Weanling albino male mice rapidly develop biochemical signs of
copper deficiency when fed a purified diet containing 0.5 mg Cu/kg. Plasma
ceruloplasmin activity of
copper-deficient (-Cu) mice was 5% of that of
copper-adequate (+Cu) control mice after only 3 d on the diet. More gradual loss of organ (liver, spleen, and thymus)
cytochrome c oxidase activity was observed during the next 4 wk.
Body weight was equivalent between +Cu and -Cu mice, but thymus weight dropped faster in -Cu mice than +Cu mice. The number of antibody producing cells to sheep erythrocytes was lower in -Cu mice compared to +Cu mice after 17 d on the diet. Spleen
cytochrome oxidase activity of -Cu mice was 50% of that of +Cu mice by 10 d on the diet. Mitogenic response of splenic and thymic lymphocytes to
concanavalin A (con A) was not greatly different between +Cu and -Cu mice. Splenocytes from -Cu mice had a 3-fold higher
thymidine incorporation rate in the absence of
mitogen compared to +Cu mice. The depressed antibody and high mitogenic background responses of -Cu mice were similar to previous work with another strain (C58) of mice that had been started on
copper-deficient treatment from birth. However, the normal proliferative response to con A stimulation in postweaning
copper deficiency differs from the previous model. Mice of both studies were very
copper-deficient as judged by liver
copper levels. Timing of the
copper-deficient treatment influences the manner in which
copper deficiency alters the immune response.