Copper distribution in the body

Copper distribution around the body appears to operate in two phases.60 In the first phase, copper ions are exported from enterocytes into the circulation. This is controlled by specific copper transporting proteins, including ATP7A, a P-type ATPase localised to the trans-Golgi network. It is also known as the Menkes protein MNK, because hereditary deficiency results in Menkes disease.99

Copper ions secreted from the intestinal mucosa are immediately bound to the high-affinity plasma proteins albumin and transcuprein.60 In physiological conditions, copper is almost always protein-bound, resulting in extremely low plasma concentrations of free ionic copper, perhaps as low as 10-18 Molar. Protein-bound copper is transported to the liver and kidney. Of the copper taken up by liver parenchymal cells, approximately 80% is excreted in the bile.100 Intestinal excretion provides the major mechanism for body copper homeostasis, urinary copper excretion being normally less than 0.1mg/d. Several pathways involving sequential protein-to-protein transfers are believed to be involved in copper transport across the hepatocyte.101 Cytoplasmic carrier proteins deliver copper to sites of synthesis of cytoplasmic cuproenzymes such as superoxide dismutase. Carrier proteins also supply copper to specific organelle-bound transporter proteins which control its incorporation into mitochondrial proteins, or entry into the hepatocyte secretory pathway.60 The trans-Golgi network protein ATP7B is involved both in bile formation and in caeruloplasmin secretion.99 Congenital deficiency of this enzyme results in Wilson's disease.

The second phase of body copper transport involves its efflux from liver and kidney and delivery to other tissues. It is secreted into the plasma, from liver and kidney cells, bound mainly to caeruloplasmin.60 From studies using radioisotopes to trace body copper transport, caeruloplasmin appears to be the main copper carrier around the body. Most tissues have been shown to have specific surface receptors for caeruloplasmin-copper, and to take it up from solution,102 either by endocytosis of the complex or by transfer of the copper to an intracellular receptor. There remains some uncertainty, however, concerning the importance of caeruloplasmin's role in body copper distribution. The protein is not thought to be crucial to copper transport because the genetic defect acaeruloplasminaemia does not severely disrupt copper metabolism. It appears that there is redundancy in the system, with copper also available to tissues from non-caeruloplasmin sources including proteins and other ligands. Current thinking is that tissues absorb copper preferentially from caeruloplasmin, but can utilise other sources if caeruloplasmin is not available.60

Hephaestin is a recently discovered membrane-bound glycoprotein. A homologue of caeruloplasmin, it appears to play a role in iron metabolism and has been most highly localised to the small intestinal villi, the site of iron absorption.103

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