Retinol and retinyl ester epidermal pools are not identically sensitive to UVB irradiation and anti-oxidant protective effect.

Background: UV irradiation can deplete epidermal vitamin A, thus the hypothesis that UV-induced depletion of vitamin A in sun-exposed skin is involved in the pathogenesis of skin cancers and skin ageing.

Objectives: In this study we addressed two questions: (1) Are retinol (ROL) and retinyl esters (RE) - the two predominant forms of vitamin A - equally sensitive to the action of UVB, and (2) could the depletion be prevented by anti-oxidants?

Methods: Hairless mice were irradiated with a single UVB dose, corresponding to the maximum of ROL and RE absorption. Retinoid content, enzyme activities catalysing the esterification of ROL (ARAT and LRAT) and the hydrolysis of RE (REH), as well as retinol-binding protein (CRBP-1) expression were determined in the epidermis.

Results: A single UVB dose induced a rapid, dose-dependent decrease in both ROL and RE in the epidermis of hairless mice, with partial replenishment after 24 h. The dose-response curve for ROL showed a high sensitivity to UV at doses not exceeding 200 mJ/cm(2), followed by a plateau, whereas RE underwent a continuous dose-dependent decrease at UVB doses up to 1 J/cm(2). A topical anti-oxidant mixture containing 0.5% ascorbate, 0.25% tocopherol and 0.25% melatonin failed to protect epidermal RE from UVB-induced depletion, whereas it did prevent ROL depletion. ARAT and REH, as well as CRBP-1, were not affected by UVB in these conditions.

Conclusion: Vitamin A storage in the epidermis comprises two forms, ROL and RE, that do not show similar sensitivity to acute UVB exposure. ROL stores comprise a UVB-resistant (possibly by CRBP) portion and a UVB-sensitive portion that can be protected by anti-oxidants. RE stores do not show such a pattern.