Abstract
Several groups of hairless mice were given UV radiation with and without pretreatment with 7,12-dimethylbenz(a)anthracene (DMBA), 5% benzoyl peroxide in a gel (Panoxyl), and gel alone, in various combinations, with appropriate control groups included, in order to see whether benzoyl peroxide, which is known to enhance chemical skin carcinogenesis after a single, small dose of DMBA, also enhances UV carcinogenesis. The mice were observed for skin tumors, and all skin lesions were histologically investigated. The percentage of tumor-bearing animals with time is called the tumor rate, the total number of tumors occurring is called the tumor yield. Continual treatment with 5% benzoyl peroxide in gel twice a week, with or without a short pretreatment period of UV radiation resulted in only 2 skin carcinomas, which is remarkable, but not significant. Both Panoxyl and gel alone enhanced tumorigenicity significantly in animals pretreated with a single dose of 51.2 micrograms DMBA. There was no difference between the enhancement caused by Panoxyl and the gel as regards the tumor rate, but when measured as final tumor yield, Panoxyl was slightly more tumor-enhancing than gel alone. However, both Panoxyl and gel protected significantly against UV tumorigenesis (all tumors). There was no difference between the protective effect of the 2 types of treatment. Neither Panoxyl nor gel alone influenced significantly UV skin carcinogenesis (malignant tumors). It is concluded that under these experimental conditions both Panoxyl and gel alone tend to protect against the tumorigenicity and do not enhance the carcinogenicity of UV radiation in hairless mice, whereas both gel and Panoxyl enhance chemical carcinogenesis. The carcinogenic mechanisms may be different for UV and chemical carcinogenesis, respectively.
Published Version
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