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Studies of the changes in systemic copper metabolism and excretion produced by the intravenous administration of trithiomolybdate in sheep

Published online by Cambridge University Press:  09 March 2007

J. Mason
Affiliation:
Biochemistry Department, Trinity College, Dublin 2, Irish Republic
M. Lamand
Affiliation:
Laboratoire des Maladies Nutritionnelles, INRA, CRZV de Theix 63122, Ceyrat, France
J. C. Tressol
Affiliation:
Laboratoire des Maladies Nutritionnelles, INRA, CRZV de Theix 63122, Ceyrat, France
G. Mulryan
Affiliation:
Biochemistry Department, Trinity College, Dublin 2, Irish Republic
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Abstract

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1. The effects of intravenous trithiomolybdate administration on the fate of 64Cu and on stable Cu metabolism were examined in sheep held in metabolism cages and fed on a low-Cu diet supplying 2·95 mg Cu/animal per d.

2. In Expt 1 the injection of trithiomolybdate, 30 mg molybdenum/sheep per d for 5 d, greatly increased plasma Cu levels and more than doubled the faecal Cu excretion. Urinary Cu excretion was unaffected. The disappearance from plasma of 64Cu injected during the trithiomolybdate administration was slowed although faecal 64Cu excretion was increased more than threefold.

3. In Expt 2 trithiomolybdate, 10 and 30 mg Mo/sheep per d for 3 d, was administered 22 h after the injection of 64Cu. Radioactivity reappeared immediately in plasma and faecal 64Cu excretion was increased.

4. In both experiments the 64Cu and the increased stable Cu in plasma were associated with albumin.

5. The experiments explain the effectiveness of thiomolybdates as ‘decoppering’ agents and provide a model for some of the systemic effects seen in ruminants exposed to increased dietary Mo. The experiments support the view that the thiomolybdates, by causing the appearance of new ligands, alter the distribution of Cu in tissues and cause an overall depletion.

Type
General Nutrition Papers
Copyright
Copyright © The Nutrition Society 1988

References

Gawthorne, J. M. (1985). In Ruminant Physiology, Concepts and Consequences, pp. 337357 [Baker, S. K., Gawthorne, J. M., Mackintosh, J. M. and Purser, D. B., editors]. Perth: University of Western Australia.Google Scholar
Gooneratne, S. R. (1986). Acta Pharmacologica et Toxiologica 59, Suppl. 7, 518523.CrossRefGoogle Scholar
Gooneratne, S. R., Christenson, D., Chaplin, R. & Trent, A. (1985). In Trace Elements in Man and Animals, pp. 342346 [Mills, C. F., Bremner, I. and Chesters, J. K., editors]. Slough: Commonwealth Agricultural Bureaux.Google Scholar
Gooneratne, S. R., Howell, J. McC. & Gawthorne, J. M. (1981). British Journal of Nutrition 46, 457480.CrossRefGoogle Scholar
Hynes, M., Lamand, M., Montel, G. & Mason, J. (1984). British Journal of Nutrition 52, 149158.CrossRefGoogle Scholar
Hynes, M., Woods, M., Poole, D., Rogers, P. & Mason, J. (1985). Journal of Inorganic Biochemistry 24, 279288.CrossRefGoogle Scholar
Kelleher, C. A. & Ivan, M. (1985). In Trace Element Metabolism in Man and Animals, pp. 364367 [Mills, C. F., Bremner, I. and Chesters, J. K., editors]. Slough: Commonwealth Agricultural Bureaux.Google Scholar
Kelleher, C. A. & Mason, J. (1986). International Journal of Biochemistry 18, 629635.CrossRefGoogle Scholar
Lamand, M., Lab, C., Tressol, J. C. & Mason, J. (1980). Annals of Veterinary Research 11, 141145.Google Scholar
Lannon, B. & Mason, J. (1986). Journal of Inorganic Biochemistry 26, 107115.CrossRefGoogle Scholar
Marcilese, N. A., Ammerman, C. G., Valsecchi, R. M., Dunavent, B. G. & Davis, G. K. (1970). Journal of Nutrition 100, 13991406.CrossRefGoogle Scholar
Mason, J. (1982). Irish Veterinary Journal 36, 164168.Google Scholar
Mason, J. (1986). Toxicology 42, 99109.CrossRefGoogle Scholar
Mason, J., Kelleher, C. A. & Letters, J. (1982 a). British Journal of Nutrition 48, 391397.CrossRefGoogle Scholar
Mason, J., Lamand, M. & Kelleher, C. A. (1982 b). Journal of Comparative Pathology 92, 509519.CrossRefGoogle Scholar
Mason, J., Lamand, M., Tressol, J. C. & Lab, C. (1978). Annals of Veterinary Research 9, 577586.Google Scholar
Mason, J., Woods, M. & Poole, D. B. R. (1986). Research in Veterinary Science 41, 108113.CrossRefGoogle Scholar
Mills, C. F., Bremner, I., El-Gallad, T. T., Dalgarno, A. C. & Young, D. W. (1978). In Trace Element Metabolism in Man and Animals, pp. 150158 [Kirchgessner, M., editor]. Weinhenstephan: Arbeitskreis für Tierernahrungsforshung.Google Scholar
Smith, B. S. W. & Wright, H. (1975). Journal of Comparative Pathology 85, 299305.CrossRefGoogle Scholar
Walshe, J. M. (1986). In Orphan Diseases/Orphan Drugs, pp. 7685 [Scheinberg, I. H. and Walshe, J. M., editors]. Manchester: Manchester University Press.Google Scholar
Wang, Z. Y., Poole, D. B. R. & Mason, J. (1986). Proceedings of the XIVth World Congress on Diseases of Cattle, pp. 845849, [Hartigan, P. J. and Monaghan, M. L., editors]. Dublin: Irish Cattle Veterinary Association.Google Scholar
Wang, Z. Y., Poole, D. B. R. & Mason, J. (1988). Journal of Inorganic Biochemistry (In the Press).Google Scholar
Woods, M. & Mason, J. (1987). Journal of Inorganic Biochemistry 30, 261272.CrossRefGoogle Scholar