Ceruloplasmin

Abstract

Despite numerous investigations [see (1) for review] little information is available on the role of blood ceruloplasmin in body function in general or its relationship to copper distribution and metabolism. It has been known since the discovery of Wilson's disease that the central nervous system is particularly sensitive to a disturbance in copper metabolism, although the significance of low ceruloplasmin to the condition is unknown. With the important finding that a copper deficiency state could be produced in animals maintained on a diet containing high molybdate and sulfate, an experimental technique became available for studying the relationship of copper to neurological function. Ewes maintained on a similar diet gave birth to lambs with sway back disease, a demyelinating condition presumably similar to Wilson's disease(2). It was the objective of the present study to determine the effects of a high molybdate and sulfate diet on blood ceruloplasmin in an effort to help elucidate the role of this copper protein.

Materials and methods. Twenty-four white albino rabbits, 14–15 weeks old, were maintained on an intake of 0.05% molybdenum, as sodium molybdate (Na₂MoO₄ · 2H₂O) and 1.8% sulfate, as sodium sulfate (Na₂SO₄) mixed with a Purina rabbit dry ration containing 2 mg % copper. Deionized distilled drinking water was provided, ad libitum.

The weight of the animals, the level of total copper in blood, serum oxidase activity, hemoglobin levels, and alkaline phosphatase levels were examined weekly. Tissue copper determinations were performed after 10 weeks on one-third of the animals, while the rest of the determinations were made after death.

The copper content of the blood and tissue was estimated by a slight modification of the method of Eden and Green(3) with extreme care being taken to avoid contamination by heavy metal.