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Chronic Dietary Copper Deficiency Alters Biochemical and Morphological Properties of Mouse Lymphoid Tissues¹

Departments of Biochemistry, Biomedical Anatomy and Medical Microbiology & Immunology, School of Medicine, University of Minnesota, Duluth, Duluth, MN 55812

Chronic copper deficiency in mice impairs both humoral and cellmediated immunity, but the mechanisms are unknown. Copper deficiency was produced in C58 mice by feeding dams a diet low in copper throughout lactation and weaning the pups to this diet. Control mice were from dams fed the same diet but with copper supplementation in the drinking water. Six-week-old mice were sampled for biochemical and morphological studies. Compared to copper-supplemented mice, copper-deficient animals were smaller, anemic and exhibited hypoceruloplasminemia. The copper-deficient mice have small thymus glands, enlarged spleens, and livers equivalent in size to copper-supplemented mice. Thymic atrophy is not caused by elevated serum corticosterone. Liver, spleen, and thymus tissues from copper-deficient mice exhibit low cytochrome oxidase (56, 38, and 45%, respectively) and superoxide dismutase activities (61, 60, and 43%, respectively) compared to tissues from copper-supplemented mice, indicating a functional copper deficiency. Electron micrographs taken of thymus and spleen from copper-deficient mice demonstrate altered morphology characterized by abnormal mitochondria and misshapen nuclei. Chronic copper deficiency alters the size, biochemistry and morphology of primary (thymus) and secondary (spleen) lymphoid tissue.

KEY WORDS: • copper-deficient mice • spleen and thymus • cuproenzymes • electron microscopy

¹ Supported by Public Health Service grant HD 15491 and by funds from the University of Minnesota Graduate School.

Manuscript received 26 January 1983.

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