Copper

BACKGROUND

Copper is a component of a number of metalloenzymes including diamine oxidase, monoamine oxidase, lysyl oxidase, ferroxidases, cytochrome c oxidase, dopamine beta monoxygenase, alphaamidating monooxygenase and cupro/zinc superoxide dismutase.

Copper is widely distributed in foods with organ meats, seafood, nuts and seeds being major contributors. Wheat bran cereals and whole grain products are also good sources. Nearly two thirds of the body's copper is found in the skeleton and muscles but the liver is also important in maintaining plasma levels (Olivares & Uauy 1996, Turnlund et al 1998).

Copper is absorbed mainly in the small intestine although some absorption may also occur in the stomach. Absorption varies with copper intake, ranging from more than 50% at intakes below 1 mg/day to less than 20% for intakes above 5 mg/day (Turnlund 1998). The composition of the diet itself has little effect on bioavailability. However, very high levels of zinc or iron, generally taken as supplements, can affect absorption in adults and infants (Botash et al 1992, Lonnerdal & Hernell 1994, Morais et al 1994 Turnlund 1999). Excretion through bile is used to regulate copper balance. Urinary copper excretion is normally very low over a wide range of intakes.

Copper deficiency results in defects in connective tissue that lead to vascular and skeletal problems, and anaemia related to defective iron metabolism. It can also affect the central nervous system (Harris 1997, Turnlund 1999) and the immune and cardiovascular systems, notably in infants (Graham & Cordano 1969, Olivares & Uauy 1996, Turnlund, 1999). Frank copper deficiency is rare in humans but has been seen in certain circumstances in infants (Shaw 1992) and under conditions of total parenteral nutrition (Fujita et al 1989). Symptoms include normocytic, hyperchromic anaemia, leukopenia and neutropenia. Other studies have observed osteoporosis in copper-deficient infants and young children (Higuchi et al 1988) and heart beat irregularities (Milne 1998).

There is no single indicator for the assessment of requirements for copper in humans (FNB:IOM 2001). Serum copper, ceruloplasmin concentration, erythrocyte superoxide dismutase activity, platelet copper, cytochrome c oxidase activity, urinary copper, leucocyte copper concentration, lysyl oxidase activity, peptidyl glycine alpha-amidating mono-oxygenase activity, diamine oxidase activity, copper balance and factorial analysis have all been used, but they generally give inconsistent results.