Díaz-Pérez Rosa Nelly, Castillo-González Juan Antonio, Carcaño-Díaz Katya, García-Juárez Jaime, Salazar-Leal Martha E, Muñoz-Maldonado Gerardo E, Montes-de-Oca-Luna Roberto, Saucedo-Cárdenas Odila, Soto-Domínguez Adolfo
Department de Histology, Faculty of Medicine, University Autonomous of Nuevo León, Monterrey, N.l, México.
Department de Pharmacology and Toxicology, Faculty of Medicine, University Autonomous of Nuevo León, Monterrey, N.l, México.
Histol Histopathol. 2016 Apr;31(4):393-402. doi: 10.14670/HH-11-681. Epub 2015 Nov 5.
The accidental ingestion of Karwinskia humboldtiana (Kh) fruit in humans and animals causes chronic or acute intoxication. Acute poisoning induces respiratory failure that progresses rapidly to death. Studies in animals intoxicated with Kh describe lesions in cerebral cortex, cerebellum, spinal cord, hippocampus and caudate nucleus. Kh intoxication in Wistar rats models the sub-lethal clinical phase observed in humans. Considering these reports, the present study analyzed the histopathological alterations within the striatum following experimental Kh intoxication. Twenty Wistar rats were divided into three groups (n =5) and were intoxicated with Kh fruit. A control group (n =5) was included. Animals were euthanized at several time points (48, 58 and 170 days post-intoxication). The brain was collected, divided and processed for conventional histology or electron microscopy. Sections were stained with hematoxylin and eosin, cresyl violet, Klüver-Barrera, and toluidine blue. Immunolabeling was performed for glial cells in the striatum, and the samples were analyzed with light microscopy. Morphometric and statistical analyses were performed. In control group, neurons, axon bundles and neuropil had a normal appearance. At 48 days, hyperchromic neurons with apparent decreased size were observed interspersed among the normal neurons. At 58 days, we observed an increased number of hyperchromic neurons and disorganization of the myelin sheath and neuropil. At 170 days, these alterations persisted in the paralysis group. In treated groups, we observed signs of gliosis and increased axonal diameters. This study is the first report that describes the histopathological alterations within the striatum caused by chronic intoxication with Kh fruit in the Wistar rat.
人类和动物意外摄入洪堡卡罗琳柿(Kh)果实会导致慢性或急性中毒。急性中毒会引发呼吸衰竭,并迅速发展至死亡。对Kh中毒动物的研究描述了大脑皮层、小脑、脊髓、海马体和尾状核中的病变。Wistar大鼠的Kh中毒模拟了人类观察到的亚致死临床阶段。考虑到这些报告,本研究分析了实验性Kh中毒后纹状体内的组织病理学改变。将20只Wistar大鼠分为三组(n = 5),用Kh果实使其中毒。设立一个对照组(n = 5)。在几个时间点(中毒后48、58和170天)对动物实施安乐死。收集大脑,进行分割并处理以用于常规组织学或电子显微镜检查。切片用苏木精和伊红、甲酚紫、Klüver-Barrera和甲苯胺蓝染色。对纹状体内的神经胶质细胞进行免疫标记,并用光学显微镜对样本进行分析。进行形态计量学和统计学分析。对照组中,神经元、轴突束和神经纤维网外观正常。在48天时,观察到大小明显减小的深染神经元散布于正常神经元之间。在58天时,我们观察到深染神经元数量增加,髓鞘和神经纤维网紊乱。在170天时,这些改变在瘫痪组中持续存在。在治疗组中,我们观察到神经胶质增生的迹象和轴突直径增加。本研究是首篇描述Wistar大鼠因Kh果实慢性中毒导致纹状体组织病理学改变的报告。