dihydroteleocidin-b and palytoxin

The activity of histidine decarboxylase (HDC) increased by a factor of 10 after a single application of 12-O-tetradecanoylphorbol-13-acetate (TPA). The HDC-inducing activity of other phorbol esters paralleled their tumor-promoting activity. Application of some indole alkaloids, which have been shown to be a new class tumor promoter, also induced the increase in HDC activity. The cell type responsible for this increase was examined. First, pieces of the skin were separated into epidermis and dermis after application of TPA. In contrast with ornithine decarboxylase, the HDC activity increased in the dermis. Second, genetically mast cell-deficient W/Wv and Sl/Sld mice were used. Although most histamine in the dermis is in the mast cells, the increase in HDC activity in W/Wv mice was comparable to that in congenic +/+ mice. However, no significant increase in HDC activity was detected in the skin of the Sl/Sld mice. Histological examination revealed that the magnitude of inflammatory cell infiltration was much less in the skin of Sl/Sld mice than in the skin of +/+ or W/Wv mice. The increase in HDC activity and the inflammatory cell response in the skin of W/Wv mice were abolished by prior X-ray irradiation, and were restored by subsequent bone marrow transplantation. Thus, inflammatory cells may be responsible for at least a part of the increase in HDC activity after application of tumor promoters.

Topics: Acrylamides; Animals; Carboxy-Lyases; Carcinogens; Cnidarian Venoms; Histamine; Histidine Decarboxylase; Leukocytes; Lyngbya Toxins; Mast Cells; Mice; Mice, Mutant Strains; Skin; Skin Neoplasms; Tetradecanoylphorbol Acetate