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Molecular Pharmacology, Vol 18, 326-330, Copyright © 1980 by the American Society for Pharmacology and Experimental Therapeutics
1 Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824
Guinea pigs fed no ascorbic acid develop scurvy due to the inherited absence of the enzyme L-gulonolactone oxidase. However, by providing this enzyme together with its substrate L-gulonolactone, synthesis of the vitamin and prevention of scurvy are demonstrated in this species. Rat liver enzyme is placed in a dialysis bag which has been surgically implanted within the animals' peritoneal cavities. Substrate is then injected into the penitoneum. Plasma concentrations of ascorbic acid are markedly increased in enzyme-treated animals compared to similar bovine albumin-treated control animals. Adrenal gland, liver, and other tissue concentrations of the vitamin are also significantly elevated. Prolonged time of survival of enzyme-treated guinea pigs fed the ascorbic acid-deficient diet is shown. Enzyme placed within the dialysis bags does not appear to be antigenic, whereas unprotected enzyme is clearly antigenic.
Note:
ACKNOWLEDGMENTS
The author would like to acknowledge and thank Gregory D. Fink,
Ph.D., for his help in developing the surgical procedures used in this
study, Susan Stein, M.S., D.V.M., for her advice regarding the maintenance of the experimental animals, and George Cardinale, Ph.D.,
Sidney Udenfriend, Ph.D., and Vincent Zannoni, Ph.D., for their comments regarding the preparation of the manuscript.