Zhan H, Pollack S, Weaver J
Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461.
Am J Hematol. 1989 Jul;31(3):203-7. doi: 10.1002/ajh.2830310311.
Transferrin donates iron to reticulocytes as follows: it binds to a receptor on the reticulocyte surface; the complex is endocytosed; both irons are released and the transferrin is recycled to the cell exterior. It has been proposed that the trigger for iron release after transferrin endocytosis is acidification of the endocytic vesicle. But this could account for removal of only one of transferrin's two irons, since only one of the irons is labile at acid pH. Moreover, iron continues to be removed from transferrin when acidification of the vesicle is blocked by a chloride-transport inhibitor. Thus a detailed explanation of iron removal from transferrin remains elusive. In earlier work we showed that iron can be removed from transferrin by whole hemolysates and also by the combined action of hemoglobin and ATP at pH 7. We now show that the iron released from transferrin by hemolysates, and by hemoglobin and ATP, is in the Fe(II) oxidation state. We also show that ADP and DPG can substitute for ATP and that NADH and NADPH can substitute for the hemoglobin, although with these substitutions Fe(II) is generated less efficiently. The reductive release of iron from transferrin is rapid enough to account for all the iron processed by a young reticulocyte. We speculate that transferrin iron may be reduced to Fe(II) before reaching the mitochondria.
它与网织红细胞表面的受体结合；该复合物被内吞；两个铁原子都被释放，转铁蛋白被循环回到细胞外。有人提出，转铁蛋白内吞后铁释放的触发因素是内吞小泡的酸化。但这只能解释转铁蛋白两个铁原子中的一个被去除，因为在酸性pH条件下只有一个铁原子不稳定。此外，当小泡酸化被氯化物转运抑制剂阻断时，铁仍会持续从转铁蛋白中被去除。因此，关于转铁蛋白中铁去除的详细解释仍然难以捉摸。在早期的研究中，我们表明全血裂解物以及血红蛋白和ATP在pH 7时的联合作用都可以从转铁蛋白中去除铁。我们现在表明，由血裂解物、血红蛋白和ATP从转铁蛋白中释放的铁处于亚铁（Fe(II)）氧化态。我们还表明，ADP和DPG可以替代ATP，NADH和NADPH可以替代血红蛋白，尽管有这些替代时Fe(II)的生成效率较低。从转铁蛋白中还原性释放铁的速度足够快，足以解释年轻网织红细胞处理的所有铁。我们推测，转铁蛋白中的铁在到达线粒体之前可能会被还原为Fe(II)。
