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镍在人肠道Caco-2细胞单层中的转运。

Transport of nickel across monolayers of human intestinal Caco-2 cells.

作者信息

Tallkvist J, Tjälve H

机构信息

Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, SE-751 23, Sweden.

出版信息

Toxicol Appl Pharmacol. 1998 Jul;151(1):117-22. doi: 10.1006/taap.1998.8453.

DOI:10.1006/taap.1998.8453
PMID:9705894
Abstract

The passage of nickel across monolayers of intestinal epithelial Caco-2 cells, originally derived from a human colonic adenocarcinoma, was studied in bicameral chambers. The results showed that the transport and accumulation of nickel were depressed in iron-loaded monolayers, indicating that the metal participates in an absorptive process for iron in the Caco-2 cells. No detectable transport of nickel in either the apical to basal or basal to apical direction occurred at 4 degreesC. Since cellular metabolism is inhibited at 4 degreesC, these data indicate that there is no passive transcellular or paracellular passage of the nickel across the monolayers. Studies in ATP-depleted monolayers showed an increased permeability of nickel, and concomitantly there was a similar increase in the permeability of the paracellular marker mannitol. These results indicate that the metabolic inhibition results in a loosening of the junctional complexes between the Caco-2 cells, resulting in a paracellular leakage of the nickel. Additional experiments showed that the transport of nickel in the basal to apical direction occurred at a higher rate than in the apical to basal direction. This indicates the presence of an extrusion mechanism that secretes the nickel from the basal to the apical side of the Caco-2 cells. Studies with Caco-2 cells and in vivo studies by other authors have shown similar results for other metals, indicating that colonic epithelial cells may have the ability to secrete some metals.

摘要

在双室培养箱中研究了镍穿过最初源自人结肠腺癌的肠上皮Caco-2细胞单层的过程。结果表明,铁负载的单层中镍的转运和积累受到抑制,这表明该金属参与了Caco-2细胞中铁的吸收过程。在4℃时,未检测到镍在顶侧到基底或基底到顶侧方向的转运。由于细胞代谢在4℃时受到抑制,这些数据表明镍没有被动跨细胞或细胞旁途径穿过单层。对ATP耗尽的单层的研究表明镍的通透性增加,同时细胞旁标志物甘露醇的通透性也有类似增加。这些结果表明,代谢抑制导致Caco-2细胞之间连接复合体的松散,从而导致镍的细胞旁渗漏。额外的实验表明,镍在基底到顶侧方向的转运速率高于顶侧到基底方向。这表明存在一种将镍从Caco-2细胞的基底侧分泌到顶侧的排出机制。对Caco-2细胞的研究以及其他作者的体内研究表明,其他金属也有类似结果,这表明结肠上皮细胞可能具有分泌某些金属的能力。

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