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电惊厥休克后[1-14C]花生四烯酸对脑磷脂酰肌醇、三酰甘油和二酰甘油标记的减少:肾上腺素能药物对该效应的增强作用以及与棕榈酸标记的比较

Reduced labeling of brain phosphatidylinositol, triacylglycerols, and diacylglycerols by [1-14C]arachidonic acid after electroconvulsive shock: potentiation of the effect by adrenergic drugs and comparison with palmitic acid labeling.

作者信息

Pediconi M F, Rodriguez de Turco E B, Bazan N G

出版信息

Neurochem Res. 1986 Feb;11(2):217-30. doi: 10.1007/BF00967970.

DOI:10.1007/BF00967970
PMID:3703102
Abstract

The effect of electroconvulsive shock on the labeling of phospholipids and neutral lipids in mice brains was examined after intracerebral injection of [1-14C] arachidonic acid or [1-14C]palmitic acid. Electroconvulsive shock reduced greatly the removal of radiolabeled arachidonic acid from the free fatty acid pool. At the same time, the incorporation of arachidonic acid was partially inhibited in triacylglycerol, diacylglycerol, and phosphatidylinositol, whereas the incorporation of [1-14C]palmitic acid was not affected. Pretreatment with desipramine and pargyline potentiated the lipid effect of electroconvulsive shock in neutral glycerides. These electroconvulsive shock-induced changes reflect alterations in the metabolism of intracerebrally injected arachidonic acid, but not of similarly injected palmitic acid. From the available data whether decreased ATP, enzyme inhibition or other factors are involved cannot be ascertained. Moreover, the electroconvulsive shock-enhanced endogenous free arachidonic acid may possibly dilute the injected radiolabeled fatty acid, thus decreasing its availability for arachidonoyl-coenzyme A synthesis. Hence, a partial inhibition of the activation-acylation of these fatty acids, primarily arachidonic acid, also may be involved in the seizure-induced accumulation of free fatty acids in the brain.

摘要

在向小鼠脑内注射[1-¹⁴C]花生四烯酸或[1-¹⁴C]棕榈酸后,研究了电惊厥休克对小鼠脑内磷脂和中性脂质标记的影响。电惊厥休克极大地减少了放射性标记的花生四烯酸从游离脂肪酸池中清除。同时,花生四烯酸在三酰甘油、二酰甘油和磷脂酰肌醇中的掺入受到部分抑制,而[1-¹⁴C]棕榈酸的掺入未受影响。用去甲丙咪嗪和帕吉林预处理可增强电惊厥休克对中性甘油酯的脂质效应。这些电惊厥休克诱导的变化反映了脑内注射的花生四烯酸代谢的改变,而非类似注射的棕榈酸代谢的改变。从现有数据无法确定是否涉及ATP降低、酶抑制或其他因素。此外,电惊厥休克增强的内源性游离花生四烯酸可能会稀释注射的放射性标记脂肪酸,从而降低其用于花生四烯酰辅酶A合成的可用性。因此,这些脂肪酸(主要是花生四烯酸)的活化酰化的部分抑制也可能与癫痫发作诱导的脑内游离脂肪酸积累有关。

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1
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引用本文的文献

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J Neural Transm Gen Sect. 1990;81(2):121-30. doi: 10.1007/BF01245832.

本文引用的文献

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