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慢性锰处理小鼠尾状核的超微结构变化

Ultrastructural Changes of Caudate Nucleus in Mice Chronically Treated with Manganese.

作者信息

Villalobos Virginia, Hernández-Fonseca Juan Pablo, Bonilla Ernesto, Medina-Leendertz Shirley, Mora Marylu, Mosquera Jesús

机构信息

Departamento de Biología, Facultad Experimental de Ciencias, Universidad del Zulia , Maracaibo , Venezuela .

出版信息

Ultrastruct Pathol. 2015;39(4):217-25. doi: 10.3109/01913123.2014.991885. Epub 2015 Jan 8.

Abstract

Manganese (Mn) is able to cross the blood-brain barrier and induces functional and structural alterations during the intoxication by this metal. Therefore, the effects of chronic administration of Mn in the caudate nucleus of mice were evaluated by electron microscopy. Male albino mice were injected intraperitoneally with MnCl2 (5 mg/kg/d) 5 d per week during 9 weeks. The control group received only 0.9% of NaCl solution. The caudate nuclei were extracted and subsequently processed to be observed on a conventional transmission electron microscope at 2, 4, 6, and 9 weeks after treatment. A high percentage of vacuolated and swollen mitochondria were found throughout all the analyzed periods. Myelin disarrangement and ultrastructural alterations related to edema were observed increased in Mn-treated mice at week 9. Granular degeneration of myelin at week 9 accompanied with deposition of electron dense granules in the neuropil was also observed. Edema in neuropil and glial cells was detected from week 2 to week 9 accompanied by swollen mitochondria. Neuronal bodies, synaptic terminals, and perivascular cells were found swollen. Decreased electron density in postsynaptic areas and decreased and dispersed synaptic vesicles in presynaptic areas were noted in Mn-treated animals. Some neurons from Mn-treated mice showed cisternae dilation of the Golgi apparatus. These results suggest that Mn-treatment produces structural alterations in the caudate nucleus that could be responsible for some of the neurotoxic effects of this metal.

摘要

锰(Mn)能够穿过血脑屏障,并在这种金属中毒期间诱发功能和结构改变。因此,通过电子显微镜评估了慢性给予锰对小鼠尾状核的影响。雄性白化小鼠在9周内每周5天腹腔注射氯化锰(5毫克/千克/天)。对照组仅接受0.9%的氯化钠溶液。在处理后2、4、6和9周提取尾状核,随后进行处理以便在传统透射电子显微镜下观察。在所有分析阶段均发现高比例的空泡化和肿胀线粒体。在第9周时,锰处理组小鼠的髓鞘排列紊乱和与水肿相关的超微结构改变增加。还观察到第9周时髓鞘颗粒变性并伴有神经毡中电子致密颗粒沉积。从第2周到第9周检测到神经毡和神经胶质细胞水肿,伴有线粒体肿胀。发现神经元体、突触终末和血管周围细胞肿胀。在锰处理的动物中,观察到突触后区域电子密度降低以及突触前区域突触小泡数量减少和分散。锰处理小鼠的一些神经元显示高尔基体池扩张。这些结果表明,锰处理会在尾状核中产生结构改变,这可能是这种金属某些神经毒性作用的原因。

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