慢性酒精中毒患者红细胞膜蛋白、酶和转运机制的改变：体内和体外研究。

Modification of erythrocyte membrane proteins, enzymes and transport mechanisms in chronic alcoholics: an in vivo and in vitro study.

机构信息

Corresponding author: Department of Biochemistry, Sri Krishnadevaraya University, Anantapur, AP 515055, India.

出版信息

Alcohol Alcohol. 2013 Nov-Dec;48(6):679-86. doi: 10.1093/alcalc/agt071. Epub 2013 Aug 21.

DOI:10.1093/alcalc/agt071

PMID:23966453

Abstract

AIM

The aim of the study was to elucidate the molecular mechanisms underlying the alcohol perturbation leading to deleterious effects on erythrocyte membrane transport in chronic alcoholics.

METHODS

Membrane bound enzyme activities such as Na(+), K(+)-ATPase, Ca(2+),Mg(2+)-ATPase and acetylcholine esterase and membrane transport analysis by in vitro and erythrocyte membrane profile analysis in controls and chronic alcoholic red cells were analyzed.

RESULTS

It was observed that decreased Na(+), K(+)-ATPase enzyme activity and increased activities of Ca(2+),Mg(2+)-ATPase and acetylcholine esterase in chronic alcoholics compared to controls. The in vitro studies of erythrocytes suggested that there is an increased uptake of glucose through chronic alcoholic red cells. However, glucose utilization by chronic alcoholic red cells was decreased. An increased sensitivity of ouabain for its binding site on Na(+), K(+)-ATPase in chronic alcoholic erythrocyte membrane was evident from this study. Though there appears to be an increased Na(+) influx in chronic alcoholic cells, the status of Na(+) transport is not altered much. However, ouabain caused slight disturbances in the transport of sodium, similar disturbances in the potassium transport resulting in much accumulation of potassium in red cells.

CONCLUSIONS

It was concluded that chronic alcohol consumption modified certain membrane bound proteins, enzymes and transport mechanisms in chronic alcoholics.

摘要

目的

本研究旨在阐明导致慢性酒精中毒患者红细胞膜转运受损的酒精干扰的分子机制。

方法

分析了对照组和慢性酒精中毒患者红细胞中膜结合酶活性（如 Na(+)、K(+)-ATP 酶、Ca(2+)、Mg(2+)-ATP 酶和乙酰胆碱酯酶）和膜转运，并进行体外分析和红细胞膜谱分析。

结果

与对照组相比，慢性酒精中毒患者的 Na(+)、K(+)-ATP 酶活性降低，Ca(2+)、Mg(2+)-ATP 酶和乙酰胆碱酯酶活性升高。对红细胞的体外研究表明，慢性酒精中毒的红细胞通过增加葡萄糖的摄取。然而，慢性酒精中毒的红细胞葡萄糖利用率降低。本研究表明，慢性酒精中毒红细胞膜上的 Na(+)、K(+)-ATP 酶对哇巴因结合位点的亲和力增加。尽管慢性酒精中毒细胞中似乎有更多的钠离子内流，但钠离子转运的状态并没有太大改变。然而，哇巴因对钠转运造成了轻微的干扰，钾转运也受到类似的干扰，导致钾在红细胞中大量积累。