Prohaska J R, Downing S W, Lukasewycz O A
J Nutr. 1983 Aug;113(8):1583-90. doi: 10.1093/jn/113.8.1583.
Chronic copper deficiency in mice impairs both humoral and cell-mediated 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 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.
小鼠慢性铜缺乏会损害体液免疫和细胞介导的免疫，但具体机制尚不清楚。通过在整个哺乳期给母鼠喂食低铜饮食，并在断奶后让幼鼠继续食用这种饮食，从而使C58小鼠产生铜缺乏。对照小鼠来自喂食相同饮食但饮用水中添加了铜的母鼠。对六周龄的小鼠进行生化和形态学研究。与补充铜的小鼠相比，铜缺乏的动物体型较小、贫血且出现血浆铜蓝蛋白血症。铜缺乏的小鼠胸腺较小，脾脏肿大，肝脏大小与补充铜的小鼠相当。胸腺萎缩并非由血清皮质酮升高引起。与补充铜的小鼠的组织相比，铜缺乏小鼠的肝脏、脾脏和胸腺组织的细胞色素氧化酶活性较低（分别为56%、38%和45%），超氧化物歧化酶活性也较低（分别为61%、60%和43%），表明存在功能性铜缺乏。对铜缺乏小鼠的胸腺和脾脏进行电子显微镜检查，结果显示其形态发生改变，特征为线粒体异常和细胞核畸形。慢性铜缺乏会改变初级（胸腺）和次级（脾脏）淋巴组织的大小、生化特性和形态。
