TY - JOUR
T1 - Effect of Dietary Benzylselenocyanate on Azoxymethane-Induced Colon Carcinogenesis in Male F344 Rats
AU - Reddy, Bandaru S.
AU - Nayini, Jaya R.
AU - Sugie, Shigeyuki
AU - El-Bayoumy, Karam
AU - Rao, Chintalapally V.
AU - Rigotty, Jeff
AU - Sohn, Ock Soon
N1 - Funding Information:
The authors thank Donna Virgil for preparation of the manuscript and Yves M. Louis for technical assistance. This is paper no. 8 in the series "Selenium in Chemoprevention of Carcinogenesis." This study was supported by National Institutes of Health (Bethesda, MD) Grant Nos. CA-17613 and CA-46589. Address reprint requests to Dr. B. S. Reddy, Naylor Dana Institute of Disease Prevention, American Health Foundation, 1Dana Rd., Valhalla, NY 10595.
PY - 1991/1/1
Y1 - 1991/1/1
N2 - The effect of dietary benzylselenocyanate (BSC) and its analogue, benzylthiocyanate (BTC), and sodium selenite during the initiation and postinitiation phases of azoxymethane (A OM)-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 adenocarcinornas 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.
AB - The effect of dietary benzylselenocyanate (BSC) and its analogue, benzylthiocyanate (BTC), and sodium selenite during the initiation and postinitiation phases of azoxymethane (A OM)-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 adenocarcinornas 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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U2 - 10.1080/01635589109514120
DO - 10.1080/01635589109514120
M3 - Article
C2 - 1645468
AN - SCOPUS:0025763086
VL - 15
SP - 129
EP - 139
JO - Nutrition and Cancer
JF - Nutrition and Cancer
SN - 0163-5581
IS - 2
ER -