United States Department of Agriculture, Science and Education Administration, Human Nutrition Laboratory, University of North Dakota, 58201, Grand Forks, North Dakota.
Biol Trace Elem Res. 1979 Dec;1(4):325-35. doi: 10.1007/BF02778834.
The interaction between nickel and iron was confirmed in rat metabolism. In a fully-crossed, two-way, three by four, factorially designed experiment, female weanling rats were fed a basal diet supplemented with iron at 0, 25, 50, and 100 μg/g and with nickel at 0, 5, and 50 μg/g. The basal diet contained about 10 ng of nickel and 2.3 μg of iron/g. After nine weeks, dietary iron affected growth, hematocrit, hemoglobin, plasma cholesterol, and in liver affected total lipids, phospholipids, and the contents of copper, iron, manganese, and zinc. By manipulating the iron content of the diet, effects of dietary nickel were shown in rats that were not from dams fed a nickel-deprived diet. Nickel affected growth, hematocrit, hemoglobin, plasma alkaline phosphatase activity, plasma total lipids, and in liver affected total lipids, and the contents of copper, manganese, and nickel. The interaction between nickel and iron affected hematocrit, hemoglobin, plasma alkaline phosphatase activity, and plasma phospholipids, and in liver affected size, content of copper, and perhaps of manganese and nickel. In severely iron-deficient rats, the high level of dietary nickel partially alleviated the drastic depression of hematocrit and hemoglobin, and the elevation of copper in liver. Simultaneously, high dietary nickel did not increase the iron level in liver and was detrimental to growth and appearance of severely iron-deficient rats. In nickel-deprived rats fed the borderline iron-deficient diet (25 μg/g) hematocrit and hemoglobin also were depressed. However, 5 μg Ni/g of diet were just as effective as 50 μg Ni/g of diet in preventing those signs of nickel deprivation. The findings in the present study suggested that nickel and iron interact with each other at more than one locus.
镍和铁在大鼠代谢中的相互作用得到了证实。在一项完全交叉的、双向的、三因素四水平的析因设计实验中，雌性断乳大鼠被喂食基础饮食，该基础饮食补充了 0、25、50 和 100μg/g 的铁和 0、5 和 50μg/g 的镍。基础饮食中约含有 10ng 镍和 2.3μg 铁/g。九周后，饮食铁影响了生长、红细胞压积、血红蛋白、血浆胆固醇以及肝脏中的总脂质、磷脂和铜、铁、锰和锌的含量。通过操纵饮食中铁的含量，展示了在不喂食镍缺乏饮食的母鼠所生的大鼠中，饮食镍的影响。镍影响了生长、红细胞压积、血红蛋白、血浆碱性磷酸酶活性、血浆总脂质以及肝脏中的总脂质，还影响了铜、锰和镍的含量。镍和铁之间的相互作用影响了红细胞压积、血红蛋白、血浆碱性磷酸酶活性和血浆磷脂，还影响了肝脏的大小、铜的含量，以及锰和镍的含量。在严重缺铁的大鼠中，高剂量的饮食镍部分缓解了红细胞压积和血红蛋白的急剧下降以及肝脏中铜的升高。同时，高剂量的饮食镍并没有增加肝脏中铁的水平，并且对严重缺铁的大鼠的生长和外观有害。在喂食边缘缺铁饮食（25μg/g）的镍缺乏大鼠中，红细胞压积和血红蛋白也降低了。然而，饮食中 5μg Ni/g 的镍与饮食中 50μg Ni/g 的镍一样有效，可预防这些镍缺乏的迹象。本研究的结果表明，镍和铁在一个以上的基因座上相互作用。
