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1,3,5-三硝基苯诱导雄性Fischer-344大鼠发生脑病。

1,3,5-Trinitrobenzene-induced encephalopathy in male Fischer-344 rats.

作者信息

Chandra A M, Qualls C W, Reddy G

机构信息

Department of Veterinary Pathology, Oklahoma State University, Stillwater 74078, USA.

出版信息

Toxicol Pathol. 1995 Jul-Aug;23(4):527-32. doi: 10.1177/019262339502300410.

DOI:10.1177/019262339502300410
PMID:7501965
Abstract

Administration of 1,3,5-trinitrobenzene (TNB) to male Fischer-344 rats produced ataxia after 6 or 7 oral doses (71 mg/kg). Light microscopic examination after 10 days revealed petechial hemorrhages in the brain stem and cerebellum and bilaterally symmetric degeneration and necrosis (malacia) with reactive gliosis in the cerebellar peduncles. The malacia was dorsal and lateral to the fourth ventricle involving the cerebellar nuclei, medial and lateral vestibular nuclei, and inferior colliculi. Blood vessels associated with the lesion had widened Virchow-Robin spaces, occasionally with extravasated erythrocytes. Rats administered daily oral doses of 35.5 mg/kg of TNB for 10 days and 35.5 and 71 mg/kg of TNB for 1 or 4 days did not have brain lesions.

摘要

给雄性Fischer-344大鼠口服1,3,5-三硝基苯(TNB),在给予6或7次口服剂量(71毫克/千克)后出现共济失调。10天后的光镜检查显示脑干和小脑有瘀点性出血,小脑脚有双侧对称性变性和坏死(软化)以及反应性胶质增生。软化位于第四脑室背侧和外侧,累及小脑核、内侧和外侧前庭核以及下丘。与病变相关的血管有增宽的Virchow-Robin间隙,偶尔有红细胞外渗。每天口服35.5毫克/千克TNB,持续10天,以及每天口服35.5和71毫克/千克TNB,持续1或4天的大鼠没有脑部病变。

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