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血红素加氧酶1的过表达增加了Caco-2细胞中的铁通量。

Heme oxygenase 1 overexpression increases iron fluxes in caco-2 cells.

作者信息

Mendiburo María José, Flores Sebastián, Pizarro Fernando, Arredondo Miguel

机构信息

Micronutrient Laboratory, Nutrition and Food Technology Institute, Universidad de Chile, Santiago, Chile.

出版信息

Biol Res. 2006;39(1):195-7. doi: 10.4067/s0716-97602006000100023.

DOI:10.4067/s0716-97602006000100023
PMID:16629181
Abstract

Heme oxygenase-1 is a microsomal enzyme that, when induced by stress, protects the cells from oxidative injury. Heme oxygenase-1 participates in the cleavage of the heme ring producing biliverdin, CO and ferrous Fe. The released Fe becomes part of intracellular Fe pool and can be stored in ferritin or released by an iron exporter. The mechanism by which heme enters cells is not completely understood, although it had been suggested that it might be internalized by an endocytosis process. In this study, we expressed a full-length Heme oxygenase-1 cDNA in Caco-2 cells and measured intracellular iron content, heme-iron uptake and transport and immunolocalization of heme oxygenase-1 in these cells. We found that heme oxygenasc-1 expressing cells showed increased apical heme iron uptake and transepithelial transport when compared to control cells. These results suggested that heme oxygenase-1 mediates heme iron influx and efflux in intestinal cells.

摘要

血红素加氧酶-1是一种微粒体酶,在受到应激诱导时,可保护细胞免受氧化损伤。血红素加氧酶-1参与血红素环的裂解,产生胆绿素、一氧化碳和亚铁离子。释放出的铁成为细胞内铁池的一部分,可储存于铁蛋白中或由铁输出蛋白释放。尽管有人提出血红素可能通过内吞作用被内化,但血红素进入细胞的机制尚未完全明确。在本研究中,我们在Caco-2细胞中表达了全长血红素加氧酶-1 cDNA,并测定了这些细胞内的铁含量、血红素铁摄取与转运以及血红素加氧酶-1的免疫定位。我们发现,与对照细胞相比,表达血红素加氧酶-1的细胞顶端血红素铁摄取和跨上皮转运增加。这些结果表明,血红素加氧酶-1介导肠道细胞中血红素铁的流入和流出。

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引用本文的文献

1
Transepithelial heme-iron transport: effect of heme oxygenase overexpression.跨上皮血红素铁转运:血红素加氧酶过表达的影响。
Eur J Nutr. 2011 Aug;50(5):363-71. doi: 10.1007/s00394-010-0144-5. Epub 2010 Nov 16.
2
Caco-2 intestinal epithelial cells absorb soybean ferritin by mu2 (AP2)-dependent endocytosis.Caco-2肠上皮细胞通过依赖于μ2(AP2)的内吞作用吸收大豆铁蛋白。
J Nutr. 2008 Apr;138(4):659-66. doi: 10.1093/jn/138.4.659.