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Diet liver function and di methyl hydrazine hydrazine induced gastro intestinal tumors in male wistar rats



Diet liver function and di methyl hydrazine hydrazine induced gastro intestinal tumors in male wistar rats



British Journal of Cancer 39(6): 731-739



Male Wistar rats fed a normal laboratory pelleted diet, when treated s.c. with 1,2-dimethylhydrazine (DMH) 10 mg/kg per wk survived the 24-wk experiment, showed no signs of chemical toxicity or macroscopic liver damage and developed mainly large-bowel tumors. Male Wistar rats treated with 20 mg/kg per wk DMH did not survive the full term of the experiment and developed ascites, pleural effusions and nodular livers. They also developed more small-bowel tumors than large-bowel tumors. The relationship between the prodominant site of tumor development and dosage of DMH was highly significant. Male Wistar rats fed with an all-liquid diet (Vivonex) and treated with 20 mg/kg per wk DMH behaved quite differently in terms of survival and site of tumor development. These rats survived the full term of the experiment, showed no signs of chemical toxicity, experienced minimal liver damage and predominantly developed large bowel tumors. The protection afforded by the all-liquid diet against DMH toxicity and small-bowel tumor induction was statistically highly significant. A series of blood tests with special reference to liver function confirmed the highly significant degree of protection against liver damage afforded by the all-liquid diet. Sections of liver from treated rats were examined, and a simple pathological scoring system was devised which showed a highly significant difference in liver histology between standard diet and liquid-diet rats treated with 20 mg/kg per wk DMH. An association between severity of liver damage from DMH and the subsequent development of small-bowel tumors was strongly suggested. The all-liquid diet protected rats from liver damage and these rats developed significantly fewer small-bowel tumors.

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