Biochemical and immunological changes in mice following postweaning copper deficiency

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Abstract
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) cytochromec 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.