The present study was designed to investigate the modulatory effect of b-sitosterol administration on 1,2-dimethylhydrazine (DMH)-induced fecal bacterial and colonic biotransformation enzyme activities. Materials and methods: The chemopreventive potential of b-sitosterol in colon carcinogenesis was assessed by injecting DMH (20 mg/kg body weight) subcutaneously into male Wistar rats and supplementing with b-sitosterol throughout the experimental period of 16 weeks at 3 different doses (5, 10, and 20 mg/kg body weight). Results: Amplified activities of fecal bacterial (b-glucuronidase, b-glucosidase, b-galactosidase, nitroreductase, hyaluronate lyase, and sulfatase) and colonic biotransformation (b-glucuronidase, b-glucosidase, b-galactosidase, and nitroreductase) enzymes were considered hallmarks of colon carcinogenesis. DMH-induced animals showed increased activities of fecal bacterial and colonic biotransformation enzymes. Treatment with b-sitosterol markedly decreased the fecal bacterial and colonic biotransformation enzymes and reverted the colonic tissue to near normal. Conclusion: The results of the present study revealed that b-sitosterol markedly inhibited DMH-induced colon carcinogenesis by its ability to ameliorate the fecal bacterial and colonic biotransformation enzymes. Hence, b-sitosterol can be a potential chemopreventive agent towards colon carcinogenesis.

The present study was designed to investigate the modulatory effect of b-sitosterol administration on 1,2-dimethylhydrazine (DMH)-induced fecal bacterial and colonic biotransformation enzyme activities. Materials and methods: The chemopreventive potential of b-sitosterol in colon carcinogenesis was assessed by injecting DMH (20 mg/kg body weight) subcutaneously into male Wistar rats and supplementing with b-sitosterol throughout the experimental period of 16 weeks at 3 different doses (5, 10, and 20 mg/kg body weight). Results: Amplified activities of fecal bacterial (b-glucuronidase, b-glucosidase, b-galactosidase, nitroreductase, hyaluronate lyase, and sulfatase) and colonic biotransformation (b-glucuronidase, b-glucosidase, b-galactosidase, and nitroreductase) enzymes were considered hallmarks of colon carcinogenesis. DMH-induced animals showed increased activities of fecal bacterial and colonic biotransformation enzymes. Treatment with b-sitosterol markedly decreased the fecal bacterial and colonic biotransformation enzymes and reverted the colonic tissue to near normal. Conclusion: The results of the present study revealed that b-sitosterol markedly inhibited DMH-induced colon carcinogenesis by its ability to ameliorate the fecal bacterial and colonic biotransformation enzymes. Hence, b-sitosterol can be a potential chemopreventive agent towards colon carcinogenesis.