox, L. He, and A. T. Poblenz)
Arsenic-Induced Dysregulation of Cell Cycle in Human Fibroblasts (J. C. States)
Mechanisms and Modulation of Chromium-Induced Apoptosis (S. R. Patierno)
Mechanisms Contributing to Systemic Autoimmune Disease: Mercury-Induced Tyrosine Phosphorylation and Disruption of the CD95/Fas Apoptotic Death Pathway (M. J. McCabe, Jr. and A. J. Rosenspire)
Conclusions
NOTES
REFERENCES
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