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慢性酒精中毒患者红细胞膜流动性和 Na+/K+-ATP 酶活性的改变。

Alterations in erythrocyte membrane fluidity and Na+/K+ -ATPase activity in chronic alcoholics.

机构信息

Department of Genetics, UT MD Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

Mol Cell Biochem. 2010 Jun;339(1-2):35-42. doi: 10.1007/s11010-009-0367-z. Epub 2010 Jan 3.

Abstract

Ethanol disorders biological membranes causing perturbations in the bilayer and also by altering the physicochemical properties of membrane lipids. But, chronic alcohol consumption also increases nitric oxide (NO) production. There was no systemic study was done related to alcohol-induced production of NO and consequent formation of peroxynitrite mediated changes in biophysical and biochemical properties, structure, composition, integrity and function of erythrocyte membranes in chronic alcoholics. Hence, keeping all these conditions in mind the present study was undertaken to investigate the role of over produced nitric oxide on red cell membrane physicochemical properties in chronic alcoholics. Human male volunteers aged 44 +/- 6 years with similar dietary habits were divided into two groups, namely nonalcoholic controls and chronic alcoholics (~125 g of alcohol at least five times per week for the past 10-12 years). Elevated nitrite and nitrate levels in plasma and lysate, changes in erythrocyte membrane individual phospholipid composition, increased lipid peroxidation, protein carbonyls, cholesterol and phospholipids ratio (C/P ratio) and anisotropic value (gamma) with decreased sulfhydryl groups and Na(+)/K(+)-ATPase activity in alcoholics was evident from this study. RBC lysate NO was positively correlated with C/P ratio (r = 0.547) and anisotropic (gamma) value (r = 0.428), Na(+)/K(+)-ATPase activity was negatively correlated with RBC lysate NO (r = -0.372) and anisotropic (gamma) value (r = -0.624) in alcoholics. Alcohol-induced overproduction of nitric oxide reacts with superoxide radicals to produce peroxynitrite, which appears to be responsible for changes in erythrocyte membrane lipids and the activity of Na(+)/K(+)-ATPase.

摘要

乙醇扰乱生物膜,导致双层结构发生扰动,同时改变膜脂的物理化学性质。但是,慢性酒精摄入也会增加一氧化氮(NO)的产生。目前还没有关于酒精引起的 NO 产生以及随后形成的过氧亚硝酸盐对红细胞膜生物物理和生物化学特性、结构、组成、完整性和功能变化的系统研究。因此,考虑到所有这些情况,本研究旨在探讨过量产生的一氧化氮在慢性酒精中毒患者红细胞膜物理化学特性中的作用。将年龄为 44 +/- 6 岁、饮食习惯相似的男性志愿者分为两组,即非酒精对照组和慢性酒精组(过去 10-12 年每周至少饮用 125 克酒精 5 次以上)。本研究表明,酒精组血浆和裂解物中硝酸盐和亚硝酸盐水平升高,红细胞膜各磷脂组成发生变化,脂质过氧化、蛋白质羰基、胆固醇和磷脂比值(C/P 比值)以及各向异性值(γ)增加,巯基和 Na(+)/K(+)-ATP 酶活性降低。红细胞裂解液中的 NO 与 C/P 比值(r = 0.547)和各向异性(γ)值(r = 0.428)呈正相关,Na(+)/K(+)-ATP 酶活性与 RBC 裂解液中的 NO(r = -0.372)和各向异性(γ)值(r = -0.624)呈负相关。酒精引起的一氧化氮过度产生与超氧自由基反应生成过氧亚硝酸盐,这似乎是导致红细胞膜脂质和 Na(+)/K(+)-ATP 酶活性变化的原因。

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