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糖尿病是否会影响二苯基己三烯渗入红细胞膜空壳?

Does diabetes mellitus affect diphenylhexatriene penetration into erythrocyte membrane ghosts?

作者信息

Watała C, Jóźwiak Z

机构信息

Department of Biophysics, University of łódź, Poland.

出版信息

Biochem Int. 1988 Mar;16(3):529-41.

PMID:3382422
Abstract

Diphenylhexatriene transverse distribution has been studied in normal and diabetic erythrocyte membrane ghosts using fluorescence polarization and fluorescence quenching methods. Acrylamide quenched the fluorescence of diphenylhexatriene according to a dynamic mechanism in agreement with Stern-Volmer equation. Nonlinear least-squares analysis based on quenching results has shown greater accessibility of fluorophore to quencher molecules in diabetic ghosts (37.2 +/- 3.2% in normal vs. 67.5 +/- 6.4% in diabetic membranes). Steady-state fluorescence anisotropy measurements evidenced the lowered membrane lipid fluidity in diabetics (anisotropy values: 0.166 +/- 0.011 in normal subjects vs. 0.193 +/- 0.018 in diabetics). A model mechanism is proposed which attributes the lowered capacity of lipid bilayer in diabetes to the increased ordering and more compact structure of membrane phospholipids. The implications of the results for the resolving of steady-state anisotropy data are discussed.

摘要

已使用荧光偏振和荧光猝灭方法研究了正常和糖尿病红细胞膜空壳中二苯基己三烯的横向分布。丙烯酰胺根据与斯特恩-沃尔默方程一致的动力学机制猝灭二苯基己三烯的荧光。基于猝灭结果的非线性最小二乘法分析表明,在糖尿病膜空壳中荧光团对猝灭剂分子的可及性更高(正常膜中为37.2±3.2%,糖尿病膜中为67.5±6.4%)。稳态荧光各向异性测量证明糖尿病患者的膜脂流动性降低(各向异性值:正常受试者为0.166±0.011,糖尿病患者为0.193±0.018)。提出了一种模型机制,将糖尿病中脂质双层能力的降低归因于膜磷脂有序性增加和结构更紧密。讨论了这些结果对稳态各向异性数据解析的意义。

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