Summary

A review is presented of various aspects of copper (Cu) metabolism. The Cu absorption from the gastrointestinal tract in monogastric animals differs from that in ruminants. This is influenced by Cu binding compounds, sulphide production in the rumen, and molybdenum and zinc concentrations of the diet. Moreover, the valence of the Cu ions may influence the availability of Cu in the intestine. Metallothionein and lysosomes are involved in the accumulation of copper in the liver. The different findings in various Cu storage diseases may reflect different mechanisms of disease. Cu‐induced liver cell damage and haemolysis may be the result of lipid peroxidation.