Dietary Protein, Aryl Hydrocarbon Hydroxylase and Chemical Carcinogenesis in Rats

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Abstract
The relationships of dietary protein to changes in hepatic aryl hydrocarbon hydroxylase activity and 7,12 dimethylbenz(a)anthracene (DMBA) carcinogenesis were studied in female Sprague-Dawley rats. Isoenergetic casein based purified diets containing 7.5, 15, or 45% protein equivalent were fed for 4 weeks, at which time rats were killed for enzyme assays. Aryl hydrocarbon hydroxylase, an enzyme system which metabolizes polycyclic aromatic hydrocarbons such as DMBA, showed increased activity as dietary protein increased. The role of protein in the initiation phase of DMBA carcinogenesis was examined in rats fed 7.5, 15, and 45% protein for 4 weeks whereupon each rat received 2.0 mg of DMBA/100 g body weight in a single oral dose. Thereafter all rats were ad libitum fed the 15% protein diet for 25 additional weeks. The percentage of rats with tumors and the number of tumors per rat were lower as protein intake was increased prior to DMBA administration. The influence of protein on the promotion phase was examined by feeding the 15% protein diet to all rats prior to DMBA administration whereupon the rats were assigned to the three experimental diets for an additional 25 weeks. With this regimen, dietary protein concentration had no effect on tumor incidence or latency during the promotion phase. Our evidence supports the hypothesis that increasing dietary protein may decrease the concentration of potential carcinogenic DMBA metabolites reaching the mammary gland by stimulating the hepatic metabolism of DMBA.