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慢性氯化镉诱导神经病变的超微结构研究

An ultrastructural study of chronic cadmium chloride-induced neuropathy.

作者信息

Sato K, Iwamasa T, Tsuru T, Takeuchi T

出版信息

Acta Neuropathol. 1978 Mar 15;41(3):185-90. doi: 10.1007/BF00690433.

Abstract

After the long-term exposure to cadmium chloride in drinking water, the Wistar rats developed peripheral polyneuropathy. The main lesion was of myelin degeneration. Ultrastructural examination of the roots and sciatic nerves revealed segmental demyelination beginning from the node of Ranvier. There was the active autophagocytosis of Schwann cells which contained a number of myelin remnants and dense bodies. There was, on the other hand, the evidence of remyelination with toxic damage, in which the thinner myelin sheaths and abnormal myelinations were observed with increase of Schwann cells containing rich ribosomes. Axoplasmic changes were minimal, but consisted of accumulation of glycogen particles which very often produced glycogenosomes in characteristic appearance with axoplasmal dysfunction.

摘要

长期饮用含氯化镉的水后,Wistar大鼠出现周围性多发性神经病。主要病变为髓鞘变性。对神经根和坐骨神经的超微结构检查显示,从郎飞结开始出现节段性脱髓鞘。雪旺细胞有活跃的自噬现象,其中含有许多髓鞘残片和致密小体。另一方面,有中毒性损伤后髓鞘再生的证据,观察到较薄的髓鞘和异常髓鞘形成,同时含有丰富核糖体的雪旺细胞增多。轴浆变化轻微,但有糖原颗粒积聚,这些颗粒常形成具有特征性外观的糖原小体,并伴有轴浆功能障碍。

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