Effect of vanadium on colonic aberrant crypt foci induced in rats by 1,2 dimethyl hydrazine

Abstract

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.

Figure 1

Grouping and different time point of the experiment.

Figure 2

Depicts the body weights of different group of animals.

Figure 3

3.1a: showing the normal colonic architecture view of rats sacrificed at end of week 16 (Low power). 3.1b: showing the normal colonic architecture view of rats sacrificed at end of week 16 (High power). 3.2a: representing the carcinogen-induced group B rats sacrificed at end of week 16 (Low power). 3.2b: representing the carcinogen-induced group B rats sacrificed at end of week 16 (High power). 3.3a: showing the treatment with vanadium group C rats sacrificed at the end of week 16 (Low power). 3.3b: showing the treatment with vanadium group C rats sacrificed at the end of week 16 (High power).

Figure 4

4.1a: showing the carcinogen-induced group B rats sacrificed at end of week 32 (Low power). 4.1b: showing the carcinogen-induced group B rats sacrificed at end of week 32 (High power). 4.2a: showing the treatment with vanadium group C rats sacrificed at the end of week 32 (Low power). 4.2b: showing the treatment with vanadium group C rats sacrificed at the end of week 32 (High power). 4.3a: showing the vanadium control group D rats with no signs of toxicity sacrificed at the end of week 32 (Low power). 4.3b: showing the vanadium control group D rats with no signs of toxicity sacrificed at the end of week 32 (High power).