A study of experimental carcinogenesis on mouse dorsal skin using: ultraviolet, PUVA and retinoid.

Abstract

ABSTRACTThe present research was designed to examine the effects of ultraviolet (UV), PUVA, and retinoid on experimental carcinogenesis and to observe the behavior of sulphydryl groups during the process of carcinogenesis.Male, four week old, ddy‐strain mice had one of the following treatments applied to their dorsal skin: twice weekly applications of 3‐methylcholanthrene (MC), a carcinogenic initiator; a single application of MC followed by twice‐weekly applications of 12‐o‐tetradecanoylphorbol‐13‐acetate, a carcinogenic promoter; or treatment with or without a single application of MC followed by twice‐weekly treatment with UV, PUVA, retinoid, or retinoid plus UV. The oncogenic and carcinogenic development was studied macroscopically, histologically and histochemically.UV obviously promoted carcinogenesis, whereas retinoid on its own did not. During MC plus UV carcinogenesis, the action of retinoid differed depending on its type. There was no influence exerted by 0.01% all‐trans retinoid. On the other hand, 0.01% 13‐cis retinoid was able to moderately inhibit cancer development (p<0.01). PUVA produced papillomas accompanied by marked dysplasia by the 28th week; however, no carcinogenesis was observed during the observation period.As a result of the histochemical time‐course observations of the cancerization process through application of DACM staining, abnormal, strongly fluorescent granules abundant in the—SH group and the S—S bond were observed in the period before any evolution to cancer cells could be seen light‐microscopically. These characteristic granules are suspected to be products resulting from cancerous changes, and therefore it is suggested that DACM staining may be a suitable marker for carcinogenesis.