肾缺血时线粒体膜流动性的改变。

Journal of Experimental Pathology Pub Date : 1990-01-01
C E Irazu, P R Rajagopalan, J K Orak, C T Fitts, I Singh
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引用次数: 0

摘要

采用荧光极化技术,以1,6-二苯基-1,3,5-己三烯为探针,测定了大鼠肾脏在常温缺血30、45、60、90分钟及再灌注24小时后,全离体线粒体荧光各向异性测量的脂质旋转迁移率(LRM)。缺血肾线粒体膜脂LRM随缺血次数的增加而稳定下降(0.1590 vs. 0.1705, 60分钟P < 0.01 < 0.001)。24小时再血流后,缺血组与对照组线粒体LRM至缺血45分钟无显著差异(0.1688 vs. 0.1705, 0.5 < P < 0.6)。然而,当肾脏缺血时间超过60分钟时,即使再灌注后,降低的LRM仍保持固定(0.1783 vs. 0.1738, 0.5小于P < 0.6)。这表明60分钟的缺血可能对线粒体膜造成不可逆的损伤,而较小程度的缺血损伤在再灌注后是可逆的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mitochondrial membrane fluidity changes in renal ischemia.

The fluorescence polarization technique with 1,6-Diphenyl-1,3,5-hexatriene as a probe, was used to determine the lipid rotational mobility (LRM) measured by fluorescence anisotropy of isolated whole mitochondria of the rat kidney following normothermic ischemia of 30, 45, 60 and 90 minutes and upon reperfusion for 24 hours. The LRM of mitochondrial membrane lipids of the ischemic kidney decreased steadily with increasing ischemic times (0.1590 vs. 0.1705, 0.01 less than P less than 0.001 at 60 minutes). Following 24 hours reflow, there were no significant differences in the LRM of mitochondria between ischemic and control groups up to 45 minutes of ischemia, (0.1688 vs. 0.1705, 0.5 less than P less than 0.6). However, when kidney was subjected to ischemic periods longer than 60 minutes, the decreased LRM remained fixed even after reperfusion (0.1783 vs. 0.1738, 0.5 less than P less than 0.6). This suggests that 60 minutes of ischemia probably produces irreversible damage to the mitochondrial membrane whereas lesser degrees of ischemic injury is reversible upon reperfusion.

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