Copper Transport and Its Disorders: Molecular and Cellular by Maria C. Linder, Norma A. Lomeli, Stephanie Donley (auth.),

By Maria C. Linder, Norma A. Lomeli, Stephanie Donley (auth.), Arturo Leone, Julian F. B. Mercer (eds.)

This ebook is a compilation of displays on the first assembly dedicated to the mo­ lecular and mobile biology of copper delivery. after we first thought of the prospective application for the assembly, we felt discussion board to combine the hot advances in molecular realizing of copper shipping with the older wisdom of copper metabolism used to be wanted. moreover we wanted to have a powerful emphasis at the ailments of copper includ­ ing the genetic illnesses, Menkes and Wilson, and different attainable wellbeing and fitness points of this met­ al visible from a molecular point of view. total we have been more than happy with the luck of the assembly, and such a lot members have been very enthusiastic. regrettably we weren't in a position to receive manuscripts from each contributor, however the choice during this e-book covers lots of the themes mentioned. The heritage of organic learn into copper dates from the latter half the final century whilst the presence of copper as an element of residing platforms was once first famous, however it was once no longer till the Nineteen Twenties that the fundamental position of copper used to be first famous. l. S. McHargue came upon that crops and animals wanted copper for optimum progress and well-being and proposed that copper was once wanted for all times (McHargue, 1925). different teams quickly proven those observations in vegetation. In animals the requirement of copper for hematopoiesis used to be stumbled on in 1928 (Hart et aI.

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McArdle et al. stimulate uptake. , 1995a). All these data supported the idea that we were studying a P-type ATPase, and that this was the Wilson disease protein ATP7B. However, closer examination of the data revealed some unexpected information. Is Cu(I) or Cu(II) Transferred by the ATPase? , 1989), and as such we believed Cu would present to the transporter as Cu(I). , 1996). A variety of factors led us to this conclusion. , 1996). Secondly, other treatments which increased Cu(l) decreased ATP dependent uptake, for example, vitamin C.

Clin. Nutr. 63, 830S-5S. H. and Sternlieb I. (1996). Wilson disease and idiopathic copper toxicosis. Am. J. Clin. Nutr. 63, 842S-845S. H. and Sternlieb, I. (1994). Is non-Indian childhood cirrhosis caused by excess dietary copper? Lancet. 344,1002-1004. L. (1992). Copper deficiency in term and preterm infants. In: Nutritional Anemias. J. Fomon, S. Zlotkin, eds. Nestle Nutrition Workshop Series Vol 30. (Vevey: Nestec Ltd, New York: Raven Press) , pp. 105-119. M. D. (1981). The inhibitory effect of bran in iron absorption in man.

Consideration of these factors in adjusting up or down the level of AREI in a given context is important since they may modify the biological effect significantly. Factors which affect biokinetics differ for each element, but basically include interaction of elements amongst themselves, interactions with other dietary factors and the effect of environmental agents which may affect biokinetics. For example excess zinc will interfere with Cu absorption (van Campen and Scaifi, 1967), thus the higher limit of Cu AREI will be greater if there is concomitantly exposure to high zinc.

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