Copper in plasma reflects its status and subsequent toxicity in the liver of LEC rats.

The possible relation of the increase in the concentration of copper (Cu) in the bloodstream with the increased supply of Cu to ceruloplasmin in the liver was examined in relation to the onset of jaundice in Long-Evans rats with a cinnamon-like coat color (LEC rats), an animal model of Wilson disease. The Cu concentration in serum and that in liver, and then that in kidneys of LEC rats were correlated, and then the relationship between the Cu concentration in serum and the malondialdehyde (MDA) concentration in the liver, a marker for lipid peroxidation, and also the activities of alanine aminotransferase and lactate dehydrogenase, marker enzymes for liver damage, were examined. An increase in the Cu concentration in liver induced significant increases in the Cu concentrations in serum and kidneys, and their relationship was different before and after the onset of jaundice, as reflected by the concentration of Cu in serum (lower than 1.5 and higher than 2.7 micrograms/ml, respectively). The relationship between the MDA concentration in liver and the Cu concentration in serum showed a characteristic change between before and after the onset of jaundice. The marker enzymes for liver damage increased significantly with age, and showed distinct responses at the Cu concentration of 1.5-2.7 micrograms/ml in serum. The results suggest that the Cu concentration in plasma reflects the on-going biological and toxicological actions of non-MT-bound Cu in the livers of LEC rats.