Effect of dietary β-sitosterol on fecal bacterial and colonic biotransformation enzymes in 1,2-dimethylhydrazine-induced colon carcinogenesis

Aim: The present study was designed to investigate the modulatory effect of beta-sitosterol administration on 1,2-dimethylhydrazine (DMH)-induced fecal bacterial and colonic biotransformation enzyme activities. Materials and methods: The chemopreventive potential of beta-sitosterol in colon carcinogenesis was assessed by injecting DMH (20 mg/kg body weight) subcutaneously into male Wistar rats and supplementing with beta-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 (beta-glucuronidase, beta-glucosidase, beta-galactosidase, nitroreductase, hyaluronate lyase, and sulfatase) and colonic biotransformation (beta-glucuronidase, beta-glucosidase, beta-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 beta-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 P-sitosterol markedly inhibited DMH-induced colon carcinogenesis by its ability to ameliorate the fecal bacterial and colonic biotransformation enzymes. Hence, beta-sitosterol can be a potential chemopreventive agent towards colon carcinogenesis.