Biliary Excretion of Cæruloplasmin Copper

Abstract

THE importance of the mechanism by which normal subjects maintain zero balance of copper is seen in patients with Wilson's disease who, lacking it, accumulate copper to the point of toxicity. In these patients, the association of chronic copper toxicity and life-long deficiency of cæruloplasmin has aroused considerable speculation about a possible role of this copper-protein in the control of either absorption or excretion of copper¹. Since earlier studies failed to indicate an effect of circulating cæruloplasmin on the absorption of copper², our attention has recently been directed on the alternative possibility that cæruloplasmin is involved in the excretory pathway of copper. Bile is a major route for the excretion of heavy metals; the question arose therefore whether cæruloplasmin copper passes directly into bile, as suggested by Jeunet, Richterich and Aebi³. This was answered by intravenously injecting cæruloplasmin labelled with copper-64 into rabbits, and correlating the disappearance of radioactivity from the blood with the appearance of radioactivity in the bile.