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American Journal of Clinical Nutrition, Vol 12, 406-412, Copyright © 1963 by The American Society for Clinical Nutrition, Inc.

The Effects of an Induced Pyridoxine and Pantothenic Acid Deficiency on Excretions of Oxalic and Xanthurenic Acids in the Urine

SANDRA R. FABER M.S.1, WENDE W. FEITLER M.S.1, ROBERTA E. BLEILER PH.D.1, MARGARET A. OHLSON PH.D.1, and ROBERT E. HODGES M.D.1

1 From the Department of Internal Medicine, College of Medicine, State University of Iowa, Iowa City, Iowa

Five healthy, adult men were made pyridoxine and pantothenic acid-deficient by use of a semisynthetic formula and desoxypyridoxine and omega-methyl pantothenic acid supplements. In addition to the weekly determination of nitrogen retention, the urinary excretions of xanthurenic and oxalic acids were studied before and after a test dose of d,l-tryptophan given weekly during the twelve week study. Pyridoxine and pantothenic acid were restored to the diet after the seventh week.

In man, as in animals, an induced pyridoxine deficiency results in oxaluria. Following the administration of test doses of tryptophan to pyridoxine-deficient subjects, the amounts of urinary oxalic acid were sharply increased for one to two days.

Excretion of xanthurenic acid increased after each test dose of tryptophan until the fifth week of study. At that time, three men became negative in nitrogen balance abruptly, and excretion of xanthurenic acid decreased to about half that observed the previous week. Two men did not lose nitrogen, and the trend of excretion of the metabolite did not change until pyridoxine was restored to the diet. In contrast, those subjects with decreased nitrogen retention excreted the greatest amounts of oxalic acid. It is postulated that catabolism of tissue may release sufficient pyridoxine to metabolize the tryptophan load, in part, but that preferential use of the vitamin must occur.




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