Abstract
Copper (Cu) is required in the diet as a trace mineral to prevent hypochromic microcytic anemia secondary to defective hemoglobin synthesis (Hart et al., 1928). This metal is also required for the normal function of a number of oxidative enzymes including catalase, peroxidase, and cytochrome oxidase. Following absorption from the gastrointestinal tract, copper is weakly bound to albumin and later more firmly bound to ceruloplasim, a specific Cu transport protein (Linder and Moor, 1977). Bile is the normal excretory route for copper and plays a primary role in copper homeostasis while liver and bone normally store excess copper.
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Weekley, L.B., Kimbrough, T.D., O’Rear, C.E., Llewellyn, G.C. (1994). Disturbances in Tryptophan Metabolism Following Chronic Ingestion of a High Copper Diet by Male Rats. In: Llewellyn, G.C., Dashek, W.V., O’Rear, C.E. (eds) Mycotoxins, Wood Decay, Plant Stress, Biocorrosion, and General Biodeterioration. Biodeterioration Research, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9450-2_50
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DOI: https://doi.org/10.1007/978-1-4757-9450-2_50
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