Davidson K A, Ewald L, Herrmann A, Ogle S P, Slaga T J
Carcinogenesis. 1984 May;5(5):609-14. doi: 10.1093/carcin/5.5.609.
The antiandrogen, cyproterone acetate (CPA), applied simultaneously with 12-O-tetradecanoylphorbol-13-acetate (TPA) to the dorsal skin of male and female SENCAR mice initiated with 7,12-dimethylbenz[a]anthracene inhibited the production of papillomas of the skin. Although 125 and 250 micrograms of CPA had no effect on the incidence of papillomas per mouse, 500 micrograms of CPA inhibited papilloma production by 95% and 91% in female mice after 20 and 37 weeks of promotion, respectively. Testosterone propionate only partially blocked the inhibitory effect of CPA. In male mice 500 micrograms and 1 mg of CPA inhibited papilloma production by 77% and 88%, respectively. In the two-stage promotion protocol 500 micrograms of CPA was ineffective as an inhibitor when it was applied with TPA during the 1st stage but inhibited papilloma production by 71% when it was applied with mezerein during the 2nd stage. CPA was also observed to inhibit TPA-stimulated epidermal DNA synthesis and inflammation but had no effect on TPA-induced epidermal ornithine decarboxylase activity.
抗雄激素醋酸环丙孕酮（CPA）与12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）同时应用于经7,12 - 二甲基苯并[a]蒽引发的雄性和雌性SENCAR小鼠的背部皮肤，可抑制皮肤乳头瘤的产生。虽然125微克和250微克的CPA对每只小鼠乳头瘤的发生率没有影响，但在促进作用20周和37周后，500微克的CPA分别使雌性小鼠的乳头瘤产生抑制了95%和91%。丙酸睾酮仅部分阻断了CPA的抑制作用。在雄性小鼠中，500微克和1毫克的CPA分别使乳头瘤产生抑制了77%和88%。在两阶段促进方案中，500微克的CPA在第一阶段与TPA一起应用时作为抑制剂无效，但在第二阶段与地锦草素一起应用时可使乳头瘤产生抑制71%。还观察到CPA可抑制TPA刺激的表皮DNA合成和炎症，但对TPA诱导的表皮鸟氨酸脱羧酶活性没有影响。
