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首页> 外文期刊>Journal of Cellular Physiology >Non-transferrin-bound iron uptake in Belgrade and normal rat erythroid cells.
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Non-transferrin-bound iron uptake in Belgrade and normal rat erythroid cells.

机译：在贝尔格莱德Non-transferrin-bound铁吸收正常大鼠红细胞细胞。

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Belgrade (b) rats have an autosomal recessive, microcytic, hypochromic anemia. Transferrin (Tf)-dependent iron uptake is defective because of a mutation in DMT1 (Nramp2), blocking endosomal iron efflux. This experiment of nature permits the present study to address whether the mutation also affects non-Tf-bound iron (NTBI) uptake and to use NTBI uptake compared to Tf-Fe utilization to increase understanding of the phenotype of the b mutation. The distribution of 59Fe2+ into intact erythroid cells and cytosolic, stromal, heme, and nonheme fractions was different after NTBI uptake vs. Tf-Fe uptake, with the former exhibiting less iron into heme but more into stromal and nonheme fractions. Both reticulocytes and erythrocytes exhibit NTBI uptake. Only reticulocytes had heme incorporation after NTBI uptake. Properly normalized, incorporation into b/b heme was approximately 20% of +/b, a decrease similar to that for Tf-Fe utilization. NTBI uptake into heme was inhibited by bafilomycin A1, concanamycin, NH4Cl, or chloroquine, consistent with the endosomal location of the transporter; cellular uptake was uninhibited. NTBI uptake was unaffected after removal of Tf receptors by Pronase or depletion of endogenous Tf. Concentration dependence revealed that NTBI uptake into cells, cytosol, stroma, and the nonheme fraction had an apparent low affinity for iron; heme incorporation behaved like a high-affinity process, as did an expression assay for DMT1. DMT1 serves in both apparent high-affinity NTBI membrane transport and the exit of iron from the endosome during Tf delivery of iron in rat reticulocytes; the low-affinity membrane transporter, however, exhibits little dependence on DMT1.
机译：贝尔格莱德(b)老鼠有一个常染色体隐性,小红细胞的,着色不足的贫血。(Tf)端依赖铁吸收是有缺陷的,因为突变的DMT1 (Nramp2)阻塞endosomal铁流出。是否允许当前研究地址突变也会影响non-Tf-bound铁(NTBI)吸收和使用比Tf-Fe NTBI吸收利用率增加的理解表型的突变。59价成完整红细胞细胞和胞质,基质、血红素和nonheme分数不同NTBI吸收与Tf-Fe吸收后,前者表现出更少的血红素铁但基质和nonheme分数。网织红细胞和红细胞展览NTBI吸收。后NTBI吸收。纳入b / b血红素大约是20%+ / b的减少Tf-Fe类似的利用率。通过bafilomycin A1、concanamycin NH4Cl,或氯喹、与endosomal一致转运体的位置;不受约束。删除Tf受体链霉蛋白酶或损耗内生的特遣部队。透露,NTBI吸收进细胞,胞质,基质,nonheme分数有明显低铁的亲和力;像一个高亲和性的过程,做了一个DMT1表达测定。明显的高亲和性NTBI膜运输和退出的铁核内体在Tf交付在鼠网织红细胞铁;然而,低亲和力膜转运体展品小DMT1的依赖。

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