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Chemoprevention of Azoxymethane-induced Colon Carcinogenesis by Dietary Feeding of S-Methyl Methane Thiosulfonate in Male F344 Rats¹

First Department of Pathology, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu City 500 [T. K., T. T., M. O., Y. H., H. M.]; School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422 [Y. N.]; and Department of Biochemistry, Gifu Pharmaceutical University, 5-6-1, Mitahora Higashi, Gifu City 502 [K. S., A. H.], Japan

Modifying effects of dietary exposure of S-methyl methane thiosulfonate (MMTS) isolated from cauliflower Brassica oleracea L. var. botrytis on rat colon carcinogenesis induced by azoxymethane (AOM) and on the expression of cell proliferation biomarkers were investigated in two experiments. In experiment 1, male F344 rats were given three s.c. injections of AOM (15 mg/kg body weight) and fed 100 ppm MMTS for 5 weeks, starting 1 week before the first dose of AOM. The frequency of colonic aberrant crypt foci was determined at 5 weeks after the start. Feeding of 100 ppm MMTS for 5 weeks significantly decreased the number of aberrant crypt foci/colon. Colonic mucosal ornithine decarboxylase activity and the number of silver-stained nucleolar organizer regions per nucleus in colonic epithelium were significantly decreased by MMTS treatment compared with those of AOM alone. In experiment 2, effects of dietary feeding of MMTS at two doses (20 and 100 ppm) during the postinitiation phase on intestinal tumorigenesis initiated with AOM were investigated by using a long-term experiment in male F344 rats. Incidences of intestinal neoplasms of rats fed MMTS-containing diets after AOM exposure were reduced in a dose-dependent manner. Feeding of MMTS during the postinitiation phase decreased the number of aberrant crypt foci/colon, colonic ornithine decarboxylase activity, 5-bromodeoxyuridine-labeling index in colonic epithelium, and polyamine level in blood compared with those of AOM alone. These results suggest that MMTS might be a possible chemopreventive agent for intestinal neoplasia.

¹ This work was supported by a grant from the Ministry of Health and Welfare, Japan.

² To whom requests for reprints should be addressed.

Received 4/24/95. Accepted 7/19/95.

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