Inhibition of D-galactose and L-phenylalanine transport by HgCl2 in rat intestine in vitro.

Revista espanola de fisiologia Pub Date : 1994-09-01
A Lugea, A Barber, F Ponz
{"title":"Inhibition of D-galactose and L-phenylalanine transport by HgCl2 in rat intestine in vitro.","authors":"A Lugea,&nbsp;A Barber,&nbsp;F Ponz","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The effect of Hg2+ on galactose and phenylalanine uptake has been studied in rat everted intestinal rings incubated for 2 minutes. The presence of 0.5 mM Hg2+ in the incubation medium inhibited the total galactose uptake from 30% to 40% and that of the phenylalanine about 70%. The inhibition was due to a reduction of galactose transport and Na(+)-dependent phenylalanine transport. Hg2+ inhibited the galactose transport in a non-competitive way, with a Vmax diminution without Km modification. The Na(+)-dependent phenylalanine transport was totally blocked in the presence of 1 mM Hg2+. The washing of the intestinal rings with 5 mM EDTA slightly decreased the inhibition produced by 0.5 mM Hg2+ on phenylalanine uptake whereas it did not modify the inhibition of galactose uptake. However, the inhibition of galactose uptake was completely reversed after washing with 10 mM cysteine. Therefore, phenylalanine transport seems to be more sensitive to HgCl2 than galactose transport. The inhibition of these intestinal transport systems by Hg2+ might be due to its interaction with ligands of the transport proteins located in the luminal membrane of enterocytes.</p>","PeriodicalId":21473,"journal":{"name":"Revista espanola de fisiologia","volume":"50 3","pages":"167-73"},"PeriodicalIF":0.0000,"publicationDate":"1994-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Revista espanola de fisiologia","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

The effect of Hg2+ on galactose and phenylalanine uptake has been studied in rat everted intestinal rings incubated for 2 minutes. The presence of 0.5 mM Hg2+ in the incubation medium inhibited the total galactose uptake from 30% to 40% and that of the phenylalanine about 70%. The inhibition was due to a reduction of galactose transport and Na(+)-dependent phenylalanine transport. Hg2+ inhibited the galactose transport in a non-competitive way, with a Vmax diminution without Km modification. The Na(+)-dependent phenylalanine transport was totally blocked in the presence of 1 mM Hg2+. The washing of the intestinal rings with 5 mM EDTA slightly decreased the inhibition produced by 0.5 mM Hg2+ on phenylalanine uptake whereas it did not modify the inhibition of galactose uptake. However, the inhibition of galactose uptake was completely reversed after washing with 10 mM cysteine. Therefore, phenylalanine transport seems to be more sensitive to HgCl2 than galactose transport. The inhibition of these intestinal transport systems by Hg2+ might be due to its interaction with ligands of the transport proteins located in the luminal membrane of enterocytes.

HgCl2体外抑制大鼠肠内d -半乳糖和l -苯丙氨酸转运的研究。
本实验研究了Hg2+对大鼠肠环旋转培养2分钟后半乳糖和苯丙氨酸摄取的影响。0.5 mM Hg2+的存在抑制了半乳糖的总摄取30% ~ 40%,苯丙氨酸的摄取约70%。抑制作用是由于半乳糖转运和Na(+)依赖性苯丙氨酸转运的减少。Hg2+以非竞争性的方式抑制半乳糖转运,在没有Km修饰的情况下降低了Vmax。在1mm Hg2+的存在下,Na(+)依赖的苯丙氨酸转运被完全阻断。用5 mM EDTA洗涤肠环可轻微降低0.5 mM Hg2+对苯丙氨酸摄取的抑制作用,但对半乳糖摄取的抑制作用没有改变。然而,用10毫米半胱氨酸洗涤后,半乳糖摄取的抑制作用完全逆转。因此,苯丙氨酸转运似乎比半乳糖转运对HgCl2更敏感。Hg2+对这些肠道运输系统的抑制可能是由于它与肠细胞腔膜上转运蛋白的配体相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信