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Dynamic microstructure of biomembranes and cellular function

生物膜的动态微观结构和细胞功能

基本信息

批准号：
02454490
负责人：
KOYAMA Tomiyasu
金额：
$ 2.11万
依托单位：
Hokkaido University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1992
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-02454490/
关键词：
biomembrane dynamic microstructure time-resolved fluorometer intramolecular oscillation Ischemia combined with reperfusion peroxidation hydration of lipid layer phospholipase coenzyme sarcoplasmic reticulum ATPase 過労筋小胞体 Ca^<2+>

项目摘要

Dynamic microstructure and its effects to cellular function were studied with a nanosecond time-resolved fluorometer. (1). Measurements of membrane viscosity (n) and wobbling angle of phospholipids (0) of plasma and mitochondrial membranes isolated from bullfrog suggested that the complex requirements of biomembranes of organelles performing different functions appear to be met by the particular dynamic microstructure of the biomembranes (1,2 ). (2). n increased and 0 decreased in rabbit heart subjected to ischemia combined with reperfusion. These changes will limit transmembrane movements of biomaterials. None of these parameters was changed in rats exposed only to ischemia (5,9). (3). Isolated cardiac mitochondria were exposed to peroxidizing conditions or adriamycin. n increased and 0 decreased, accompanied with strong decreases in the DPH fluorescence intensity and life time. The hydration of phospholipid layers of mitochondria occurs as a consequence of lipid peroxidation and also … More by adriamycin (3). (4). A quinoyl compound, idebenone pretreatment, suppressed the peroxidation- induced changes in the dynamic microstructure. Protection of phospholipids against peroxidation by antioxidative substances is effective in keeping nearly normal physical properties in the dynamic microstructure of cardiac mitochondrial membranes (4). (5). Phospholipids in cardiac mitochondria strongly decreased after a prolonged swim due to an activity increase in phospholipase A_2. The dynamic microstructure, however, showed no changes despite the remarkable decrease in phospholipids. This was probably because cholesterol was lost from mitochondrial membranes concurrently with phospholipids and the ratio of cholesterol to phospholipids did not change (7). Preadministration of a coenzyme, CoQ_<10> suppressed the exercise-induced decrease in mitochondrial phospholipids (8). (6). Lipid titration of sarcoplasmic reticulum with phospholipids having shorter acyl chains produced a lipid exchange by 70 % and caused an increase in the intramolecular oscillation of Ca-ATPase (6,11). Also a titration with an arachidonoyl phospholipid caused an increase in the intramolecular oscillation accompanied with a reduction in ATPase activity (10). The conformation and the suitable intramolecular oscillation of the ATPase are maintained with the adequate physical properties of surrounding phospholipids and the conformation changes in ATPase which permit an increase in intramolecular oscillation cause a decrease in the ATPase activity. Less

使用纳秒时间分辨荧光计研究动态微观结构及其对细胞功能的影响。 (1).对从牛蛙中分离出的质膜和线粒体膜的膜粘度 (n) 和磷脂摆动角 (0) 的测量表明，执行不同功能的细胞器生物膜的复杂要求似乎可以通过生物膜的特定动态微观结构来满足 (1,2 )。（2）。兔心脏缺血再灌注后n增加，0减少。这些变化将限制生物材料的跨膜运动。在仅暴露于缺血的大鼠中，这些参数均未发生改变 (5,9)。（3）。分离的心脏线粒体暴露于过氧化条件或阿霉素。 n增加而0减少，伴随着DPH荧光强度和寿命的强烈下降。线粒体磷脂层的水合作用是脂质过氧化以及阿霉素作用的结果 (3)。（4）。喹酰基化合物艾地苯醌预处理可抑制过氧化引起的动态微观结构变化。抗氧化物质保护磷脂免遭过氧化，可有效保持心脏线粒体膜动态微结构的近乎正常物理特性 (4)。（5）。长时间游泳后，由于磷脂酶 A_2 活性增加，心脏线粒体中的磷脂大幅减少。然而，尽管磷脂显着减少，但动态微观结构没有表现出任何变化。这可能是因为胆固醇与磷脂同时从线粒体膜丢失，并且胆固醇与磷脂的比率没有改变 (7)。预施用辅酶CoQ_ 10 抑制了运动引起的线粒体磷脂的减少(8)。（6）。使用具有较短酰基链的磷脂对肌浆网进行脂质滴定，产生 70% 的脂质交换，并导致 Ca-ATP 酶的分子内振荡增加 (6,11)。此外，用花生四烯酰磷脂进行滴定会导致分子内振荡增加，同时 ATP 酶活性降低 (10)。 ATP酶的构象和适当的分子内振荡通过周围磷脂的足够的物理性质得以维持，并且允许分子内振荡增加的ATP酶的构象变化引起ATP酶活性的降低。较少的