Effect of Various Levels of Dietary Butylated Hydroxyanisole on Methylazoxymethanol Acetate-Induced Colon Carcinogenesis in CF1 Mice<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

Abstract

The effect of dietary butylated hydroxyanisole (BHA) on methylazoxymethanol (MAM) acetate-induced colon carcinogenesis was studied in female CF1 mice fed the NIH-07 open formula diet and the AIN-76 semipurified diet. BHA levels in the experimental diets were 0.6% in the AIN-76 diet and 0.03, 0.1, 0.3, and 0.6% in the NIH-07 diet. Starting at 5 weeks of age, groups of mice were fed diets with or without BHA. At 7 weeks of age, all animals except vehicle-treated controls were given ip injections of MAM acetate (15 mg/kg body wt), four times in 11 days (low dose) and eight times in 22 days (high dose). Animals were fed their experimental diets until 2 weeks after carcinogen treatment, when those receiving the BHA diets were fed their respective control diets without BHA until termination of the experiment. With a low dose of carcinogen, BHA in the NIH-07 diet inhibited lung tumor incidences in a dose-related manner; with a high dose of carcinogen the inhibition was apparent with 0.1-0.6% BHA. Lung tumor incidence was lower in the low carcinogen treated group fed the AIN-76 diet containing 0.6% BHA than in the animals fed the diet without BHA. Colon tumor incidence was lower in mice fed the NIH-07 diet containing 0.3 and 0.6% BHA and treated with a low dose of carcinogen than in the animals fed no BHA; colon tumor multiplicity (adenomas/animal and adenomas/tumor-bearing animal) was inhibited in mice fed the diets containing 0.03-0.6% BHA. In groups given a high dose of MAM acetate, the NIH-07 diet with 0.03-0.6% BHA and the AIN-76 diet with 0.6% BHA greatly inhibited colon tumor incidence and multiplicity.