Verschoyle R D, Brown A W, Thompson C A
Arch Toxicol. 1984 Dec;56(2):109-12. doi: 10.1007/BF00349081.
2,4,5-tribromoimidazole and its 1-n-butylcarboxylate and 1-dimethylcarbamoyl derivatives, when administered to rats, induced poisoning typical of uncouplers of oxidative phosphorylation. At 48 h rats surviving a single toxic dose of 20-60 mg/kg developed permanent incoordination of the hindlimbs in the absence of brain oedema. Neuropathologic examination of brain and spinal cord from perfused fixed rats at 24 h revealed neuronal necrosis and chromatolysis in the vestibular nucleus, the outer parietal neocortex and red nucleus. Chromatolysis and necrosis in these areas had increased at 72-96 h and were also observed in the deeper layers of the neocortex, the medial entorhinal cortex, the reticular formation, the grey matter of the spinal cord extending into the ventral horns, the dorsal, and ventral cochlear nuclei and the deep cerebellar nuclei, in decreasing order of severity. Neuronal necrosis was accompanied by an increased glial response, including neuronophagia and at 16 days with astroglial hypertrophy and hyperplasia.
2,4,5-三溴咪唑及其1-正丁基羧酸酯和1-二甲基氨基甲酰衍生物给大鼠用药时，会引发典型的氧化磷酸化解偶联剂中毒症状。单次给予20 - 60 mg/kg毒性剂量后存活48小时的大鼠，在无脑水肿的情况下出现后肢永久性共济失调。对24小时灌注固定大鼠的脑和脊髓进行神经病理学检查发现，前庭核、外侧顶叶新皮质和红核出现神经元坏死和染色质溶解。这些区域的染色质溶解和坏死在72 - 96小时时增加，并且在新皮质深层、内侧内嗅皮质、网状结构、延伸至腹角的脊髓灰质、背侧和腹侧耳蜗核以及小脑深部核团也有观察到，严重程度依次降低。神经元坏死伴随着胶质细胞反应增强，包括噬神经元现象，在16天时出现星形胶质细胞肥大和增生。
