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Copper Deficiency during Perinatal Development: Effects on the Immune Response of Mice¹

Department of Biochemistry ^* Department of Medical Microbiology and Immunology, University of Minnesota, Duluth, MN 55812

Dietary copper (Cu) was restricted in Swiss albino mice during five discrete intervals over a 9-wk period of perinatal development: gestation only (G), lactation only (L), 3 wk postiactation (PL), 1 wk after birth through post-lactation (2/3L + PL), and lactation plus postiactation (L + PL). Biochemical and immunological status of mice in copper-deficient (-Cu) treatment groups in models G and L did not differ from that of copper-adequate (+Cu) controls. Signs of severe copper deficiency, such as low liver copper levels, and significant reductions in activity of plasma ceruloplasmin and splenocyte Cu-Zn superoxide dismutase were most evident in 6-wk-old mice from two groups, -Cu 2/3L + PL and -Cu L + PL. Mice in these groups were anemic and had small thymuses and enlarged spleens compared to controls receiving +Cu treatment. The -Cu mice demonstrated impaired antibody (plaqueforming cells, PFC) response to sheep erythrocytes, and the attenuation was proportional to copper deficiency, as judged by liver copper levels. Total plasma IgM levels were not greatly altered by -Cu treatment except in model L + PL. Total IgG levels were markedly reduced in this group and in the -Cu 2/3L + PL group. The PFC response of mice in the -Cu PL group was normal even though signs of copper deficiency were evident; however, the PFC response was reduced when -Cu treatment was extended to 5 wk and was reversible by switching to +Cu treatment. Splenocyte reactivity to B- and T-cell mitogens was not greatly different between groups. Incorporation of thymidine into DNA in the absence of mitogen was higher in -Cu mice. It is evident that severity of copper deficiency is related to degree of impaired immunity. Furthermore, severity of copper deficiency is dependent on duration and time of initiation of dietary copper restriction.

KEY WORDS: • perinatal copper deficiency • mice • mitogen reactivity • antibody production • immunoglobulins

¹ Supported by grant HD 20975 from the National Institutes of Health.

Manuscript received 30 September 1988. Revision accepted 6 March 1989.

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