Abstract
Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis, the rat shows only minimal hepatic abnormalities on copper loading. To investigate the possibility that copper loading may potentiate the effects of a superimposed hepatitis, groups of rats received D-galactosamine (GalN) 0.85g/Kg ip, with or without previous oral copper supplementation, as copper acetate increasing to 0.2%(w/v) in the drinking water over 7 weeks.This regimen increased the hepatic copper to 557±143ug/g (control 55±10)(P<.002). Serum GOT levels for the non-copper-loaded rats rose from 64.8±2.1 to 2860±729 IU/L 24 hrs after the GalN, whereas in copper-loaded rats sGOT only rose to 122±31 IU/L. 24 hrs after GalN, non-copper-loaded rats had developed an intense hepatic inflammatory infiltration with extensive necrosis. In contrast, the copper-loaded rats showed only mild portal tract inflammation and focal necrosis.Faecal aerotolerant bacterial counts were reduced on copper-loading, suggesting that a decrease in gut-derived endotoxin is related to the protective effect of copper. Alternatively this may result from impairment of prostaglandin synthesis by copper. The effect of copper on the liver may be the sum of its cytotoxic and its anti-inflammatory actions.
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