These minerals are cations that might compete for uptake in the digestive tract, thereby reducing absorption. These minerals might also affect copper utilization and excretion. For example, molybdenum has long been known to result in copper deficiency in ruminants but has little effect in nonruminants. Along with zinc for maintenance therapy, tetrathiomolybdate is now being used in the initial treatment of patients with the neurological or psychiatric form of Wilson disease.
Tetrathiomolybate acts by blocking absorption of copper when given with food and by complexing with serum copper when given separately from food Brewer et al. Similar to other metals, the bioavailability of copper in soils or suspended particulates in water is likely to be a function of its mineral or surface sorbed form, solubility, and particle size Davis et al.
As demonstrated for lead, solubility and bioavailability can vary greatly, depending on chemical and physical form Ruby et al. Copper acetate and sulfate are considerably more soluble and thus more bioavailable than cupric oxide Johnson et al. Copper in soil and sediments also adsorbs strongly to soil components, such as clay minerals, hydrous iron, and manganese oxides Tyler and McBride , resulting in reduced solubility and mobility. Studies of absorption, transport and metabolism of copper have provided insights into the biochemical mechanisms for coping with copper deficiency and excess.
The retention of copper from the diet is influenced by age, amount and form of copper in the diet, and genetic background. The liver plays a central role in copper homeostasis by varying the excretion of copper into the bile for loss in the stool. The newly discovered chaperones for copper have provided insight into how copper ions in cells are guided to their target proteins.
Studies are needed to elucidate mechanisms of copper absorption, distribution, and excretion in humans. Research should be conducted on the genetic basis of the absorption mechanism and on whether variation in absorption efficiency has a genetic basis. Research is needed to define extrahepatic processes for uptake and distribution. The ability of copper to induce proteins involved in its metabolism and transport should be investigated. Particular emphasis should be given to the investigation of metal response elements on copper transport proteins.
Research is needed to identify how the form of copper i. Amaravadi, R. Glerum and A. Alda, J. Chloride or bicarbonate -dependent copper uptake through the anion exchanger in human blood cells. Baker, D. Odle, M. Funk, and T. Research note: bioavailability of copper in cupric oxide, cuprous oxide, and in a copperlysine complex.
Bremner, I. Absorption, transport and distribution of copper. Ciba Foundation Symposium Amsterdam: Excerpta Medica. Brewer, G. Wilson disease. Medicine 71 3 — Dick, V. Yuzbasiyan-Gurkan, V. Johnson and Y. Therapy with zinc in presymptomatic patients from the time of diagnosis. Johnson, J. Brunberg, K. Kluin, and J. Treatment of Wilson's disease with zinc: XV. Long-term follow-up studies.
Johnson, R. Dick, K. Kluin, J. Fink, and J. Treatment of Wilson Disease with ammonium tetrathiomolybdate. Initial therapy in 33 neurologically affected patients and follow-up with zinc therapy. Dick, and Y. Treatment of Wilson's disease with zinc: XI. Interaction with other anticopper agents. Yuzbasiyan-Gurkan, R. Dick, Y. Wang, and V. Does a vegetarian diet control Wilson's disease? Cordano, A. Clinical manifestations of nutritional copper deficiency in infants and children.
Cousins, R. Absorption, transport, and hepatic metabolism of copper and zinc: Special reference to metallothionein and ceruloplasmin. Culotta, V. Klomp, J. Strain, R. Casareno, B. Krems, and Gitlin J. The copper chaperone for superoxide dismutase. Lin, P. Schmidt, L. Klomp, R. Casareno, and J. Intracellular pathways of copper trafficking in yeast and humans. Dancis, A. Yuan, D.
Haile, C. Askwith, D. Eide, C. Moehle, J. Kaplan, and R. Molecular characterization of a copper transport protein in S. Cell — Haile, D. S Yuan, and R. The Saccharomyces cerevisiae copper transport protein Ctr1p. Biochemical characterization, regulation by copper, and physiologic role in copper uptake.
Davis, A. Drexier JW, M. Ruby, and A. Micromineralogy of mine wastes in relation to lead bioavailability, Butte, Montana. Deneke, S. Regulation of cellular glutathione. DiSilvestro, R. Physiological ligands for copper and zinc.
Dunn, M. Green and R. Leach, Jr. Kinetics of copper metabolism in rats: a compartmental model. Eide, D. The molecular biology of metal ion transport in Saccharomyces cerevisiae. Fields, M. Holbrook, D. Scholfield, J. Smith, Jr. Effect of fructose or starch on copper absorption and excretion by the rat. Fischer, P. Giroux, and M. Effect of zinc supplementation on copper status in adult man. Freedman, J. Resistance of cultured hepatoma cells to copper toxicity.
Purification and characterization of the hepatoma metallothionein. Acta 2 — Intracellular copper transport in cultured hepatoma cells. Fuentealba, I. Haywood, and J. Variations in the intralobular distribution of copper in the livers of copper-loaded rats in relation to the pathogenesis of copper storage diseases. Georgatsou, E. Mavrogiannis, G. Fragiadakis, and D. Gross, J. Myers, L. Kost, S. Kuntz, and N. Biliary copper excretion by hepatocyte lysosomes in the rat.
