Inhibition of Tumor Promoter-mediated Processes in Mouse Skin and Bovine Lens by Caffeic Acid Phenethyl Ester

Krystyna Frenkel, Huachen Wei, Ramesh Bhimani, Jingjing Ye, Jingjing Ye, Jose A. Zadunaisky, Mou Tan Huang, Thomas Ferraro, Allan H. Conney, Dezider Grunberger

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Caffeic acid phenethyl ester (CAPE) was isolated from propolis (a product of honeybee hives) that has been used in folk medicine as a potent antiinflammatory agent CAPE is cytotoxic to tumor and virally transformed but not to normal cells. Our main goal was to establish whether CAPE inhibits the tumor promoter (12-0-tetradecanoylphorbol-13-acetate)-induced processes associated with carcinogenesis. Topical treatment of SENCAR mice with very low doses (0.1-6.5 nmol/topical treatment) of CAPE strongly inhibits the following 12-0-tetradecanoylphorbol-13-acetate-mediated oxidative processes that are considered essential for tumor promotion: (a) polymorphonuclear leukocyte infiltration into mouse skin and ears, as quantified by myeloperoxidase activity; (b) hydrogen peroxide (H202) production; and (c) formation of oxidized bases in epidermal DNA, as measured by 5-hydroxymethyluracil and 8-hydroxylguanine. A 0.5-nmol dose of CAPE suppresses the oxidative burst of human polymorphonuclear leukocytes by 50%. At higher doses (1-10 umol), CAPE inhibits edema and ornithine decarboxylase induction in CD-I and SENCAR mice. Interestingly, we discovered that 12-0-tetradecanoylphorbol-13-acetate-induced H202 production in bovine lenses also is inhibited by CAPE. Cumulatively, these findings point to CAPE as being a potent chemopreventive agent, which may be useful in combatting diseases with strong inflammatory and/or oxidative stress components, Le., various types of cancer and possibly cataract development.

Original languageEnglish
Pages (from-to)1255-1261
Number of pages7
JournalCancer Research
Issue number6
StatePublished - Mar 1993
Externally publishedYes


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