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Journal of Nutrition Vol. 87 No. 4 December 1965, pp. 419-423
Copyright © 1965 by American Society for Nutrition
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Vitamin B6 Depletion in Man: Urinary Excretion of Quinolinic Acid and Niacin Metabolites1

R. R. Brown2, Norma Yess3, J. M. Price4, Hellen Linkswiler, Patricia Swan and L. V. Hankes

Division of Clinical Oncology, University of Wisconsin Medical School, School of Home Economics, University of Wisconsin, Madison, Wisconsin and Division of Biochemistry, Medical Research Center, Brookhaven National Laboratory, Upton, Long Island, New York

The effect of vitamin B6 depletion on the conversion of tryptophan to niacin by 6 male subjects was studied during a 55-day experiment. The urinary excretion of quinolinic acid, nicotinic acid, N1-methylnicotinamide and N-methyl-2-pyridone-5-carboxamide was measured (a) during a 5-day pre-depletion period when the subjects ate self-selected diets; (b) during depletion while they consumed a diet containing only 0.16 mg of vitamin B6 daily, (c) when they were fed diets supplemented with 0.6 or 0.9 mg of pyridoxine/day; and (d) when they received 50 mg of pyridoxine daily. The urinary levels of the 4 metabolites were determined before and after loading with 2 g of L-tryptophan during each of these periods. Post-tryptophan quinolinic acid excretion levels and yields (post-tryptophan values minus basal values) were significantly elevated during vitamin B6 depletion and these returned to pre-depletion levels upon repletion and saturation with pyridoxine. During the height of depletion, N1-methylnicotinamide values were not significantly different from values during repletion or saturation but differed from pre-depletion values probably because the subjects were eating self-selected diets during the pre-depletion period. The excretion levels of the 4 metabolites in other periods were not statistically different. The results of this experiment suggest a possible requirement for vitamin B6 coenzymes in the metabolism of quinolinic acid.

1 Published with the approval of the Director of the University of Wisconsin Agricultural Experiment Station. Supported in part by a grant from the American Cancer Society; by Public Health Service Research Grant no. CA-03274 from the National Cancer Institute; and nos. AM-01499 and AM-06675 from the National Institute of Arthritis and Metabolic Diseases; and by a grant from the U.S. Atomic Energy Commission.

2 Supported by Public Health Service Research Career Development Award no. CA-K3-18,404 from the National Institutes of Health.

3 Present address: Department of Nutrition, Harvard University School of Public Health, Boston, Massachusetts.

4 American Cancer Society — Charles S. Hayden Foundation Professor of Surgery in Cancer Research.

Manuscript received 30 July 1965.




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