Mulhern S A, Raveche E S, Smith H R, Lal R B
Division of Nutrition, Food and Drug Administration, Washington, DC 20204.
Am J Clin Nutr. 1987 Dec;46(6):1035-9. doi: 10.1093/ajcn/46.6.1035.
NZB mice were exposed from birth to a diet either adequate or deficient in copper. By age 6 wk the mice exposed to the copper-deficient diet showed symptoms characteristic of copper deficiency (anemia, hypoceruloplasminemia, and achromatrichia). The splenic lymphocytes from the copper-deficient group had reduced numbers of cells expressing the following surface markers: Ly-5, Ly-1, B-220, and sIg. Less than 10% of the splenic lymphocytes in this group were cycling, as determined by flow cytometry analysis. The spontaneous 96-h anti-ss-DNA levels in the copper-deficient group were lower than those in the control group. The exogenous colony-forming units (CFUs) were significantly enhanced in the copper-deficient mice. The decreased splenic lymphoid populations, decreased anti-ss-DNA titers, and increased exogenous CFUs in the copper-deficient mice appear to be due to an increase in erythropoiesis at the expense of lymphopoiesis.
从出生起，将NZB小鼠置于铜含量充足或缺乏的饮食环境中。到6周龄时，食用缺铜饮食的小鼠出现了铜缺乏的典型症状（贫血、低铜蓝蛋白血症和毛发褪色）。缺铜组脾脏淋巴细胞表达以下表面标志物的细胞数量减少：Ly-5、Ly-1、B-220和表面免疫球蛋白。通过流式细胞术分析确定，该组脾脏淋巴细胞中循环细胞不到10%。缺铜组的自发96小时抗单链DNA水平低于对照组。缺铜小鼠的外源性集落形成单位（CFU）显著增加。缺铜小鼠脾脏淋巴细胞群体减少、抗单链DNA滴度降低以及外源性CFU增加，似乎是由于以淋巴细胞生成减少为代价的红细胞生成增加所致。
