A COPPER-DEFICIENT DIET PREVENTS HEPATIC COPPER ACCUMULATION AND DYSFUNCTION IN LONG-EVANS CINNAMON (LEC) RATS WITH AN ABNORMAL COPPER-METABOLISM AND HEREDITARY HEPATITIS

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 th e Cu metabolism linked to hepatic injury in LEC rats. The hepatic Cu c oncentration at 30 days after birth was 94+/-4 Cu mu g/g liver in LEC rats, whereas that of Fischer rats at the same age was 7+/-1 Cu mu g/g . From 30 days after birth, all rats were fed a semisynthetic diet wit h two different levels of Cu, 0.5 or 30 mu g/g food, for 35 days. In L EC rats fed a Cu-deficient diet (0.5 mu g/g), the hepatic Cu concentra tion was 39+/-7 mu g/g. The Cu-normal diet (30 mu g/g) LEC group had a concentration of 357+/-15 mu g/g in the hepatic Cu. The group had sig nificantly higher aspartate aminotransferase (ASAT), alanine aminotran sferase (ALAT) and gamma-glutamyl transferase (GGT) levels than did th e 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.