摘要
AIM: To investigate the chemo preventive effects of vanadium on rat colorectal carcinogenesis induced by 1,2-dimethylhydrazine (DMH).METHODS: Male Sprague-Dawley Rats were randomly divided into four groups. Rats in Group A received saline vehicle alone for 16 weeks. Rats in Group B were given DMH injection once a week intraperitoneally for 16 weeks;rats in Group C, with the same DMH treatment as in the Group B, but received 0.5-ppm vanadium in the form ammonium monovanadate ad libitum in drinking water. Rats in the Group D received vanadium alone as in the Group C without DMH injection.RESULTS: Aberrant crypt foci (ACF) were formed in animals in DMH-treated groups at the end of week 16.Compared to DMH group, vanadium treated group had less ACF (P＜0.001). At the end of week 32, all rats in DMH group developed large intestinal tumors. Rats treated with vanadium contained significantly few colonic adenomas and carcinomas (P＜0.05) compared to rats administered DMH only. In addition, a significant reduction (P＜0.05) in colon tumor burden (sum of tumor sizes per animal) was also evident in animals of Group C when compared to those in rats of carcinogen control Group B. The results also showed that vanadium significantly lowered PCNA index in ACF (P＜0.005). Furthermore, vanadium supplementation also elevated liver GST and Cyt P-450 activities (P＜0.001 and P＜0.02, respectively).CONCLUSION: Vanadium in the form of ammonium monovanadate supplemented in drinking water ad libitum has been found to be highly effective in reducing tumor incidence and preneoplastic foci on DMH-induced colorectal carcinogenesis. These findings suggest that vanadium administration can suppress colon carcinogenesis in rats.
AIM:To investigate the chemo preventive effects of vanadium on rat colorectal carcinogenesis induced by 1,2- dimethylhydrazine (DMH). METHODS:Male Sprague-Dawley Rats were randomly divided into four groups.Rats in Group A received saline vehicle alone for 16 weeks.Rats in Group B were given DMH injection once a week intraperitoneally for 16 weeks; rats in Group C,with the same DMH treatment as in the Group B,but received 0.5-ppm vanadium in the form ammonium monovanadate ad libitum in drinking water.Rats in the Group D received vanadium alone as in the Group C without DMH injection. RESULTS:Aberrant crypt foci (ACF) were formed in animals in DMH-treated groups at the end of week 16. Compared to DMH group,vanadium treated group had less ACF (P<0.001).At the end of week 32,all rats in DMH group developed large intestinal tumors.Rats treated with vanadium contained significantly few colonic adenomas and carcinomas (P<0.05) compared to rats administered DMH only.In addition,a significant reduction (P<0.05) in colon tumor burden (sum of tumor sizes per animal) was also evident in animals of Group C when compared to those in rats of carcinogen control Group B.The results also showed that vanadium significantly lowered PCNA index in ACF (P<0.005).Furthermore,vanadium supplementation also elevated liver GST and Cyt P-450 activities (P<0.001 and P<0.02,respectively). CONCLUSION:Vanadium in the form of ammonium monovanadate supplemented in drinking water ad libitum has been found to be highly effective in reducing tumor incidence and preneoplastic foci on DMH-induced colorectal carcinogenesis.These findings suggest that vanadium administration can suppress colon carcinogenesis in rats.
基金
financial assistance of Department of Science & Technology,Government of India for during execution of the study(Ref No.SP/SO/B36/2000 dated 4/7/2002)
