Diet and its relationship to cancer have received much attention in recent years. Although one dietary factor, cholesterol, has been indicted in the development of numerous types of cancer, including actinic, no direct or consistent data have been forthcoming to substantiate such a relationship. Thus, several levels of dietary cholesterol, as well as antioxidant additives, were tested for effect on ultraviolet light (UV) carcinogenesis. Six hundred hairless mice were divided into 12 groups of 50 animals each. The animals received a restricted, semipurified, isocaloric diet containing 0, 0.01, and 2% cholesterol with or without antioxidants (2%, w/w). A regimen of escalating UV irradiation was used until an accumulative dose of 145 J/sq cm had been delivered. Animals were evaluated weekly for actinic lesions and biweekly for body weights, hematocrits, and serum cholesterol levels. A cumulative distribution frequency, based upon the asymptotic theory of extreme values, was used to determine tumor occurrence with time of study. It was found that the tumor development time for 50% of the animals for each dietary cholesterol level used was significantly different, with a longer development period occurring with increasing cholesterol level. Although not as pronounced as previous studies utilizing commercial diets, dietary antioxidants significantly suppressed UV-induced tumor formation. These data indicate that dietary cholesterol does not enhance UV carcinogenesis but rather has a slight, but significant, moderating effect. This effect could result from direct participation of dietary cholesterol in the carcinogenic process or, alternatively, could occur as the result of sterol-altered epidermal parameters which effectively diminish the UV dose reaching respective target sites.

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Supported by USPHS Grant CA-20907 from the National Cancer Institute.

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