Antiinflammatory drug effects on ultraviolet light-induced epidermal ornithine decarboxylase and DNA synthesis.
Ornithine decarboxylase which forms putrescine by the decarboxyalation of ornithine, is the first and probably the rate-limiting enzyme in the biosynthesis of the other polyamines, spermidine and spermine. Epidermal ornithine decarboxylase activity is greatly elevated in response to tumor promoting agents and ultraviolet light. The purpose of this paper is to report modification of ultraviolet-induced epidermal ornithine decarboxylase activity by antiinflammatory agents. Topical triamcinolone acetonide and indomethacin were found to significantly inhibit the UV-B induction of epidermal ornithine decarboxylase in hairless mice when applied following ultraviolet light irradiation. The corticosteroid also showed inhibition of ultraviolet light increased epidermal DNA synthesis. Indomethacin failed to show any inhibition of DNA synthesis. It is suggested that these assays may be used to study drugs that may modulate some ultraviolet light effects on the epidermis.
D000818:Animals; D002262:Carboxy-Lyases / Q000096:biosynthesis*; D004247:DNA / Q000096:biosynthesis; D004790:Enzyme Induction / Q000187:drug effects; D004817:Epidermis / Q000187:drug effects* / Q000528:radiation effects; D007213:Indomethacin / Q000494:pharmacology*; D051379:Mice; D008819:Mice, Nude; D009955:Ornithine Decarboxylase / Q000096:biosynthesis*; D014222:Triamcinolone Acetonide / Q000494:pharmacology*; D014466:Ultraviolet Rays
D004247:DNA; D002262:Carboxy-Lyases; D009955:Ornithine Decarboxylase; D014222:Triamcinolone Acetonide; D007213:Indomethacin