Copper Metabolism: Intake - dietary 3.2 mg/day food
0.4 mg/day water
Output - excreted through bile ( 80%)
- excreted by the kidneys ( 4%)
Copper is absorbed from the small intestine. It is stored in the body in bone marrow and other tissues. Most of the serum copper is bound to Caeruloplasmin, the rest is loosely bound to Albumin. Copper can also bind to Transferrin (raised Cu levels can be found in Fe deficiency anaemias). Copper also has biological functions associated with enzyme activity; uricase, the monoamine oxidases, ascorbic acid oxidases and tyrosinase.
Women of child bearing age have higher Copper levels than men (Oestrogen therapy leads to levels of up to 47 μmol/L). Newborn infants have lower serum Copper levels 3 – 9 μmol/L.
Increases of serum Copper can be seen in a variety of disorders (usually as a result of increases in caeruloplasmin levels) e.g. sub-acute and chronic infections, acute leukaemia, aplastic anaemia, heamochromatosis and in Hodgkins disease where a response to treatment can be judged by a fall in serum Copper levels (often to normal levels)
Urine Copper is increased in proteinurias and nephrosis and Wilson’s disease.
Low serum Copper levels occur when there is poor synthesis of proteins, or dietary lack or absorption is impaired.
Copper is of particular interest in Wilson’s disease and Menkes syndrome.
Wilson’s disease is a copper storage disease in which Copper is unable to bind to caeruloplasmin. There is an increase in the amount of Copper absorbed from the diet which then becomes deposited in the tissues, particularly the liver and brain (leading to gross mental deficiency). Treatment is by chelation with agents such as penicillamine.
In Menkes syndrome (kinky hair disease) dietary Copper is unable to pass through the gut mucosa, serum Copper levels are very low, as is the urine Copper level.
Lipids/Trace Metals
PCU
5 days
4226