Ponka P, Schulman H M
J Biol Chem. 1985 Nov 25;260(27):14717-21.
Fe-salicylaldehyde isonicotinoylhydrazone (SIH), which can donate iron to reticulocytes without transferrin as a mediator, has been utilized to test the hypothesis that the rate of iron uptake from transferrin limits the rate of heme synthesis in erythroid cells. Reticulocytes take up 59Fe from [59Fe]SIH and incorporate it into heme to a much greater extent than from saturating concentrations of [59Fe]transferrin. Also, Fe-SIH stimulates [2-14C]glycine into heme when compared to the incorporation observed with saturating levels of Fe-transferrin. In addition, delta-aminolevulinic acid does not stimulate 59Fe incorporation into heme from either [59Fe]transferrin or [59Fe]SIH but does reverse the inhibition of 59Fe incorporation into heme caused by isoniazid, an inhibitor of delta-aminolevulinic acid synthase. Taken together, these results suggest the hypothesis that some step(s) in the pathway of iron from extracellular transferrin to intracellular protoporphyrin limits the overall rate of heme synthesis in reticulocytes.
铁-水杨醛异烟酰腙（SIH）能够在没有转铁蛋白作为介质的情况下将铁提供给网织红细胞，已被用于检验以下假说：从转铁蛋白摄取铁的速率限制了红细胞系细胞中血红素合成的速率。网织红细胞从[59Fe]SIH摄取59Fe并将其掺入血红素的程度比从饱和浓度的[59Fe]转铁蛋白中摄取并掺入的程度要大得多。此外，与在饱和水平的铁-转铁蛋白观察到的掺入情况相比，Fe-SIH能刺激[2-14C]甘氨酸掺入血红素。另外，δ-氨基乙酰丙酸既不刺激59Fe从[59Fe]转铁蛋白或[59Fe]SIH掺入血红素，但确实能逆转由δ-氨基乙酰丙酸合酶抑制剂异烟肼引起的59Fe掺入血红素的抑制作用。综上所述，这些结果提示了这样一个假说：从细胞外转铁蛋白到细胞内原卟啉的铁转运途径中的某些步骤限制了网织红细胞中血红素合成的总体速率。
