Black C, Glass J, Nunez M T, Robinson S H
J Lab Clin Med. 1979 Apr;93(4):645-51.
Three aspects of iron metabolism were studies in reticulocytes from iron-deficient, phlebotomized, and phenylhydrazine-treated rats: (1) the number of transferrin binding sites; (2) the uptake of 59Fe-transferrin; and (3) the ability of cytosol to mobilize 59Fe from 59Fe-labeled reticulocyte plasma membrane. The number of transferrin binding sites, assayed by measuring the binding of 125I-labeled transferrin to reticulocytes, were similar in iron-deficient and phlebotomy-induced reticulocytes, 66,000 and 75,000 binding sites/cell, respectively, but were about doubled, 120,000 binding sites/cell, in phenylhydrazine-induced reticulocytes. Uptake of 59Fe into iron-deficient reticulocytes was about one-half that for phlebotomy-induced reticulocytes and one-quarter that for phenylhydrazine-induced reticulocytes, the rates of uptake being measured as 21,540, 41,233, and 79,600 molecules of 59Fe per minute per cell, respectively. The mobilizing activity of cytosol free iron-deficient reticulocytes was also about one-half that of cytosol from phlebotomy-induced reticulocytes and about one-quarter that of cytosol from phenylhydrazine-induced reticulocytes. These results indicate that instead of a compensatory increase in these aspects of iron metabolism, the iron-deficient reticulocyte had a decreased ability to transport iron.
对缺铁、放血和用苯肼处理的大鼠网织红细胞的铁代谢三个方面进行了研究：（1）转铁蛋白结合位点的数量；（2）59Fe-转铁蛋白的摄取；（3）细胞溶质从59Fe标记的网织红细胞质膜中动员59Fe的能力。通过测量125I标记的转铁蛋白与网织红细胞的结合来测定转铁蛋白结合位点的数量，缺铁和放血诱导的网织红细胞中的数量相似，分别为66,000和75,000个结合位点/细胞，但在苯肼诱导的网织红细胞中约增加一倍，为120,000个结合位点/细胞。缺铁网织红细胞对59Fe的摄取约为放血诱导的网织红细胞的一半，为苯肼诱导的网织红细胞的四分之一，摄取速率分别测定为每分钟每细胞21,540、41,233和79,600个59Fe分子。缺铁网织红细胞的细胞溶质游离铁的动员活性也约为放血诱导的网织红细胞细胞溶质的一半，为苯肼诱导的网织红细胞细胞溶质的四分之一。这些结果表明，缺铁网织红细胞在这些铁代谢方面没有代偿性增加，而是运输铁的能力下降。
