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Science 20 April 1979:
Vol. 204. no. 4390, pp. 332 - 335
DOI: 10.1126/science.432648
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Articles

Science, Vol 204, Issue 4390, 332-335
Copyright © 1979 by American Association for the Advancement of Science

articles

Iron deficiency prevents liver toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin

GD Sweeny, KG Jones, FM Cole, D Basford, and F Krestynski

The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes hepatocellular damage and porphyria in C57B1/6J mice, among a wide range of toxic effects. We compared the effect of TCDD toxicity in iron-deficient mice with that in mice receiving a normal diet. Porphyria did not develop in the iron-deficient animals, and these animals were also protected from hepatocellular damage and certain other toxic effects of TCDD.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
A porphomethene inhibitor of uroporphyrinogen decarboxylase causes porphyria cutanea tarda.
J. D. Phillips, H. A. Bergonia, C. A. Reilly, M. R. Franklin, and J. P. Kushner (2007)
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Non-Ahr Gene Susceptibility Loci for Porphyria and Liver Injury Induced by the Interaction of `Dioxin' with Iron Overload in Mice.
S. W. Robinson, B. Clothier, R. A. Akhtar, A. L. Yang, I. Latour, C. Van Ijperen, M. F. W. Festing, and A. G. Smith (2002)
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Interaction between Iron Metabolism and 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Mice with Variants of the Ahr Gene: A Hepatic Oxidative Mechanism.
A. G. Smith, B. Clothier, S. Robinson, M. J. Scullion, P. Carthew, R. Edwards, J. Luo, C. K. Lim, and M. Toledano (1998)
Mol. Pharmacol. 53, 52-61
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Iron-mediated Mechanisms of Liver Injury by Polyhalogenated Aromatic Chemicals.
A.G. Smith (1989)
Human and Experimental Toxicology 8, 149-150
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