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Journal of Nutrition Vol. 71 No. 1 May 1960, pp. 95-100
Copyright © 1960 by American Society for Nutrition
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A Mechanism for the Copper-Molybdenum Interrelationship1

A. W. Halverson2, J. H. Phifer and K. J. Monty

McCollum-Pratt Institute, The Johns Hopkins University, Baltimore, Maryland

Excessive dietary molybdate produced a profound depression of growth and a low incidence of anemia and diarrhea in rats fed a low copper diet. Supplementing the diet with copper prevented anemia and diarrhea, but did not restore growth. Administration of excessive dietary cystine to rats fed the high molybdate-low copper diet led to critical conditions of anemia and diarrhea and to some fatalities. These toxic effects of cystine were prevented or reversed by copper, and the joint administration of cystine and copper, alleviated the growth depression due to molybdate. The observations are discussed in terms of the postulate that the reduced level of sulfide oxidase in the tissues of rats receiving excessive molybdate permits an abnormal accumulation of sulfide. This accumulation leads to the formation of copper sulfide and the subsequent appearance of symptoms of copper deficiency.


1 Contribution no. 273 from the McCollum-Pratt Institute. Supported in part by a contract with the United States Atomic Energy Commission and a grant from the National Institutes of Health.

2 Fellow of the National Institutes of Health, on leave from Station Biochemistry, South Dakota State College, Brookings.

Manuscript received 16 January 1960.





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