INFLUENCE OF A DIETARY FIBER ON DEVELOPMENT OF DIMETHYLHYDRAZINE-INDUCED ABERRANT CRYPT FOCI AND COLON-TUMOR INCIDENCE IN WISTAR RATS

Citation
I. Thorup et al., INFLUENCE OF A DIETARY FIBER ON DEVELOPMENT OF DIMETHYLHYDRAZINE-INDUCED ABERRANT CRYPT FOCI AND COLON-TUMOR INCIDENCE IN WISTAR RATS, Nutrition and cancer, 21(2), 1994, pp. 177-182
Citations number
23
Categorie Soggetti
Nutrition & Dietetics",Oncology
Journal title
ISSN journal
01635581
Volume
21
Issue
2
Year of publication
1994
Pages
177 - 182
Database
ISI
SICI code
0163-5581(1994)21:2<177:IOADFO>2.0.ZU;2-M
Abstract
Formation of aberrant crypt foci (ACF) in archived colon tissue from a nimals in a previous study was examined. The animals were fed a semisy nthetic casein-based diet in which the carbohydrate pool was substitut ed with a dietary beet fiber (Fibeta) as the only source of fiber. Ora l doses of dimethylhydrazine dihydrochloride (DMH-2HCl, 20 mg/kg body wt) once a week for 10 weeks were used as initiator. The rats were fed different levels of the fiber in a preinitiation period, during initi ation, or in a postinitiation period. In general, the results showed a statistically significant inverse relation between duration of intake of high-fiber diet and number of animals with ACF, as well as the tot al number of ACF and number of small A CF (1-3 crypts) per affected an imal. The previously reported data showed no protective effect of the dietary fiber at any stage of the colorectal carcinogenic process. The lack of correlation between the outcome of ACF and tumors could be re lated to the observation that statistically significant differences be tween groups were seen only in the total number of ACF and number of s mall ACF. The hypothesis that ACF are preneoplastic lesions needs to b e supported by further experimental data. The present state of knowled ge could indicate that ACF represent true preneoplastic lesions progre ssing into colon tumors or that ACF and colon tumors represent two par allel independent events as a consequence of the cancer initiation (i. e., the ACF not being preneoplastic lesions per se).