Ischemia/reperfusion-induced changes in membrane proteins and lipids of gerbil cortical synaptosomes.
Ischemia/reperfusion-induced changes in membrane proteins and lipids of gerbil cortical synaptosomes.
复制标题
缺血/再灌注引起沙鼠皮质突触体膜蛋白和脂质的变化。
DOI：
10.1016/0306-4522(94)00385-i
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发表时间：
1995
期刊：
影响因子：
3.3
通讯作者：
Butterfield,DA
中科院分区：
文献类型：
--
作者：
Hall,NC;Carney,JM;Cheng,MS;Butterfield,DA
应用电子顺磁共振技术研究了短暂性双侧颈动脉闭塞对成年沙鼠和老年沙鼠突触体膜蛋白和脂质的物理状态的影响。通过阻断成年沙鼠和老年沙鼠的双侧颈总动脉，再灌注时间为0 ~ 24小时，造成短暂性缺血。分离大脑皮层突触体，用蛋白特异性自旋探针（2,2,6,6-四甲基-4-马酰亚胺-哌啶-1-氧基）和脂质特异性自旋探针（5-羟基硬脂酸）标记。成年沙鼠模型和老年沙鼠模型的蛋白质物理状态变化在再灌注60 min时达到峰值，老年沙鼠模型的变化更强烈，但在24 h后没有恢复到对照组值。老年沙鼠模型和成年沙鼠模型的脂质特异性标记均出现双相变化。老龄沙鼠组织的第一阶段变化发生时间（再灌注30分钟）早于成年沙鼠组织（再灌注3 - 6小时），而第二阶段变化发生在再灌注12小时，成年沙鼠和老年沙鼠都是如此。这些结果与假设一致，即蛋白质氧化和脂质过氧化是缺血后再灌注过程中产生的自由基的直接结果，蛋白质氧化可能因周围脂质过氧化而加剧。磷脂酶a2的活化与膜磷脂组织的改变有关。
The effects of transient bilateral carotid occlusion on the physical state of synaptosomal membrane proteins and lipids were studied in adult and aged gerbils employing electron paramagnetic resonance. Transient ischemia was produced in adult and aged gerbils by bilateral occlusion of the common carotid arteries with reperfusion times ranging from 0 to 24 h. Synaptosomes of the cerebral cortices were isolated and labeled with a protein-specific spin probe (2,2,6,6-tetramethyl-4-maleimido-piperidine-1-oxyl) and a lipid-specific spin probe (5-doxylstearic acid). Changes in the physical state of the protein peaked at 60 min reperfusion for both adult and aged gerbil models, with a more intense change in aged, but did not return to control values by 24 h. A biphasic change occurred with the lipid-specific label in both the aged and adult models. The onset of the first phase of change occurred at an earlier time (30 min reperfusion) for aged gerbil tissue than for adult tissue (between 3 and 6 h reperfusion), while the second phase of change occurred at 12 h reperfusion for both adult and aged. These results are consistent with the hypothesis that protein oxidation and lipid peroxidation are direct results of free radicals produced during the reperfusion following ischemia and that protein oxidation may be intensified by peroxidation of the surrounding lipids. Phospholipase A2activation is implicated to cause changes in membrane phospholipid organization as seen in these studies.