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[维生素E缺乏诱导游离脂肪酸对脑突触体损伤作用的增强]

[Increase in the damaging effect of free fatty acids on brain synaptosomes induced by vitamin E deficiency].

作者信息

Skrypin V I, Brusovanik V I, Dzhaparidze L M, Erin A N, Selishcheva A A

出版信息

Biull Eksp Biol Med. 1986 Nov;102(11):547-9.

PMID:3779076
Abstract

Using fluorescent probes it has been shown that free fatty acids cause depolarization of synaptosomes isolated from the rat brain. At the same time free fatty acids stimulated 45Ca2+ transport into synaptosomes. It has been demonstrated that synaptosomes isolated from the brain of E-deficient rats were more sensitive to the action of free fatty acids. Depolarization of synaptosomes isolated from the brain of both control and E-deficient rats were reduced by the addition of exogenous alpha-tocopherol.

摘要

使用荧光探针已表明,游离脂肪酸会导致从大鼠大脑分离出的突触体去极化。与此同时,游离脂肪酸刺激了45Ca2+转运到突触体中。已经证明,从维生素E缺乏的大鼠大脑中分离出的突触体对游离脂肪酸的作用更敏感。添加外源性α-生育酚可降低从对照大鼠和维生素E缺乏大鼠大脑中分离出的突触体的去极化。

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1
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Biull Eksp Biol Med. 1986 Nov;102(11):547-9.
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The protective effect of vitamin E, idebenone and reduced glutathione on free radical mediated injury in rat brain synaptosomes.维生素E、艾地苯醌和还原型谷胱甘肽对大鼠脑突触体自由基介导损伤的保护作用。
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[Vitamin E: comparison of efficiency of incorporation of alpha-tocopherol in the organs in comparison to gamma-tocopherol].[维生素E:与γ-生育酚相比,α-生育酚在各器官中的掺入效率比较]
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