Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat
Effects of iron deficiency and iron overload on manganese uptake and deposition in the brain and other organs of the rat
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DOI：
10.1007/bf02784167
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发表时间：
1996-10-01
影响因子：
3.9
通讯作者：
Morgan, EH
中科院分区：
文献类型：
--
作者：
Chua, ACG;Morgan, EH
锰在低浓度时是一种必需的微量元素，但在高浓度时具有神经毒性。它具有几种类似铁(Fe)的化学和生化特性，而且有证据表明这两种金属之间存在代谢相互作用，特别是在肠道吸收的水平上。这项研究的目的是确定在大鼠大脑和其他器官从血浆中摄取的过程中，锰和铁是否相互作用。从妊娠第18~19天开始，饲喂对照组(70mgFe/kg)、缺铁(5~10mgFe/kg)和加铁(20g羰基铁/kg)饲料，加或不加含锰饮用水(2g锰/L)，断奶后继续饲喂相同的饮食方案。测定了15和63日龄大鼠的脑、肝、肾中的锰和非血红素铁水平，以及这些器官和股骨对血浆中的锰-54和铁-59的摄取。器官中非血红素铁的水平远高于锰的水平，肝脏和肾脏中的非血红素铁水平随着铁负荷的增加而增加。然而，在大脑中，锰的增加更大。铁缺乏和铁负荷均导致15d/只大鼠脑内锰浓度升高，而铁负荷在63d时也有这种作用，锰负荷对非血红素铁浓度没有显著影响。与以二铁转铁蛋白形式注射的Fe-59相比，以MnCl2与血清混合的形式注射的Mn-54从循环中清除得更快。在15天龄大鼠中，脑、肝、肾和股骨对锰-54的摄取随铁负荷的增加而增加，而63天龄大鼠则未见此现象。补充锰可增加对照组和缺铁组大鼠脑、肝、肾对Fe-59的摄取，但对缺铁组大鼠无明显影响。结论是，锰和铁在从血浆转移到脑和其他器官的过程中相互作用，这种相互作用本质上是协同的，而不是竞争的。因此，过量摄入铁和锰可能会加剧一种金属单独造成组织损伤的风险，特别是在大脑中。
Manganese (Mn) is an essential trace element at low concentrations, but at higher concentrations is neurotoxic. It has several chemical and biochemical properties similar to iron (Fe), and there is evidence of metabolic interaction between the two metals, particularly at the level of absorption from the intestine. The aim of this investigation was to determine whether Mn and Fe interact during the processes involved in uptake from the plasma by the brain and other organs of the rat. Dams were fed control (70 mg Fe/kg), Fe-deficient (5-10 mg Fe/kg), or Fe-loaded (20 g carbonyl Fe/kg) diets, with or without Mn-loaded drinking water (2 g Mn/L), from day 18-19 of pregnancy, and, after weaning the young rats, were continued on the same dietary regimens. Measurements of brain, liver, and kidney Mn and nonheme Fe levels, and the uptake of Mn-54 and Fe-59 from the plasma by these organs and the femurs, were made when the rats were aged 15 and 63 d. Organ nonheme Fe levels were much higher than Mn levels, and in the liver and kidney increased much more with Fe loading than did Mn levels with Mn loading. However, in the brain the increases were greater for Mn. Both Fe depletion and loading led to increased brain Mn concentrations in the 15-d/rats, while Fe loading also had this effect at 63 d. Mn loading did not have significant effects on the nonheme Fe concentrations. Mn-54, injected as MnCl2 mixed with serum, was cleared more rapidly from the circulation than was Fe-59, injected in the form of diferric transferrin. In the 15-d-rats, the uptake of Mn-54 by brain, liver, kidneys, and femurs was increased by Fe loading, but this was not seen in the 63-d rats. Mn supplementation led to increased Fe-59 uptake by the brain, Liver, and kidneys of the rats fed the control and Fe-deficient diets, but not in the Fe-loaded rats. It is concluded that Mn and Fe interact during transfer from the plasma to the brain and other organs and that this interaction is synergistic rather than competitive in nature. Hence, excessive intake of Fe plus Mn may accentuate the risk of tissue damage caused by one metal alone, particularly in the brain.