Copper is an essential trace element required for the activity of certain oxido-reductases including cytochrome oxidase, superoxidase dismutase, tyrosinase, dopamine b-hydroxylase, and lysyl oxidase. And playing a role in energy production, connective tissue formation, iron metabolism, making and metabolising neurotransmitters, forming and maintaining myelin sheaths, melanin formation, antioxidant function, and regulation of gene expression.
Copper interacts with several other nutrients, including being required for iron metabolism and red blood cell formation; High amounts of zinc in the diet reduces copper amounts. And a copper deficiency is associated with anaemia that is unresponsive to iron supplementation.
We consume about 2g copper per day and excrete 1.9g in the faeces. Absorbed copper is taken into the tissues to balance losses in the urine, hair and skin. It is complexed with albumin or amino acids in the blood and is taken up by the tissues.
The liver forms a copper-binding protein, caeruloplasmin. As well as transporting copper to the liver, caeruloplasmin catalyses the oxidation of iron (Fe) (II) to Fe (III). Problems with this protein have been reported to produce iron overload. Copper requires specific ATPases to cross cell and organelle membranes. Many copper requiring enzymes are in mitochondria or vesicles.
Two inherited diseases of copper metabolism include Wilson’s disease and Menke’s disease. Both result in decreased serum copper levels. Wilson’s disease is more common and less serious. Wilson’s disease manifests with muscular rigidity, tremor, lack of coordination, and damage to the basal ganglia and liver. Wilson’s disease exhibits increased urinary and hepatic copper and is treated with metal-ion chelators.
Menke’s disease usually results in death before the third birthday. Menke’s disease results from the inability of the body to carry copper across membranes to the enzymes which require it. Lysyl oxidase is required for the cross linking of elastin and its inability to perform (due to copper deficiency) results in arterial rupture. In both Wilson’s disease and Menke’s disease, patients are susceptible to free radical attack due to accumulation of uncomplexed copper (II).
Penelope Espinoza Hallett, Naturopath
BHsc (C.M.) AdvDip. Nat/N.D, Dip. Aroma, Dip. C.H., Cert. R.M., Cert. R.M., Cert. SBM, mNHAA