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American Journal of Clinical Nutrition, Vol 24, 444-454, Copyright © 1971 by The American Society for Clinical Nutrition, Inc.
1 From the Chemistry Division, U.S. Army Medical Research and Nutrition Laboratory, Fitzsimons General Hospital, Denver, Colorado, and the Metabolism-Nutrition Section of the Department of Internal Medicine, University Hospitals, University of Iowa, Iowa City, Iowa
Experimental scurvy was investigated in five volunteer, adult, male human subjects who were maintained on a diet devoid of vitamin C. The metabolism of the vitamin was followed through the use of isotopically labeled ascorbic acid during the depletion and repletion of these subjects.
The radioisotope data obtained on each subject showed that there was direct relationship between clinical signs of scurvy and the pool size of ascorbic acid. There was also a definite relationship between the whole blood ascorbic acid values and the body pool of ascorbic acid when the body pool was in excess of 300 mg. Reductions in the ascorbic acid body pool below a level of 300 mg and until repleted back again to this level were not associated with any further changes in whole blood ascorbic acid levels. Frank signs of clinical scurvy were observed in all subjects when the body pool of ascorbic acid had been depleted to a level of 300 mg. Upon repletion of the ascorbate pool beyond a level of 300 mg, clinical symptomatology of scurvy began to recede. The rate of depletion was an exponential process, whereas the rate of repletion of ascorbic acid was found to be a linear process and proportional to the level of daily ascorbic acid intake. When the subjects were fed high intakes of ascorbic acid, only a limited quantity of the ingested vitamin equilibrated with the ascorbate body pool.
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