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Study on pathogenesis of urolithiasis with special reference to oxalate handling in biomembranes

尿石症发病机制的研究，特别是生物膜中草酸盐的处理

基本信息

批准号：
02807148
负责人：
KAWAMURA Juichi
金额：
$ 1.02万
依托单位：
Mie University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1991
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-02807148/
关键词：
Oxalate Red Blood Cell Membrane Oxalate Influx Rate Renal Proximal Tubule Brush Border and Basolateral Membrane Vesicles Intestinal Epithelial Membrane Vesicles Sodium-Oxalate Cotransport System Oxalate : Bicarbonate Exchange System 輸送系

项目摘要

In this study we investigated mechanisms of oxalate transport in red blood cell membrane, intestinal and renal epithelial membranes which relate to oxalate absorption and excretion.1. Oxalate influx rate in red blood cell membrane increased in calcium oxalate stone formers compared to that in healthy controls. This influx was inhibited by an inhibitor of anion exchange system such as DIDS.2. There are oxalate : OH^- exchange and oxalate : HCO_3^- exchange systems both in the brush border membrane vesicles of the intraluminal side and in the basolateral membrane vesicles of the contraluminal side, in the renal proximal tubule Oxalate : OH^- exchange system shares the common transport pathway with oxalate : HCO_3^- exchange system.3. Oxalate absorption is accelerated by an increment of sodium concentration in the intestinal epithelial cells, suggesting the existence of sodium-oxalate cotransport system in the intestine. This result coincides with the fact that urinary oxalate excretion is exaggerated by adding sodium chloride during oxalate loading test.An increased oxalate influx rate in red blood cell membrane in calcium oxalate stone formers may share the common abnormality in biomembrane with the intestinal epithelium where oxalate absorption increases and with the renal epithelium where oxalate excretion increases.Further investigations are required to analyse an abnormal transporter of oxalate within cells in calcium oxalate stone formers.

在这项研究中，我们研究了草酸在红细胞膜、肠上皮膜和肾上皮膜中的转运机制，这些机制与草酸的吸收和排泄有关。草酸钙结石患者红细胞膜草酸内流速度较正常对照组增加。这种内流被阴离子交换系统的抑制剂如DIDS2所抑制。在肾小管近端小管草酸：羟基交换系统和草酸：HCO3+交换系统中，在管腔内侧刷状缘膜泡和对侧基外侧膜泡中均存在草酸：羟基交换和草酸：HCO3+交换系统。肠道上皮细胞对草酸的吸收随着钠浓度的增加而加快，提示肠道中存在钠-草酸共转运系统。这一结果与在草酸盐负荷试验中加入氯化钠会放大尿液草酸排泄的事实相吻合。草酸钙结石患者红细胞膜草酸内流速度增加可能与草酸盐吸收增加的肠上皮和草酸排泄增加的肾上皮具有共同的生物膜异常。草酸钙结石患者细胞内草酸转运异常的分析有待进一步研究。