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Research Article Free access | 10.1172/JCI105556

Studies on Zinc Deficiency: Changes in Trace Elements and Enzyme Activities in Tissues of Zinc-deficient Rats

Ananda S. Prasad, Donald Oberleas, Paul Wolf, Jerome P. Horwitz, Ray Collins, and Janice M. Vazquez

Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Department of Pathology, Wayne State University School of Medicine, Detroit, Mich.

Veterans Administration Hospital, Dearborn, Mich.

Detroit Institute of Cancer Research, Detroit, Mich.

†

Address requests for reprints to Dr. Ananda S. Prasad, Dept. of Medicine, Wayne State University School of Medicine, 1400 Chrysler Freeway, Detroit, Mich. 48207.

*

Submitted for publication August 8, 1966; accepted December 15, 1966.

Supported in part by U. S. Public Health Service grants AM 08142-03 and CA 02624, the Jennie Grogan Mendelson Memorial Fund, Detroit General Hospital Research Corporation grant M-16, and Nutrition Foundation grant 331.

Find articles by Prasad, A. in: PubMed | Google Scholar

Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Department of Pathology, Wayne State University School of Medicine, Detroit, Mich.

Veterans Administration Hospital, Dearborn, Mich.

Detroit Institute of Cancer Research, Detroit, Mich.

†

Address requests for reprints to Dr. Ananda S. Prasad, Dept. of Medicine, Wayne State University School of Medicine, 1400 Chrysler Freeway, Detroit, Mich. 48207.

*

Submitted for publication August 8, 1966; accepted December 15, 1966.

Supported in part by U. S. Public Health Service grants AM 08142-03 and CA 02624, the Jennie Grogan Mendelson Memorial Fund, Detroit General Hospital Research Corporation grant M-16, and Nutrition Foundation grant 331.

Find articles by Oberleas, D. in: PubMed | Google Scholar

Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Department of Pathology, Wayne State University School of Medicine, Detroit, Mich.

Veterans Administration Hospital, Dearborn, Mich.

Detroit Institute of Cancer Research, Detroit, Mich.

†

Address requests for reprints to Dr. Ananda S. Prasad, Dept. of Medicine, Wayne State University School of Medicine, 1400 Chrysler Freeway, Detroit, Mich. 48207.

*

Submitted for publication August 8, 1966; accepted December 15, 1966.

Supported in part by U. S. Public Health Service grants AM 08142-03 and CA 02624, the Jennie Grogan Mendelson Memorial Fund, Detroit General Hospital Research Corporation grant M-16, and Nutrition Foundation grant 331.

Find articles by Wolf, P. in: PubMed | Google Scholar

Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Department of Pathology, Wayne State University School of Medicine, Detroit, Mich.

Veterans Administration Hospital, Dearborn, Mich.

Detroit Institute of Cancer Research, Detroit, Mich.

†

Address requests for reprints to Dr. Ananda S. Prasad, Dept. of Medicine, Wayne State University School of Medicine, 1400 Chrysler Freeway, Detroit, Mich. 48207.

*

Submitted for publication August 8, 1966; accepted December 15, 1966.

Supported in part by U. S. Public Health Service grants AM 08142-03 and CA 02624, the Jennie Grogan Mendelson Memorial Fund, Detroit General Hospital Research Corporation grant M-16, and Nutrition Foundation grant 331.

Find articles by Horwitz, J. in: PubMed | Google Scholar

Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Department of Pathology, Wayne State University School of Medicine, Detroit, Mich.

Veterans Administration Hospital, Dearborn, Mich.

Detroit Institute of Cancer Research, Detroit, Mich.

†

Address requests for reprints to Dr. Ananda S. Prasad, Dept. of Medicine, Wayne State University School of Medicine, 1400 Chrysler Freeway, Detroit, Mich. 48207.

*

Submitted for publication August 8, 1966; accepted December 15, 1966.

Supported in part by U. S. Public Health Service grants AM 08142-03 and CA 02624, the Jennie Grogan Mendelson Memorial Fund, Detroit General Hospital Research Corporation grant M-16, and Nutrition Foundation grant 331.

Find articles by Collins, R. in: PubMed | Google Scholar

Department of Medicine, Wayne State University School of Medicine, Detroit, Mich.

Department of Pathology, Wayne State University School of Medicine, Detroit, Mich.

Veterans Administration Hospital, Dearborn, Mich.

Detroit Institute of Cancer Research, Detroit, Mich.

†

Address requests for reprints to Dr. Ananda S. Prasad, Dept. of Medicine, Wayne State University School of Medicine, 1400 Chrysler Freeway, Detroit, Mich. 48207.

*

Submitted for publication August 8, 1966; accepted December 15, 1966.

Supported in part by U. S. Public Health Service grants AM 08142-03 and CA 02624, the Jennie Grogan Mendelson Memorial Fund, Detroit General Hospital Research Corporation grant M-16, and Nutrition Foundation grant 331.

Find articles by Vazquez, J. in: PubMed | Google Scholar

Published April 1, 1967 - More info

Published in Volume 46, Issue 4 on April 1, 1967
J Clin Invest. 1967;46(4):549–557. https://doi.org/10.1172/JCI105556.
© 1967 The American Society for Clinical Investigation
Published April 1, 1967 - Version history
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Abstract

Zinc content of testes, bones, esophagus, kidneys, and muscles was decreased, whereas iron content was increased in the testes of zinc-deficient rats compared to restrictedly fed control rats. Histochemical enzyme determinations revealed reduced activities of certain enzymes in the testes, bones, esophagus, and kidneys. In the testes, lactic dehydrogenase (LDH), malic dehydrogenase (MDH), alcohol dehydrogenase (ADH), and NADH diaphorase; in the bones, LDH, MDH, ADH, and alkaline phosphatase; in the esophagus, MDH, ADH, and NADH diaphorase; and in the kidneys, MDH and alkaline phosphatase were decreased in zinc-deficient rats compared to restrictedly fed controls. Succinic dehydrogenase (SDH) revealed no significant changes under the conditions of our experiments in various groups of rats that were investigated.

In a “repleted” group of rats, content of zinc in testes and bones increased significantly, compared to the deficient group. The iron content of the testes decreased after repletion with zinc. In the testes, bones, esophagus, and kidneys, the activities of various enzymes increased after repletion with zinc.

Inasmuch as the major manifestations of zinc deficiency syndrome in the rat include growth retardation, testicular atrophy, and esophageal parakeratosis, our results suggest that the content of zinc in the above tissues most likely controls the physiological processes through the formation of zinc-dependent enzymes.

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