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Inhibition by 1,-25-Dihydroxyvitamin D₃ of Induction of Epidermal Ornithine Decarboxylase Caused by 12-O-Tetradecanoylphorbol-13-acetate and Teleocidin B¹

Department of Cancer Cell Research, Institute of Medical Science, University of Tokyo, Shirokanedai, Minato-ku, Tokyo 108 [K. C., H. H., T. K.], and Department of Biochemistry, School of Dentistry, Showa University, Hatanodai, Shinagawa-ku, Tokyo 142 [T. S.], Japan

Topical application of 1,25-dihydroxyvitamin D₃ [1,25-(OH)₂D₃], an active form of vitamin D₃, markedly inhibited induction of ornithine decarboxylase caused by 12-O-tetradecanoylphorbol-13-acetate (TPA) and teleocidin B in mouse skin. The degree of inhibition was dependent on the dose and time of application of 1,25(OH)₂D₃. Application of 1 µg 1,25(OH)₂D₃ within 30 min before or after treatment with 10 µg TPA caused about 72% inhibition of ODC induction at 4 hr. Similar degrees of inhibition were obtained with dose ratios of 1,25(OH)₂D₃ to TPA of 1:3, 1:10, and 1:30. The dose required for 50% inhibition was 0.063 µg, or 0.15 nmol, which is about one-half that of retinoic acid, a known inhibitor of induction of ODC activity by TPA. 1,25(OH)₂D₃ had a specific inhibitory effect, in which 100 times higher doses or more of other derivatives of vitamin D₃, such as 1-hydroxyvitamin D₃, 25-hydroxyvitamin D₃, 24R,25-dihydroxyvitamin D₃, and vitamin D₃, were required to inhibit ODC induction by TPA. 1,25(OH)₂D₃ did not inhibit epidermal hyperplasia induced by TPA.

¹ Supported in part by a grant for Cancer Research from the Ministry of Education, Science and Culture of Japan.

² To whom requests for reprints should be addressed.

Received 9/ 7/83. Accepted 12/28/83.

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