The Influence of Topical and Oral Retinoid Treatment on Photocarcinogenicity in Hairless Albino Mice

Abstract

The etiological role of sunlight in human skin cancer is well established (3). The action spectrum of carcinogenic light irradiation lies between 280 and 320 nm (UV-B) (9, 10). Higher wave lengths of up to 400 nm (UV-A) increase the above-mentioned carcinogenic effect (12) as do chemicals which are known to be either photoactive, cancer initiating or cancer promoting agents (4, 5, 6). Epstein (7) has demonstrated that topical tretinoin in high concentrations can accelerate the tumorigenic process of UV-B light. Forbes et al. (8) have shown that topically applied tretinoin, even at very low concentrations, enhanced the carcinogenic effect of simulated sunlight in hairless albino mice. In a first investigation the influence on sunlight carcinogenesis by topical treatment with motretinid, an aromatic retinoid, was studied in comparison with tretinoin. The aim of a similar experiment was to study the influence of oral treatment with etretinate, another aromatic retinoid, on photocarcinogenesis. This is of particular importance since the combined clinical application of etretinate and UV-B irradiation induces a high percentage of complete remissions in severe psoriasis (11).