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Reports

Effect of dietary benzylselenocyanate on azoxymethane‐induced colon carcinogenesis in Male F344 rats

, , , , , & show all
Pages 129-139 | Received 16 Aug 1990, Accepted 30 Oct 1990, Published online: 04 Aug 2009
 

Abstract

The effect of dietary benzylselenocyanate (BSCJ and its analogue, benzylthiocyanate (BTC), and sodium selenite during the initiation and postinitiation phases of azoxymethane (AOM)‐induced intestinal carcinogenesis was studied in male F344 rats. Animals intended for initiation study were fed the high‐fat (23.5% corn oil) diets containing 25, 50, and 100 ppm BSC (10, 20, and 40 ppm selenium, respectively) and 100 ppm BTC and 4 ppm selenium (as sodium selenite in drinking water); those intended for postinitiation study were fed the high‐fat control diet. Two weeks later, all animals were injected subcutaneously with AOM (15 mg/kg body wt) once weekly for two weeks. Three days after the last AOM injection, animals in the initiation and postinitiation studies were transferred respectively to the high‐fat diet and high‐fat diets containing BSC and BTC and sodium selenite in drinking water. This regimen was continued until 36 weeks post‐AOM injection. BSC inhibited the small intestinal and colon adenocarcinoma incidence and multiplicity of colon adenocarcinomas when fed during the postinitiation phase. Sodium selenite inhibited the incidence and multiplicity of colon adenocarcinomas only during the postinitiation phase. BTC had no inhibitory effect when fed during the initiation and postinitiation phases. The colonic mucosal ornithine decarboxylase activity was significantly inhibited by the administration of all three compounds, BSC (78%), BTC (62%), and sodium selenite (44%). It is concluded that the BSC has an inhibitory effect on the intestinal carcinogenesis in animals fed the high‐fat diet.

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