Manganese metabolism is impaired in the Belgrade laboratory rat

Manganese metabolism is impaired in the Belgrade laboratory rat
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DOI:
10.1007/s003600050085
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发表时间:
1997-07-01
期刊:
JOURNAL OF COMPARATIVE PHYSIOLOGY B-BIOCHEMICAL SYSTEMIC AND ENVIRONMENTAL PHYSIOLOGY
影响因子:
--
通讯作者:
Morgan, EH
Morgan, EH
中科院分区:
其他
文献类型:
--
作者:
Chua, ACG;Morgan, EH

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纯合子贝尔格莱德大鼠具有低色素性贫血,这是由于通过未成熟红系细胞的细胞膜的铁转运受损。本研究旨在探讨红系细胞和其他类型细胞中是否也存在锰代谢异常。实验用纯合子(双B)和杂合子(+/B)Belgrade大鼠和Wistar大鼠进行,包括体外网织红细胞对锰的吸收,十二指肠原位闭合袢对锰的吸收,静脉注射与转铁蛋白(Tf)结合或与血清混合的放射性Mn后,血浆清除和几个器官的摄取。在几个实验中,用Fe-59标记的Fe进行了类似的测量,与+/B或Wistar大鼠相比,bb大鼠网织红细胞的Mn摄取和十二指肠的Mn吸收受损。Mn-Tf的血浆清除比Mn-血清慢得多,但两者都快于Fe-Tf的清除。B/B大鼠肾脏、大脑和股骨对Mn-54的摄取低于Wistar或+/B大鼠,但在双B大鼠中,肝脏对Mn-54的摄取更大。肾脏、大脑和股骨对Fe-59的吸收也存在类似的差异,但肝脏对Fe-59的吸收也受损。结论:B/B大鼠的遗传异常影响了Mn和Fe的代谢,Mn和Fe在红系组织、十二指肠粘膜细胞中具有相似的转运机制。肾和血脑屏障。
Homozygous Belgrade rats have a hypochromic anaemia due to impaired iron transport across the cell membrane of immature erythroid cells. This study aimed at investigating whether there are also abnormalities of Mn metabolism in erythroid and other types of cells, The experiments were performed with homozygous (bib) and heterozygous (+/b) Belgrade rats and Wistar rats and included measurements of Mn uptake by reticulocytes in vitro, Mn absorption from in situ closed loops of the duodenum, and plasma clearance and uptake by several organs after intravenous injection of radioactive Mn bound to transferrin (Tf) or mixed with serum. Similar measurements were made with Fe-59-labelled Fe in several of the experiments, Mn uptake by reticulocytes and absorption from the duodenum was impaired in bb rats compared with +/b or Wistar rats. The plasma clearance of Mn-Tf was much slower than Mn-serum, but both were faster than the clearance of Fe-Tf. Uptake of Mn-54 by the kidneys, brain and femurs was less in b/b than Wistar or +/b rats, but uptake by the liver was greater in bib rats. Similar differences were found for Fe-59 uptake by kidneys, brain and femurs but Fe-59 uptake by the liver was also impaired in the liver. II is concluded that the genetic abnormality present in b/b rats affects Mn metabolism as well as Fe metabolism and that Mn and Fe share similar transport mechanisms in the cells of erythroid tissue, duodenal mucosa. kidney and blood-brain barrier.