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丙烯酰胺所致大鼠浦肯野细胞损伤的超微结构特征:细胞神经病理学中的一种新现象。

Ultrastructural features of the Purkinje cell damage caused by acrylamide in the rat: a new phenomenon in cellular neuropathology.

作者信息

Cavanagh J B, Gysbers M F

出版信息

J Neurocytol. 1983 Jun;12(3):413-37. doi: 10.1007/BF01159383.

DOI:10.1007/BF01159383
PMID:6875619
Abstract

Dosing rats with acrylamide leads to the formation in Purkinje cells of juxtanuclear clusters of tubular and vesicular smooth endoplastic reticulum (SER). A microtubule organizing centre forms in relation to these clusters and together they appear to move to the cell surface, where protrusions of plasmalemma form, often with overlying synaptic attachments, containing densely packed tubular and vesicular SER membranes. Usually the microtubule organizing centre immediately underlies this. Subsequently, appearances suggest that astroglial intrusions occur internal to the protrusions described above to which the tubulo-vesicular material appears to be transferred. During these events the organization of the cytoplasm of the Purkinje cell is grossly disturbed with apparent loss and disarray of rough endoplasmic reticulum (RER) and of polyribosomes. This temporal sequence of events can be followed after a single dose of acrylamide. In chronically intoxicated animals vacuolation and swelling of dendrites takes place and the Purkinje cell may die after all stages of the cellular transformations have been present. These unique events appear to be confined to Purkinje cells and are considered probably to be the result of a primary disturbance to SER synthesis caused by acrylamide. It is argued that the changes taking place in acrylamide intoxication in neurons that lead to degeneration in long axons are probably of the same general kind.

摘要

给大鼠注射丙烯酰胺会导致浦肯野细胞中形成近核的管状和泡状滑面内质网(SER)簇。一个微管组织中心与这些簇相关形成,并且它们似乎一起移动到细胞表面,在那里质膜形成突起,通常带有覆盖的突触附着,包含密集堆积的管状和泡状SER膜。通常微管组织中心紧邻其下方。随后,有迹象表明星形胶质细胞侵入上述突起内部,管状泡状物质似乎被转移到这些突起中。在这些过程中,浦肯野细胞的细胞质组织受到严重干扰,粗面内质网(RER)和多核糖体明显丢失和紊乱。单次注射丙烯酰胺后可以观察到这些事件的时间顺序。在慢性中毒的动物中,树突会出现空泡化和肿胀,并且在细胞转化的所有阶段都出现后,浦肯野细胞可能会死亡。这些独特的事件似乎仅限于浦肯野细胞,并且被认为可能是丙烯酰胺对SER合成的原发性干扰的结果。有人认为,丙烯酰胺中毒时神经元中发生的导致长轴突退变的变化可能属于同一类一般性质的变化。

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Arch Toxicol. 1992;66(1):57-66. doi: 10.1007/BF02307271.