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Sodium Butyrate Inhibits Carcinoma Development in a 1,2-Dimethylhydrazine-Induced Rat Colon Cancer

Hospitat Universitario de Canarias, Universidad de La Laguna, Tenerife, Spain

J.J. Afonso, MD

Hospitat Universitario de Canarias, Universidad de La Laguna, Tenerife, Spain

H. Alvarez-Arguelles, MD

Hospitat Universitario de Canarias, Universidad de La Laguna, Tenerife, Spain

C. Hernández, PHD

Hospitat Universitario de Canarias, Universidad de La Laguna, Tenerife, Spain

F. González, MD

Hospitat Universitario de Canarias, Universidad de La Laguna, Tenerife, Spain

Background: Butyric acid is one of the most important by-products of dietary fiber degradation. It is an important trophic agent for the intestinal mucosa under different experimental conditions. Data obtained from several in vitro studies strongly suggest that butyrate can be a potential therapeutic agent in controlling the growth of some cancer cells. However, to date, in vivo animal studies have failed to show conclusive results. Methods: We evaluated the effects of intracecal administration of butyrate in an experimental model of colonic carcinogenesis induced by 1,2-dimethylhydrazine (DMH), administered at the site where it is naturally produced, the cecum. We studied the incidence of colon tumors and their main histologic features. Results: Direct application of sodium butyrate significantly decreased the total number of tumors and the incidence of malignancies and carcinoma in the colon. Conclusions: Butyrate may inhibit the growth of tumors induced by DMH. (Journal of Parenteral and Enteral Nutrition 22: 14-17, 1998)

Journal of Parenteral and Enteral Nutrition, Vol. 22, No. 1, 14-17 (1998)
DOI: 10.1177/014860719802200114


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