人血小板匀浆中游离花生四烯酸浓度的调节。

Regulation of the concentration of free arachidonic acid in homogenates of human platelets.

作者信息

Preuss I, Patscheke H

机构信息

Institute for Clinical Chemistry, Klinikum Mannheim, University of Heidelberg, Germany.

出版信息

Agents Actions Suppl. 1992;37:34-40. doi: 10.1007/978-3-0348-7262-1_5.

DOI:10.1007/978-3-0348-7262-1_5

PMID:1632309

Abstract

With the intention to study the regulation of the availability of free arachidonic acid through the enzymes of the Lands cycle, we established a model system in homogenates of human platelets. Phospholipase A2, arachidonoyl-CoA synthetase and lysophosphatidyl acyltransferase proved to be simultaneously active and a steady turnover of arachidonic acid was the consequence. EGTA suppressed the deacylating activity that acted on endogenous membrane phospholipids and prevented eicosanoid formation from previously esterified exogenous arachidonoyl-CoA. The reacylating enzymes took part in the control of eicosanoid biosynthesis by re-esterification of liberated arachidonic acid. Blockade of the reacylation by apyrase made arachidonic acid completely available for further metabolization into 12-HETE and thereby induced an increase in the eicosanoid release.

摘要

为了研究通过兰兹循环的酶对游离花生四烯酸可用性的调节，我们在人血小板匀浆中建立了一个模型系统。结果证明磷脂酶A2、花生四烯酰辅酶A合成酶和溶血磷脂酰酰基转移酶同时具有活性，花生四烯酸的稳定周转就是其结果。乙二醇双（2-氨基乙基醚）四乙酸（EGTA）抑制了作用于内源性膜磷脂的脱酰基活性，并阻止了由先前酯化的外源性花生四烯酰辅酶A形成类二十烷酸。再酰化酶通过对释放的花生四烯酸进行再酯化参与类二十烷酸生物合成的控制。腺苷三磷酸双磷酸酶（apyrase）对再酰化的阻断使花生四烯酸完全可用于进一步代谢为12-羟基二十碳四烯酸（12-HETE），从而导致类二十烷酸释放增加。