Abstract
This afternoon is devoted mainly to the pathological consequences associated of abnormal copper metabolism, which, by the way, offers some insight into the mechanism by which copper is taken up into the organism, distributed within the organism, utilized and excreted from the organism. That the intestinal uptake of copper is not merely a process of diffusion is evident from the natural experiment of the Menkes1 kinky hair syndrome in which apparently the absorption of copper is defective (1). It has been possible to gain information from an experimental model which has enabled detailed studies of the intestinal absorption mechanism of copper by comparing mouse mutants to normal animals. Questions concerning the mechanisms of pathogenesis of Wilson’s disease have not been unequivocally answered. It appears doubtful as to whether intestinal absorption mechanisms of copper are involved in the pathological processes since Bush et al. (2) showed that the time course of the appearance of copper in the plasma is not different from that of healthy individuals. However, the intermediate metabolism of copper by the organism does appear to be abnormal.
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T.J. Goka, R.E. Stevenson, P.M. Hefferan and R.R. Howell, Proc. Nat. Acad. Sci. U.S. 73, 604 (1976).
J.A. Bush, J.P. Mahoney, H. Markowitz, C.J. Gubler, G.E. Cartwright, M.M. Wintrobe, J. Clin. Invest. 34, 1766 (1955).
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© 1982 The Humana Press Inc.
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Forth, W. (1982). Introduction to the Afternoon Session on Physiological Aspectes of Copper Metabolism. In: Sorenson, J.R.J. (eds) Inflammatory Diseases and Copper. Experimental Biology and Medicine, vol 2. Humana Press. https://doi.org/10.1007/978-1-4612-5829-2_7
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DOI: https://doi.org/10.1007/978-1-4612-5829-2_7
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