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[在脂质过氧化激活过程中α-生育酚对突触体的稳定作用机制]

[Mechanism of the stabilization of synaptosomes with alpha-tocopherol during activation of lipid peroxidation].

作者信息

Davitashvili N G, Erin A N, Prilipko L L

出版信息

Biokhimiia. 1986 Mar;51(3):472-7.

PMID:3697420
Abstract

Using the fluorescent probe technique, it was shown that activation of lipid peroxidation decreases the value of transmembrane potential of rat brain synaptosomes. Depolarization of synaptosomes may be due to the impairment of the "barrier" properties of synaptosomal membranes and the decrease in Na,K-ATPase activity. alpha-Tocopherol and its model derivative devoid of the phytol chain--2,2,5,7,8-pentamethyl-6-oxychromanol--stabilize the transmembrane potential value during inhibition of lipid peroxidation. alpha-Tocopherol acetate causes no stabilizing or inhibiting effects. Unlike 2,2,5,7,8-pentamethyl-6-oxychromanol, alpha-tocopherol exerts a structuralizing action which manifests itself in the stabilization of the synaptosomal membrane potential during incomplete inhibition of lipid peroxidation. The previously established ability of alpha-tocopherol to protect synaptosomes from the damaging action of phospholipases and the experimental results of this work permit to regard vitamin E as a universal stabilizer of brain synaptosomal membranes.

摘要

运用荧光探针技术表明,脂质过氧化的激活会降低大鼠脑突触体跨膜电位的值。突触体的去极化可能是由于突触体膜“屏障”特性受损以及钠钾-ATP酶活性降低所致。α-生育酚及其不含叶绿醇链的模型衍生物——2,2,5,7,8-五甲基-6-氧代色满醇——在脂质过氧化受抑制期间可稳定跨膜电位值。α-生育酚乙酸酯无稳定或抑制作用。与2,2,5,7,8-五甲基-6-氧代色满醇不同,α-生育酚具有一种结构化作用,这种作用在脂质过氧化未完全受抑制期间突触体膜电位的稳定中得以体现。先前已证实α-生育酚具有保护突触体免受磷脂酶破坏作用的能力,以及本研究的实验结果,这使得我们可以将维生素E视为脑突触体膜的通用稳定剂。

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