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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
HEPATIC VITAMIN A IN THE RAT AS AFFECTED BY THE ADMINISTRATION OF DIBENZANTHRACENE
J C Abels1, A T Gorham, S L Eberlin
1Memorial Hospital for the Treatment of Cancer and Allied Diseases, New York.
Abstract:
1. The decreased concentrations of vitamin A in the livers of rats given dibenzanthracene probably are due to a particular effect of the carcinogen on the ability of the liver to store the vitamin and not to the production of general hepatic dysfunction. 2. The administration of dibenzanthracene to normal rats does not (a) increase significantly their hepatic content of total fat nor decrease that of phospholipid; (b) impair the ability of their livers to fabricate serum albumin; (c) impair the capacity of their livers to esterify cholesterol or phenol; (d) interfere with the hepatic synthesis and conjugation of glucuronic acid; or (e) interfere with the hepatic storage of riboflavin. 3. The simultaneous ingestion of yeast by the dibenzanthracene-treated rats further depletes their hepatic stores of vitamin A. This depletion conceivably is due to the fact that yeast alone also might deplete the liver of its vitamin A and thus a summation of two similar effects is attained. 4. The results suggest a competition between vitamin A and dibenzanthracene for some substance, possibly a protein, to which vitamin A may be bound in the liver.
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