ABSTRACT
Findings indicating an impaired host defense system in copper deficiency come from studies in humans and animals. Children with the Menkes syndrome, a rare congenital disease resulting in copper deficiency, frequently die from pneumonia. While the critical mechanism of copper interaction in immunity will require further study, the present evidence suggests that such investigations will elucidate key regulatory events in the normal immune response. Using a low-copper basal diet similar to that used for mice by Lukasewycz and coworkers, a series of experiments were completed using weanling inbred Lewisrats. Anemia, depressed serum or plasma ceruloplasmin activity, depressed serum or plasma copper and iron, depressed liver copper, elevated liver iron, depressed cytochrome c oxidase activity, and copper and zinc superoxide dismutase in lymphoid cells have been commonly found in young male copper-deficient rats. Proliferation of spleen lymphoid and cervical lymph node cells stimulated by Con A was influenced by low dietary copper.
