Dynamic microstructure of biomembranes and cellular function

用纳秒时间分辨荧光仪研究了动态微结构及其对细胞功能的影响。（一）.从牛蛙中分离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的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）。（二）、缺血再灌注兔心n增加，0减少。这些变化将限制生物材料的跨膜运动。在仅暴露于局部缺血的大鼠中，这些参数均未发生变化（5，9）。（三）、分离的心肌线粒体暴露于过氧化条件或阿霉素。n增加，0减少，伴随着显着降低的DPH荧光强度和寿命。线粒体磷脂层的水合作用是脂质过氧化的结果， ...更多信息 阿霉素（3）。（四）、一种喹酰化合物艾地苯醌预处理，抑制过氧化诱导的动态微观结构的变化。通过抗氧化物质保护磷脂免受过氧化作用，可有效保持心脏线粒体膜动态微观结构中接近正常的物理特性（4）。（五）、长时间游泳后心肌线粒体磷脂含量显著降低，这与磷脂酶A_2活性增加有关。然而，尽管磷脂显著减少，但动态微观结构没有变化。这可能是因为胆固醇与磷脂同时从线粒体膜中丢失，胆固醇与磷脂的比例没有变化（7）。预先给予辅酶CoQ_1<10>可抑制运动诱导的线粒体磷脂减少（8）。（六）、用具有较短酰基链的磷脂对肌浆网进行脂质滴定，产生了70%的脂质交换，并导致Ca-ATP酶分子内振荡增加（6，11）。此外，用花生四烯酸磷脂滴定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与周围磷脂的适当物理性质保持在一起，并且ATP酶中允许分子内振荡增加的构象变化导致ATP酶活性降低。少

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