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


CONCLUSIONS
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.
Kanna
P-Suresh
PS
Division of Biochemistry, Department of Pharmaceutical Technology, Jadavpur University, Kolkata-700032 (Calcutta), India.
Mahendrakumar
C B
CB
Chakraborty
T
T
Hemalatha
P
P
Banerjee
Pratik
P
Chatterjee
M
M
D019813:1,2-Dimethylhydrazine / Q000633:toxicity; D000236:Adenoma / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control; D000818:Animals; D002273:Carcinogens / Q000633:toxicity; D002277:Carcinoma / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control; D003106:Colon / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D003110:Colonic Neoplasms / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D008297:Male; D011230:Precancerous Conditions / Q000139:chemically induced / Q000201:enzymology / Q000473:pathology / Q000517:prevention & control*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014638:Vanadates / Q000494:pharmacology*
D002273:Carcinogens; D018809:Proliferating Cell Nuclear Antigen; D014638:Vanadates; D003577:Cytochrome P-450 Enzyme System; D005982:Glutathione Transferase; D019813:1,2-Dimethylhydrazine