Oral administration of sodium butyrate reduces chemically-induced preneoplastic lesions in experimental carcinogenesis

OBJECTIVE: The objective was to assess the effects of oral administration of sodium butyrate on colon carcinogenesis. METHODS: Carcinogenesis in adult male Wistar rats was induced with 1.2-dimethylhydrazine injections at a dose of 40mg/kg of body weight. A solution of sodium butyrate (3.4%) was given ad libitum for 4 weeks (butyrate group, n=16) instead of water (control group, n=9). Rats were killed 17 weeks after 1.2-dimethylhydrazine administration. Aberrant crypt foci and expression of the messenger ribonucleic acid (mRNA) of cyclins D1 and E were quantified in the colon. Alterations in the fatty acid profile of the colon, liver, intra-abdominal fat and feces were also analyzed. RESULTS: A significant decrease in aberrant crypt foci was found in the group taking butyrate. No differences were found between the groups in the mRNA expression of cyclins D1 and E. Nevertheless, butyrate intake decreased the content of stearic and oleic acids in the intra-abdominal fat and docosahexaenoic acid in the liver. Moreover, these rats presented higher percentages of linoleic acid in the intra-abdominal fat than control rats. CONCLUSION: The data indicate that butyrate use in rats reduced preneoplastic lesions and changes in the intra-abdominal fat and fatty acid profile of the liver, commonly found in colon carcinogenesis.