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Molecular Pharmacology, Vol 8, 374-379, Copyright © 1972 by the American Society for Pharmacology and Experimental Therapeutics

Aryl Hydrocarbon Hydroxylase, Epoxide Hydrase, and 7,12-Dimethylbenz[a]anthracene-Produced Skin Tumorigenesis in the Mouse

D. W. NEBERT 1, W. F. BENEDICT 1, J. E. GIELEN 1, F. OESCH 2, and J. W. DALY 2

1 Section on Developmental Pharmacology, Laboratory of Biomedical Sciences, National Institute of Child Health and Human Development
2 Section on Pharmacodynamics, Laboratory of Chemistry, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Besthesda, Maryland 20014

Mouse skin tumorigenesis initiated by 7,12-dimethylbenz[a]anthracene and promoted by repeated applications of phorbol ester is unrelated to genetic diffrences in the extent of aryl hydrocarbon hydroxylase induction by polycyclic hydrocarbons in inbred or hybrid C57BL/6N and DBA/2N mice. Thus, if aryl metabolism of 7,12-dimethylbenz[a] anthracene is a necessary step in the initiation of chemical carcinogenesis, the constitutive level of the hydroxylase activity in the skin of these mice is sufficient, Levels of hepatic epoxide hydrase activity are the same among inbred and hybrid C57BL/6N and DBA/2N mice and, in contrast to the hydroxylase, are not inducible by 3-methylcholanthrene. Epoxide hydrase activity could not be detected in the skin of these mice.

Note:
ACKNOWLEDGMENT We thank Francine Goujon and Noreen Morris for valuable technical assistance.

Submitted on January 18, 1972




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D. M. Jerina and J. W. Daly
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Science, August 16, 1974; 185(4151): 573 - 582.
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