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Inhibition by Retinoids of Anthralin-induced Mouse Epidermal Ornithine Decarboxylase Activity and Anthralin-promoted Skin Tumor Formation¹

Life Sciences Division, SRI International, Menlo Park, California 94025

The retinoids all-trans-retinoic acid, 13-cis-retinoic acid, 4-[2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1E-propen-1-yl]benzoic acid, 6-[1-(4-carboxyphenyl)-1E-propen-2-yl]-3,4-dihydro-4,4-dimethyl-2H-1-benzothiopyran, and 6-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-2-naphthalenecarboxylic acid inhibited the induction of ornithine decarboxylase in CD-1 mouse epidermis treated with the weak tumor promoter anthralin (444 nmol). Enzyme activity reached maximal levels 48 h after the application of the promoter. This activity was most effectively inhibited when retinoids were applied to the epidermis 24 h after the promoter.

These retinoids also inhibited the appearance of papillomas in mouse epidermis in the two-stage tumorigenesis model using 7,12-dimethyl-benz(a)anthracene (200 nmol) as the initiator and anthralin (444 nmol) as the promoter during the 32-week period of promotion. Comparison of the doses of retinoids required to inhibit anthralin-induced ornithine decarboxylase by 50% and those required to inhibit anthralin-induced tumor promotion by 50% demonstrated that these values correlated.

¹ Research supported by USPHS Grants CA30512 and CA32428, awarded by the Division of Cancer Etiology, National Cancer Institute, Department of Human Health Services.

² To whom requests for reprints should be addressed.

Received 3/ 3/87. Revised 8/24/87. Accepted 8/28/87.

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