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Division of Nutritional Science, Department of Internal Medicine, College of Medicine, University of Illinois, Urbana, IL 61801
The mucosa of the intestine responds to polycyclic aromatic hydrocarbons (PAH) with the rapid induction of benzo(a)pyrene hydroxylase (BPH). Studies were conducted to determine if dietary fiber would reduce exposure of the intestine to dietary benzo(a)pyrene (BP) as indicated by intestinal BPH activity. In all studies, female Sprague-Dawley rats were fed a fiber-free purified diet for 7 d, whereupon they were switched to experimental diets for 48 h. After 48 h their small intestinal mucosa was assayed for BPH activity. Diets for the initial study contained 0, 100, 400, 800, or 1200 mg BP/kg diet, each with and without 10% soft white wheat bran. Enzyme induction with 100 and 400 mg BP/kg diet was partially inhibited by bran, but with higher concentrations of BP there was no protective effect. The inhibition in BP-induced intestinal BPH activity was observed with 10% wheat bran but not with 3.3 or 6.6%. Subsequent studies showed no significant inhibition in BPH induction with cellulose or lignin, whereas all forms of wheat bran (hard red, soft white, or finely ground soft white) caused significant inhibition. In the final study, a diet containing charcoal-broiled beef, a known source of PAH, was compared with diets containing raw beef or soybean protein, each with and without 10% soft white wheat bran. BPH activity remained low with raw beef and soybean protein whether or not fiber was added. However, intestinal BPH activity was raised ninefold by charcoal-broiled beef. The addition of bran reduced BPH activity to 65% of that observed with the fiber-free, charcoal-broiled beef diet. These data are compatible with the conclusion that wheat bran reduces exposure of the intestine to dietary PAH.
KEY WORDS: dietary fiber wheat bran cellulose lignin benzo(a)pyrene hydroxylase benzo(a)pyrene beef soy protein
1 Supported by the National Cancer Institute of the National Institutes of Health, Grant Nos. CA19692, CA23326.
2 Present address: Dana Farber Cancer Institute and Harvard Medical School, 44 Binney St., Boston, MA 02115.
3 To whom reprint requests should be addressed.
Manuscript received 8 June 1988. Revision accepted 18 November 1988.