慢性乙醇对鸡胚脑、心、肝磷脂酶A2-和c活性的影响。

R Natsuki
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引用次数: 0

摘要

采用底物1-棕榈- 1-2-N-(4-硝基苯并-2-氧- 1,3 -二唑氨基已酰磷脂酰胆碱(ndd - pc)测定了鸡胚脑、心、肝亚细胞组分中磷脂酶A2 (PLA2)和C (PLC)的活性,并评价了慢性乙醇处理对其活性的影响。通过测定外源NBD-PC中N-(4-硝基苯并-2-氧- 1,3 -二唑)氨基己酸(nbd -己酸)和1-棕榈1-2-NBD氨基己醇(NBD-DG)的释放量,测定各组分PLA2和PLC活性。微粒体膜流动性由二苯六烯各向异性(γ)估计。细胞质、线粒体和微粒体亚细胞组分通过对脑、心和肝的匀浆进行差速离心制备。乙醇处理鸡胚的脑组织、心脏和肝脏微粒体亚细胞组分的PLA2和PLC特异性活性显著高于未处理鸡胚的相应组分。经乙醇处理的鸡胚脑组织和心脏线粒体亚细胞组分的PLA2和PLC特异性活性显著高于相应的对照组分。与对照组相比,经乙醇处理的鸡胚的脑组织和心脏微粒体显著降低了γ。这些结果表明,膜流动性的变化显然是PLA2和PLC活性变化的先决条件。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of chronic ethanol on phospholipase A2- and C-activity in chick embryo brain, heart and liver.

The activities of phospholipase A2 (PLA2) and C (PLC) in subcellulal fractions from chick embryo brain, heart and liver were determined using the substrate 1-palmitoy 1-2-N-(4-nitrobenzo-2-oxa-1, 3-diazole amino caproyl-phsphatidylcholine (NBD-PC), and the effect of chronic ethanol treatment on these activities was evaluated. PLA2 and PLC activities of each fraction were assayed by measuring release of N- (4-nitrobenzo-2-oxa-1, 3-diazole) amino caproic acid (NBD-caproic acid) and of 1-palmitoy 1-2-NBD amino caproyl glycerol (NBD-DG) from exogenous NBD-PC. The microsomal membrane fluidity was estimated from diphenylhexatriene anisotropy (gamma). Cytosolic, mitochondorial, and microsomal subcellular fractions were prepared by differential centrifugation of homogenates of the brain, heart, and liver. Microsomal subcellular fractions from the brain, heart and liver of ethanol treated chick embryo showed significantly higher PLA2 and PLC specific activities than did corresponding fractions from non-treated chick embryo. Mitochondrial subcellular fractions from the brain and heart of ethanol-treated chick embryo also showed significantly higher PLA2 and PLC specific activities than the corresponding control fractions. Microsomal fractions from the brain and heart of ethanol-treated chick embryo decreased significantly the gamma than those of control. These results suggest that the change in the membrane fluidity is an apparent prerequisite for the changes of PLA2 and PLC activities.

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