Inhibitory Effect of B-Glucuronidase Inhibitor on Colon Tumor Induction by Azoxymethane in Rats

抄録

To explore the significance of microflora l β-glucuronidase in colonic carcinogenesis, the effect of β-glucuronidase inhibitor on colon carcinogenesis was evaluated. Starting at 5 weeks of age, male Donryu strain rats were fed either a semisynthetic diet or the same diet containing 0.1% ie-glucuronidase inhibitor as N-cyclohexy1-5-o-acetyl-2,4-o- (p-methoxybenzylidene) -Dglucarol-amide-6,3-lactone (C-GAL). All animals were given subcutaneous injections of 7.4mg azoxymethane (AOM) /Kg body weight once a week for 11 weeks and followed for an additional 20 weeks. Most animals receiving the colonic carcinogen developed tumors in the colon, and a few also developed tumors in the small intestine. However, the number of tumors in the large intestine of rats given C-GAL at the same time as AOM was significantly lower than in the control, especially in the proximal half of the colon, but those given C-GAL after AOM treatment had almost the same number of colon tumors as the controls. It is concluded that since bacterial -glucuronidase activity in the feces of rats given O.1% C-GAL was significantly inhibited, intestinal microfloral β-glucuronidase plays an important role in colonic carcinogenesis caused by AOM.