Major excretory pathway in experimental copper overload. Harris, E. Role of ligands in the translocation of metals. Bioinorganic Medicine, Vol. Berthon, ed. New York: Marcel Dekker. O'Dell and R. Sunde, eds.
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Harris, D. The influence of amino acids on copper uptake by rat liver slices. Harris, Z. Takahashi, H. Miyajima, M. Serizawa, R. MacGillivray and J. Aceruloplasminemia: molecular characterization of this disorder of iron metabolism. USA 92 7 — Hassett, R. Evidence for Cu II reduction as a component of copper uptake by Saccharomyces cerevisiae. Haywood, S. A non-random distribution of copper within the liver of rats. Hillman, L. Martin and B. Effect of oral copper supplementation on serum copper and ceruloplasmin concentrations in premature infants.
Hogan, G. Role of copper binding, absorption, and translocation in copper tolerance of agrostis gigantea roth. Holt, D. Dinsdale, and M. Intestinal uptake and retention of copper in the suckling rat, Rattus rattus. Distribution and binding. Holtzman, N. Studies on the rate of release and turnover of ceruloplasmin and apoceruloplasmin in rat plasma. Hoogenraad, T.
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Koevoet, and E. Oral zinc sulphate as long-term treatment in Wilson's disease hepatolenticular degeneration. Oral zinc in Wilson's disease [letter].
Lancet 2 — Management of Wilson's disease with zinc sulfate. Experience in a series of 27 patients.
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Houwen, R. Dijkstra, F. Kuipers, E. Smit, R. Havinga and R. Two pathways for biliary copper excretion in the rat. The role of glutathione. Humbert W. Aprahamian, C. Stock, and J. Copper accumulation in primary biliary cirrhosis. An electron and X-ray microanalytical study. Histochemistry 74 1 — Irie S. Liver endothelium desialates ceruloplasmin. IOM Institute of Medicine. Nutrition during pregnancy. Part I: Weight Gain. Part II: Nutrient Supplements. Iyengar V. Brewer, R. Dick, and O. Studies of cholescystokinin-stimulated biliary secretions reveal a high molecular weight copper-binding substance in normal subjects that is absent in patients with Wilson's disease.
Johnson, M. Smith, and J. Copper, iron, zinc, and manganese in dietary supplements, infant formulas, and ready-to-eat breakfast cereals. L'Abbe M. The effects of dietary zinc on the activity of copper-requiring metalloenzymes in the rat. Bioavailability of copper. Copper nutrition during infancy and childhood. Bell, and C. Copper absorption from human milk, cow's milk, and infant formulas using a suckling rat model. Murata Y. Yamakawa, T. Lizuka, H. Kodama, T. Abe, Y. Seki, and M. Failure of copper incorporation into ceruloplasmin in the Golgi apparatus of LEC rat hepatocytes.
Recommended Dietary Allowances, 10th Ed. Washington, D. Oestreicher P. Copper and zinc absorption in the rat: Mechanism of mutual antagonism. Percival, S. Copper and immunity. Percival S. Ascorbate enhances copper transport from ceruloplasmin into human K cells. Copper transport from ceruloplasmin: Characterization of the cellular uptake mechanism. Regulation of Cu, Zn superoxide dismutase with copper. Caeruloplasmin maintains levels of functional enzyme activity during differentiation of K cells. Structure-function analyses of the ATX1 metallochaperone.
Reinstein, N. Lonnerdal, C. Keen and L. Zinc-copper interactions in the pregnant rat: fetal outcome and maternal and fetal zinc, copper and iron.
Rolfs A. Metal ion transporters in mammals: structure, function and pathological implications. Ruby M. Davis, R. Schoof, S. Eberle, and C. Estimation of lead and arsenic bioavailability using a physiologically based extraction test. Schoof, J. Drexier, W. Brattin, M. Goldade, G. Post, M.
Recommendations to Prevent and Control Iron Deficiency in the United States
Berti, M. Carpenter, D. Edwards, D. Cragin, and W. In press. When iron stores are exhausted, the condition is called iron depletion. Further decreases may be called iron-deficient erythropoiesis and still further decreases produce iron deficiency anemia. Blood loss is the most common cause of iron deficiency. In men and postmenopausal women, iron deficiency is almost always the result of gastrointestinal blood loss. In menstruating women, genitourinary blood loss often accounts for increased iron requirements. Oral contraceptives tend to decrease menstrual blood loss, whereas intrauterine devices tend to increase menstrual bleeding.
Other causes of genitourinary bleeding and respiratory tract bleeding also increase iron requirements. For blood donors, each donation results in the loss of to mg of iron. During periods of growth in infancy, childhood and adolescence, iron requirements may outstrip the supply of iron from diet and stores. Iron loss from tissue growth during pregnancy and from bleeding during delivery and post partum averages mg. Breastfeeding increases iron requirements by about 0. Your "iron level" is checked before each blood donation to determine if it is safe for you to give blood.
Iron is not made in the body and must be absorbed from what you eat. The adult minimum daily requirement of iron is 1. Only about 10 to 30 percent of the iron you consume is absorbed and used by the body. The daily requirement of iron can be achieved by taking iron supplements. Ferrous sulfate mg, taken orally once a day, and by eating foods high in iron. Foods high in vitamin C also are recommended because vitamin C helps your body absorb iron.
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