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Increased retention of orally administered zinc and raised blood cell zinc concentrations in iron-deficient rats

Published online by Cambridge University Press:  09 March 2007

C. J. F. Spry  and
K. G. Piper
C. J. F. Spry
Affiliation:
Nuffield Department of Clinical Medicine
K. G. Piper
Affiliation:
Nuffield Department of Clinical Biochemistry, Radclifle Infirmary, Oxford
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Abstract

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1. Rats were made severely iron-deficient by feeding with Fe-deficient diets, which contained adequate amounts of zinc.

2. Ten days after an oral dose of 250 μg65Zn the Fe-deficient rats had retained 17% whereas control rats had retained only 8% of the dose.

3. When unlabelled Zn was given intravenously to the Fe-deficient and control rats there was a reduction in retention of the orally administered 65Zn. This effect was not produced when Fe was given before the oral dose of 65Zn.

4. Total body Zn, whole blood Zn and plasma Zn concentrations of the rats were measured by atomic absorption spectrophotometry. Both the Fe-deficient rats and the control rats had the same total body Zn calculated as a proportion of body-weight. The plasma Zn concentrations were normal in all the animals. Blood cell Zn concentrations in the Fe-deficient animals were raised.

5. The blood cell Zn concentration was directly related to the reticulocyte count in all the rats.

6. It was concluded that Fe and Zn are absorbed by different metabolic pathways, and that there is an increased turnover of Zn in the Fe-deficient rats, possibly related to the short lifespan and increased Zn concentration of Fe-deficient rat erythrocytes. In the rat abnormalities of Zn concentration can only be considered significant if Fe status is also known.

Type
Research Article
Information
British Journal of Nutrition , Volume 23 , Issue 1 , March 1969 , pp. 91 - 96
Copyright
Copyright © The Nutrition Society 1969

References

Becker, W. M. & Hoekstra, W. G. (1966). J. Nutr. 90, 301.CrossRefGoogle Scholar
Charlton, R. W., Jacobs, P., Torrance, J. D. & Bothwell, T. H. (1965). J. clin. Invest. 44, 543.CrossRefGoogle Scholar
Coble, Y. D., VanReen, R., Schulert, A. R., Koshakji, R. P., Farid, Z. & Davis, J. T. (1966). Am. J. clin. Nutr. 19, 415.CrossRefGoogle Scholar
Furchner, J. E. & Richmond, C. R. (1962). Hlth Phys. 8, 85.CrossRefGoogle Scholar
McCall, M. G., Newman, G. E., O'Brien, J. R. P., Valberg, L. S. & Witts, L. J. (1962). Br. J. Nutr. 16, 297.CrossRefGoogle Scholar
McKee, L. C., Wasson, M. & Heyssel, R. M. (1968). Br. J. Haemat. 14, 87.CrossRefGoogle Scholar
Orr, H. (1967). Hlth Phys. 13, 15.CrossRefGoogle Scholar
Piper, K. G. & Higgins, G. (1967). Proc. Ass. clin. Biochem. 4, 190.Google Scholar
Prasad, A. S. (1966). Zinc Metabolism, p. 250. Illinois: Charles C. Thomas.Google Scholar
Sahagian, B. M., Harding-Barlow, I. & Mitchell Perry, H. (1966). J. Nutr., 90 259.CrossRefGoogle Scholar
Sanstead, H. H., Prasad, A. S., Schulert, A. R., Farid, Z., Miale, A. Jr, Bassilly, S. & Darby, W. J. (1967). Am. J. clin. Nutr. 20, 422.CrossRefGoogle Scholar
Valberg, L. S., Card, R. T., Paulson, E. J. & Szivek, J. (1967). Br. J. Haemat. 13, 115.CrossRefGoogle Scholar
Van Campen, D. R. & Mitchell, E. A. (1965). J. Nutr. 86, 120.CrossRefGoogle Scholar
Warner, G. T. & Oliver, R. (1962). Br. J. Radiol. 35, 349.CrossRefGoogle Scholar