EFFECTS OF FLAVONOIDS AND ANTIOXIDANTS ON 12-O-TETRADECANOYLPHORBOL-13-ACETATE-CAUSED EPIDERMAL ORNITHINE DECARBOXYLASE INDUCTION AND TUMOR PROMOTION IN RELATION TO LIPOXYGENASE INHIBITION BY THESE COMPOUNDS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 75  (3) , 214-222
Abstract
The effects of flavonoids, antioxidants and related compounds on 12-O-tetradecanoylphorbol-13-acetate (TPA)-caused epidermal ornithine decarboxylase (ODC) induction, DNA synthesis and skin tumor promotion, and on epidermal lipoxygenase activity, were investigated using CD-1 mice. Morin, fisetin, kaempferol and n-propyl gallate potently inhibited epidermal lipoxygenase activity, and esculetin, butylated hydroxyanisole (BHA), .alpha.-naphthol and 2,3-dihydroxynaphthalene (2,3-DHNA) moderately inhibited it. .alpha.-Tocopherol, (+)-catechin, (-)epicatechin and butylated hydroxytoluene (BHT) were inactive. Similarly, morin, fisetin, kaempferol and n-propyl gallate markedly inhibited TPA-caused ODC induction. Esculetin, BHA, .alpha.-naphthol, 2,3-DHNA and .alpha.-tocopherol inhibited it less potently, but significantly. (+)Catechin, (-)epicatechin and BHT failed to inhibit or only slightly inhibited TPA-caused ODC induction. TPA-caused DNA synthesis was not inhibited by morin, esculetin, (+)-catechin or .alpha.-tocopherol. The TPA-induced skin tumor promotion was markedly inhibited by morin and slightly suppressed by esculetin and .alpha.-tocopherol, but (+)-catechin was inactive. Thus, the inhibitory effects of flavonoids and antioxidants on the TPA-caused ODC induction and tumor promotion were roughly parallel with their activities of lipoxygenase inhibition. A lipoxygenase product(s) is probably involved in the mechanism of TPA-caused ODC induction and tumor promotion.

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