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Low-molecular-mass iron complexes in blood plasma of iron-deficient pigs do not originate directly from nutrient iron.
Metallomics ( IF 3.4 ) Pub Date : 2019-10-11 , DOI: 10.1039/c9mt00152b
Nathaniel Dziuba 1 , Joanne Hardy 2 , Paul A Lindahl 3
Affiliation  

Nutrient iron entering the blood binds transferrin (TFN)d, which delivers iron to cells in the body. In healthy individuals, ∼30% of TFN is iron-bound while the remainder is unbound (apo-TFN). TFN saturates the plasma of individuals with iron-overload diseases such as hereditary hemochromatosis, prompting release of a poorly-defined low-molecular-mass (LMM) iron species called non-transferrin-bound iron (NTBI). An experiment was devised to directly detect NTBI in plasma of iron-deficient pigs and to assess the role of the liver which is known to bind NTBI. Catheters were surgically installed in the portal vein (PV) and either the caudal vena cava or the cranial vena cava. After the animals recovered, 57Fe II ascorbate was injected into the stomach via a feeding tube. Blood was removed through the catheters before and after injection; plasma became 57Fe-enriched after injection. 57Fe-enriched plasma was passed through a 10 kDa cutoff membrane and the flow-through solution (FTS) was subjected to size-exclusion liquid chromatography (LC). The eluent flowed into an ICP-MS where 56Fe and 57Fe were detected. Low-intensity iron peaks with masses of 400–1600 Da were observed, but none became enriched in 57Fe after injection. Rather, the injected 57Fe bound to apo-TFN. Viewed naively, this implies that nutrient-derived 57Fe in healthy mammals passes from the intestines to apo-TFN without first entering the blood as a LMM intermediate. In this case, nutrient iron exported from intestinal enterocytes of healthy individuals may quickly bind apo-TFN such that LMM iron species do not accumulate in blood plasma. Some 57Fe from the FTS may have adsorbed onto the column. In any event, the LMM iron species in plasma that eluted from the column must have originated from iron stored within the body, perhaps in macrophages – not directly from nutrient iron absorption. The liver absorbed and released LMM iron species, but the effect was modest, consistent with its role as a dynamic iron buffer. Passage through the liver also altered the distribution of different forms of TFN present in the PV.

中文翻译:

缺铁猪血浆中的低分子质量铁络合物并不直接来自营养铁。

进入血液的营养铁与转铁蛋白 (TFN) d结合,将铁输送到体内的细胞。在健康个体中,约 30% 的 TFN 与铁结合,而其余部分则未结合 (apo-TFN)。TFN 使患有铁超载疾病(例如遗传性血色素沉着病)的个体的血浆饱和,促使释放一种定义不明确的低分子质量(LMM)铁物质,称为非转铁蛋白结合铁(NTBI)。设计了一项实验来直接检测缺铁猪血浆中的 NTBI,并评估已知结合 NTBI 的肝脏的作用。通过手术将导管安装在门静脉(PV)和尾腔静脉或颅腔静脉中。动物康复后,通过饲管将57 Fe II 抗坏血酸注射入胃中。注射前后通过导管除去血液;注射后血浆变得富含57 Fe。使富含57 Fe 的血浆通过 10 kDa 截止膜,并对流通溶液 (FTS) 进行尺寸排阻液相色谱 (LC) 分析。洗脱液流入ICP-MS,检测到56 Fe 和57 Fe。观察到质量为 400-1600 Da 的低强度铁峰,但注射后没有富集57 Fe。相反,注入的57 Fe 与 apo-TFN 结合。简单地看,这意味着健康哺乳动物中营养来源的57 Fe 从肠道传递到 apo-TFN,而没有首先作为 LMM 中间体进入血液。在这种情况下,从健康个体的肠细胞输出的营养铁可以快速结合apo-TFN,使得LMM铁物质不会在血浆中积累。FTS 中的一些57 Fe 可能已吸附到色谱柱上。无论如何,从柱中洗脱出来的血浆中的 LMM 铁物质必定源自体内储存的铁,可能是巨噬细胞中的铁,而不是直接来自营养铁吸收。肝脏吸收并释放 LMM 铁物质,但效果不大,与其作为动态铁缓冲剂的作用一致。通过肝脏还改变了 PV 中不同形式的 TFN 的分布。
更新日期:2019-10-11
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