COPPER DEFICIENCY IMPAIRS SURVIVAL IN ENDOTOXIN-TREATED RATS

Copper (Cu) deficiency causes low activities of antioxidant enzymes, an effect which could weaken resistance against endotoxin induced injury. Weanling rats fed 0.2 ppm Cu for 6 weeks showed poor survival (2/12) 20 h after injection ip with 10 mg/kg endotoxin. Rats fed 15 ppm Cu showed good survival after this treatment (10/10). At 3 h after endotoxin injection, Cu-deficient rats displayed much larger increases than adequates in serum alanine aminotransferase activities, an indicator of liver injury. Deficient rats had low activities of 3 antioxidant enzymes: serum ceruloplasmin, hepatic Cu-Zn superoxide dismutase and serum extracellular superoxide dismutase. The last activities were reduced 3 h after endotoxin treatment in both Cu-adequate and deficient rats, but the final levels were much lower in the deficients. Thus, rats with low activities of Cu enzymes with potential antioxidant function showed poor survival of endotoxemia.