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Hepatic iron accumulation in copper-deficient rats

Published online by Cambridge University Press:  24 July 2007

Darryl M. Williams
Affiliation:
Departments of Internal Medicine and Biochemistry, Louisiana State University Medical Center in Shreveport, PO Box 33932, Shreveport, Louisiana 71130-3932, USA
F. Scott Kennedy
Affiliation:
Departments of Internal Medicine and Biochemistry, Louisiana State University Medical Center in Shreveport, PO Box 33932, Shreveport, Louisiana 71130-3932, USA
Brenda G. Green
Affiliation:
Departments of Internal Medicine and Biochemistry, Louisiana State University Medical Center in Shreveport, PO Box 33932, Shreveport, Louisiana 71130-3932, USA
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Abstract

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1. Studies of anaemia and tissue iron distribution were carried out in copper-deficient rats and pair-fed control animals given Fe orally or parenterally in varying doses.

2. The anaemia of Cu deficiency was partially but incompletely corrected by oral Fe supplementation of one-to five-fold normal dietary levels or by intramuscular Fe supplementation.

3. Serum Fe increased in Cu-deficient animals as the dose of supplemental Fe was increased.

4. Hepatic Fe accumulation occurred in Cu-deficient rats which were administered with either oral Fe in two-to five-fold excess or low doses of intramuscular Fe. This difference was not seen in animals receiving high doses of intramuscular Fe, but similar relativedifferences were seen in Cu-deficient and Cu-replete rats which had been given no Fe supplementation.

5. Duodenal Fe was not increased in Cu deficiency. Bone marrow Fe was present in Cu-deficient animals receiving either parenteral or oral Fe supplementation.

6. Present studies suggest that a decrease in caeruloplasmin (EC 1. 16. 3. 1) activity does not wholly explain the anaemia of Cu deficiency.Fe accumulation may be restricted to the liver, suggesting that Cu may be required for normal intracellular Fe metabolism.

Type
Research Article
Copyright
Copyright © The Nutrition Society 1983

References

Baker, E., Morton, A. G. & Tavill, A. S. (1980). British Journal of Haematology 45, 607620.CrossRefGoogle Scholar
Cartwright, G. E. (1968). Diagnostic Laboratory Hematology, 4th ed. New York: Grune & Stratton.Google Scholar
Cartwright, G. E. & Lee, G. R. (1971). British Journal of Haematology 21, 147152.CrossRefGoogle Scholar
Chase, M. S., Gubler, C. J., Cartwright, G. E. & Wintrobe, M. M. (1952). Journal of Biological Chemistry 199, 757763.CrossRefGoogle Scholar
Danks, D. M., Campbell, P. E., Stevens, B. J., Mayne, V. & Cartwright, E. (1972). Pediatrics 50, 188201.CrossRefGoogle Scholar
Evans, J. L. & Abraham, P. A. (1973). Journal of Nutrition 103, 196201.CrossRefGoogle Scholar
Jacobs, A. & Worwood, M. (1978). In Metals and the Liver, pp. 351 [Powell, L. W., editor]. New York: Marcel Dekker.Google Scholar
Lee, G. R., Nacht, S., Christensen, D., Hansen, S. P. & Cartwright, G. E. (1969). Proceedings of the Society for Experimental Biology and Medicine 131, 918923.CrossRefGoogle Scholar
Lee, G. R., Nacht, S., Lukens, J. N. & Cartwright, G. E. (1968). Journal of Clinical Investigation 47, 20582069.CrossRefGoogle Scholar
Lee, G. R., Williams, D. M. & Cartwright, G. E. (1976). In Trace Elements in Human Health and Disease vol. 1 Zinc and Copper, pp. 373393. [Prasad, A. S. and Oberleas, D., editors]. New York: Academic Press.Google Scholar
Marston, H. R., Allen, S. H. & Swaby, S. L. (1971). British Journal of Nutrition 25, 1530.CrossRefGoogle Scholar
Mills, C. F. & Murray, G. (1960). Journal of the Science of Food and Agriculture 11, 547552.CrossRefGoogle Scholar
O'Reilly, S., Pollycove, M. & Bank, W. J. (1968). Neurology 18, 634644.CrossRefGoogle Scholar
Osaki, S. & Johnson, D. A. (1969). Journal of Biological Chemistry 244, 57575765.CrossRefGoogle Scholar
Owen, C. A. Jr (1973). American Journal of Physiology 224, 514518.CrossRefGoogle Scholar
Pinkerton, P. H., Spence, I., Ogilvie, J. C., Ronald, W. A., Marchant, P. & Ray, P. K. (1970). Journal of Clinical Pathology 23, 6876.CrossRefGoogle Scholar
Prohaska, J. R. (1981). Nutrition Research 1, 159167.CrossRefGoogle Scholar
Ravin, H. A. (1961). Journal of Laboratory and Clinical Medicine 58, 161168.Google Scholar
Roeser, H. P., Lee, G. R., Nacht, S. & Cartwright, G. E. (1970). Journal of Clinical Investigation 49, 24082417.CrossRefGoogle Scholar
Smith, S. E. & Medlicott, M. (1944). American Journal of Physiology 141, 354358.CrossRefGoogle Scholar
Topham, R. W., Woodruff, J. H., Neatrour, G. P., Calisch, M. P., Russo, R. B. & Jackson, M. R. (1980). Biochemical and Biophysical Research Communications 96, 15321539.CrossRefGoogle Scholar
Weisenberg, E., Halbreich, A. & Mager, J. (1980). Biochemical Journal 188, 633641.CrossRefGoogle Scholar
Williams, D. M.Burk, R. F., Jenkinson, S. G. & Lawrence, R. A. (1981). Journal of Nutrition 111, 979983.CrossRefGoogle Scholar
Williams, D. M., Lee, G. R. & Cartwright, G. E. (1974). American Journal of Physiology 227, 10941097.CrossRefGoogle Scholar
Williams, D. M., Loukopoulos, D., Lee, G. R. & Cartwright, G. E. (1976). Blood 48, 7785.CrossRefGoogle Scholar