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Copper and molybdenum in subcellular fractions of rat liver

Published online by Cambridge University Press:  09 March 2007

C. F. Mills
Affiliation:
Rowett Research Institute, Bucksburn, Aberdeen
R. L. Mitchell
Affiliation:
Macaulay Institute for Soil Research, Craigiebuckler, Aberdeen
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Abstract

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1. Black-hooded weanling rats were given a copper-deficient diet or diets providing 3 ppm Cu with or without supplements containing combinations of molybdate, sulphate and sulphide salts to provide 35 ppm molybdenum and 2μg atoms sulphur/g. Changes in weight and blood haemoglobin concentration were studied during 48 d of treatment. The subcellular distribution of Cu and Mo in the liver was subsequently determined.

2. Rats fed on the Cu-deficient diet had a lower growth rate than animals receiving 3 ppm Cu and suffered a decline in blood haemoglobin concentration; Mo supplementation of the diet providing 3 ppm Cu produced similar adverse effects on growth but not on Hb. Effects of Mo on growth were exacerbated by a sulphide supplement which also decreased the rate of the gain in Hb concentration. This concentration of dietary sulphide was without effect when Mo was omitted from the diet.

3. The Cu-deficient diet decreased both the Cu concentration and proportion of total liver Cu in mitochondria + microsome and supernatant fractions of liver.

4. Mo-supplemented diets greatly increased both the Cu and Mo contents of all liver fractions. This phenomenon is considered in relation to previous suggestions that an unavailable Cu–Mo complex can form in tissues as a response to Mo accumulation.

Type
General Nutrition
Copyright
Copyright © The Nutrition Society 1971

References

REFERENCES

Brinkman, G. L., Miller, R. F. & Engel, R. W. (1961). Proc. Soc. exp. Biol. Med. 107, 666.CrossRefGoogle Scholar
Dowdy, R. P., Kunz, G. A. & Sauberlich, H. E. (1969). J. Nutr. 99, 491.CrossRefGoogle Scholar
Dowdy, R. P. & Matrone, G. (1968 a). J. Nutr. 95, 191.CrossRefGoogle Scholar
Dowdy, R. P. & Matrone, G. (1968 b). J. Nutr. 95, 197.CrossRefGoogle Scholar
Gregoriadis, G. & Sourkes, T. L. (1967). Can. J. Biochem. 45, 1841.CrossRefGoogle Scholar
Halverson, A. W., Phifer, J. H. & Monty, K. J. (1960). J. Nutr. 71, 95.CrossRefGoogle Scholar
Miller, R. F., Price, N. O. & Engel, R. W. (1956). J. Nutr. 60, 539.CrossRefGoogle Scholar
Mills, C. F. (1960). Proc. Nutr. Soc. 19, 162.CrossRefGoogle Scholar
Mills, C. F., Monty, K. J., Ichihara, A. & Pearson, P. B. (1958). J. Nutr. 65, 129.CrossRefGoogle Scholar
Mills, C. F. & Murray, G. (1960). J. Sci. Fd Agric. 11, 547.CrossRefGoogle Scholar
Mitchell, R. L. (1964). Tech. Commun. Commonw. Bur. Soils no. 44A.Google Scholar
Siegel, L. M. & Monty, K. J. (1961). J. Nutr. 74, 167.CrossRefGoogle Scholar
Thiers, R. E. & Vallee, B. L. (1957). J. biol. Chem. 226, 911.CrossRefGoogle Scholar