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通过冷冻断裂研究大鼠氯苯丁胺肌病的早期变化。

Early changes in chlorphentermine myopathy of rat studied by freeze fracturing.

作者信息

Schmalbruch H

出版信息

Muscle Nerve. 1978 Sep-Oct;1(5):421-2. doi: 10.1002/mus.880010516.

Abstract

Chlorphentermine interferes with the metabolism of phospholipids. When administered to the rat in daily doses for 5 days, it causes necrosis of muscle fibers that are rich in mitochondria. Before the onset of necrosis, the following characteristics of freeze-fractured muscle preparations were observed: multilayered lipid globules and single-layered lipid membranes without membrane particles; different stages of exocytosis of lipid through the plasma membrane of the muscle fibers; and areas of plasma membrane that were devoid of particles of intramembranous proteins. These latter areas may arise secondary to exocytosis, to fusion of lipid vesicles with the plasma membrane, or to a direct action of chlorphentermine on the membrane. It is not known whether these areas give rise to membrane defects and fiber necrosis.

摘要

氯苯丁胺干扰磷脂的代谢。当以每日剂量给大鼠连续给药5天时,它会导致富含线粒体的肌纤维坏死。在坏死发生之前,观察到冷冻断裂肌标本有以下特征:多层脂质球和无膜颗粒的单层脂质膜;脂质通过肌纤维质膜胞吐的不同阶段;以及缺乏膜内蛋白质颗粒的质膜区域。后一种区域可能继发于胞吐作用、脂质小泡与质膜的融合或氯苯丁胺对膜的直接作用。尚不清楚这些区域是否会导致膜缺陷和纤维坏死。

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