Abstract
Induction of epidermal ornithine decarboxylase (ODC) by a topical application of 12-0-tetradecanoylphorbol-13-acetate (TPA) was inhibited by treatment of mouse skin with phenidone (30 μmol/mouse), nordihydroguaiaretic acid (NDGA, 30 μmol/mouse) or BW 755C (30 μmol/mouse). Inhibition of TPA-induced ODC by indomethacin (1.12 μmol/mouse) was counteracted by PGE2 (140 μmol/mouse). This counteracting effect of PGE2 was reversed by the treatment of mice with NDGA (30 μmol/mouse) or phenidone (30 μmol/mouse). ODC activity which was suppressed by NDGA or phenidone at a dose of 180 μmol/mouse was not further inhibited by indomethacin (1.12 μmol/mouse). The counteracting action of PGE (140 nmol/mouse) was not observed in mice treated with NDGA or phenidone at a dose of 180 μmol/mouse. The above findings strongly suggest that not only cyclooxygenase product (i.e., PGE2) but also lipoxygenase product(s) are involved in the mechanism of ODC induction. NDGA and a phospholipase A2 inhibitor, p-bromophenacyl bromide, markedly suppressed promoter effect of TPA on skin tumor formation by dimethylbenzanthracene. These results suggests the involvement of phospholipase A2 and lipoxygenase products in the mechanism of tumor promotion.
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