Schmalbruch H
J Neuropathol Exp Neurol. 1980 Jan;39(1):65-81. doi: 10.1097/00005072-198001000-00006.
In soleus muscles of rats treated for 2 to 11 days with high doses of chloroquine or chlorphentermine, muscle fibres showed autophagocytosis followed by segmental contracture and necrosis. Vascuolar degeneration, "splitting", and internal nuclei were absent. At variance with findings in progressive muscular dystrophy, the incidence of intramembrane particles was unchanged and membrane defects in necrotizing fibres were absent. Autophagic vacuoles were formed by cup-shaped cisternae derived from tubules that often enclosed single mitochondria. Golgi complexes occurred in the centre of the fibres; dilated vesicles of the sarcoplasmic reticulum contained an electrondense substance, possibly lysosomal enzymes. Exocytosis of autophagic vacuoles and of almost undigested mitochondria was observed. The changes in the plasma membrane were as in other cells: a bulge was formed that was cleared of intramembrane particles; the membrane fused with the limiting membrane of the autophagic vacuole, the content of which was expelled through an orifice. Inside autophagic vacuoles, persisting phospholipids arranged themselves into protein-free lipid bilayers, that formed concentric membranes or single-layered vesicles. Both drugs are known to inhibit degradation of phospholipids; the findings indicate that the rate of autophagocytosis and exocytosis were enhanced as well. Fibre necrosis was probably due to the fact that fibres eventually became unable to maintain their integrity.
在用高剂量氯喹或氯苯丁胺处理2至11天的大鼠比目鱼肌中，肌纤维出现自噬作用，随后出现节段性挛缩和坏死。无血管变性、“分裂”及核内移现象。与进行性肌营养不良的发现不同，膜内颗粒的发生率未变，坏死纤维中也无膜缺陷。自噬泡由源自小管的杯状池形成，这些池常包绕单个线粒体。高尔基体位于纤维中央；肌浆网的扩张囊泡含有电子致密物质，可能是溶酶体酶。观察到自噬泡及几乎未被消化的线粒体的胞吐作用。质膜的变化与其他细胞相同：形成一个凸起，膜内颗粒消失；膜与自噬泡的界膜融合，自噬泡内容物通过一个小孔排出。在自噬泡内，残留的磷脂排列成无蛋白的脂质双层，形成同心膜或单层囊泡。已知这两种药物均抑制磷脂降解；研究结果表明自噬作用和胞吐作用的速率也增强了。纤维坏死可能是由于纤维最终无法维持其完整性。
