A copper deficient diet prevents hepatic copper accumulation and dysfunction in Long-Evans Cinnamon (LEC) rats with an abnormal copper metabolism and hereditary hepatitis.

Abstract

Long-Evans Cinnamon (LEC) rats that develop spontaneous hepatitis due to an inherently abnormal Cu metabolism have recently been established. This investigation concerns the effects of a Cu-deficient diet on the Cu metabolism linked to hepatic injury in LEC rats. The hepatic Cu concentration at 30 days after birth was 94 +/- 4 Cu micrograms/g liver in LEC rats, whereas that of Fischer rats at the same age was 7 +/- 1 Cu micrograms/g. From 30 days after birth, all rats were fed a semisynthetic diet with two different levels of Cu, 0.5 or 30 micrograms/g food, for 35 days. In LEC rats fed a Cu-deficient diet (0.5 microgram/g), the hepatic Cu concentration was 39 +/- 7 micrograms/g. The Cu-normal diet (30 micrograms/g) LEC group had a concentration of 357 +/- 15 micrograms/g in the hepatic Cu. The group had significantly higher aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and gamma-glutamyl transferase (GGT) levels than did the LEC rats given the Cu-deficient diet. These results suggest that the occurrence of acute hepatitis in LEC rats can be prevented by feeding the animals a Cu-deficient diet.