In this study of the role of microfloral
beta-glucuronidase in colonic
carcinogenesis, the effect of
beta-glucuronidase inhibitor was evaluated. Starting at 5 weeks of age, male Donryu rats were fed either a semisynthetic diet or the same diet containing 0.1%
beta-glucuronidase inhibitor as N-cyclohexyl-5-O-acetyl-2,4-O-p-methoxybenzylidene) -D-glucaro-1-
amide-6,3-
lactone (
C-GAL). All animals were given s.c.
injections of 7.4 mg
azoxymethane (AOM) per 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 the rats given
C-GAL at the same time as AOM was significantly lower than in the control rats, 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 did the controls. It is concluded that, since bacterial
beta-glucuronidase activity in the feces of rats given 0.1%
C-GAL was significantly inhibited, intestinal microfloral
beta-glucuronidase may play an important role in colonic
carcinogenesis caused by AOM.