Lack of inhibition of ultraviolet radiation-induced ornithine decarboxylase activity by retinoic acid.

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Abstract— Normally present at low levels, ornithine decarboxylase (ODC) activity is induced to higher levels in animal skin by such disparate agents as tumor promoter 12–0‐tetradecanoylphorbol‐13‐acetate (TPA), UV radiation, and hair plucking. Retinoids are known to inhibit induction by TPA. Repeated applications of retinoic acid (RA) in acetone have also been reported to inhibit UV‐induced ODC in hairless mice. As a preliminary study, it was of interest to know whether RA in a cream vehicle would have the same effect. Groups of Skh‐hairless‐1 albino mice were irradiated once with Westinghouse FS‐20 lamps (0.045 Joules/cm/). Immediately post‐irradiation, RA was applied to the dorsum in different concentrations (0.001%, 0.002%, 0.02%), vehicles (cream and acetone) and on various time schedules (1–5 times). Sacrifice was by cervical dislocation 24 h later. Epidermis was obtained by mild heat separation and two epidermal sheets were pooled for each extract. In all experiments, the 70‐fold increase in UV‐induced ODC activity was further increased by retinoic acid by a factor ∼ 1.6. Since ODC levels are usually elevated in proliferating systems, the results are in concordance with the fact that both UV radiation and RA induce epidermal hyperplasia.