Scottish Trace Element and Micronutrient Reference Laboratory
Scotland's specialised laboratory for trace elements and vitamins in health and disease
Metabolism of Copper
On average, about 30% of dietary Cu is absorbed. It is transported to the liver in portal blood bound to albumin. In the liver the metal is redistributed amongst the various Cu-metalloproteins. Intracellular regulation of Cu transport is mediated by metallothionein. The 'blue' glycoprotein, caeruloplasmin is exported from the liver and is the main plasma Cu fraction (95% of the total concentration of 15-25 µmol/l). This protein is an acute phase reactant increasing in response to infection, injury and in chronic inflammatory conditions. The plasma concentration of caeruloplasmin is increased by the action of steroid hormones for example in pregnancy and with the use of the contraceptive pill. The main route of Cu excretion is in bile and other intestinal fluids. The faecal output normally equals the total dietary intake. Urinary excretion is less than 1.0 µmol/day.
The dietary requirement is from 1-3 mg Cu per day. Since Cu is present in most foodstuffs dietary deficiency was thought unlikely in the general public. However, earlier estimates of total Cu dietary intake were erroneously high and Cu intestinal absorption is adversely affected by other dietary constituents. Some workers consider that subclinical Cu depletion may be widespread and is a risk factor for cardiovascular disease.
Severely malnourished children and adults on prolonged intravenous nutrition, have been found to respond to copper supplementation. Deficiency presents as a microcytic hypochromic anaemia resistant to iron therapy. There is a marked neutropenia. Intestinal malabsorption of copper is common in any condition resulting in severe diarrhoea.
Children, particularly neonates, fed with diet deficient in copper, are at risk of developing bone disease due to the inability to form collagen effectively.
Acute ingestion of copper salts produces nausea, vomiting and diarrhoea. A severe intravascular haemolysis develops leading to renal failure. Such effects have been observed after accidental or intentional poisoning with copper sulphate. Copper poisoning has also occurred in patients during renal dialysis due to use of contaminated water and the leaching of copper from dialysis membranes. In situations of acute overload the total plasma copper concentration will be greatly increased. The caeruloplasmin Cu fraction will not increase. Calculation of the proportion of non-caeruloplasmin bound Cu is then of value. (Normally less than 10% of total).