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神经退行性疾病中的脑汞含量。

Brain mercury in neurodegenerative disorders.

作者信息

Fung Y K, Meade A G, Rack E P, Blotcky A J

机构信息

Department of Oral Biology, University of Nebraska Medical Center, College of Dentistry, Lincoln 68583-0740, USA.

出版信息

J Toxicol Clin Toxicol. 1997;35(1):49-54. doi: 10.3109/15563659709001165.

DOI:10.3109/15563659709001165
PMID:9022652
Abstract

BACKGROUND

Trace element neurotoxicity has long been invoked as an etiologic factor for Alzheimer's disease. This study was conducted to determine the concentrations of mercury in seven different brain regions from deceased patients histologically confirmed with Alzheimer's disease or multiple sclerosis as compared to control subjects without known central nervous system and renal disorders. Brain mercury concentrations in all deceased subjects can arise from amalgam restorations, diet, and the working environment.

METHODS

Autopsy frozen specimens (control, Alzheimer's disease and multiple sclerosis) from seven brain regions, which included frontal cortex, temporal cortex, occipital cortex, putamen, hippocampus, corona radiata and corpus callosum were assayed for the concentrations of selenium using instrumental neutron activation analysis and mercury using radiochemical neutron activation analysis.

RESULTS

We found that the concentrations of mercury and the mercury/selenium molar ratios were significantly lower in the hippocampi of multiple sclerosis patients as compared to aged-matched controls. However, no statistically significant differences were detected for the concentrations of mercury and the mercury/ selenium molar ratios for the remaining six brain regions among these groups.

CONCLUSIONS

Since brain mercury concentrations from deceased subjects with either Alzheimer's disease or multiple sclerosis are not significantly higher than controls, the present study provides no scientific support that mercury plays a significant role in the pathogenesis of these neurologic disorders.

摘要

背景

长期以来,微量元素神经毒性一直被认为是阿尔茨海默病的一个病因。本研究旨在确定经组织学确诊为阿尔茨海默病或多发性硬化症的已故患者与无已知中枢神经系统和肾脏疾病的对照受试者相比,七个不同脑区中的汞浓度。所有已故受试者脑中的汞浓度可能来自汞合金修复体、饮食和工作环境。

方法

使用仪器中子活化分析法测定来自额叶皮质、颞叶皮质、枕叶皮质、壳核、海马体、放射冠和胼胝体这七个脑区的尸检冷冻标本(对照、阿尔茨海默病和多发性硬化症)中的硒浓度,使用放射化学中子活化分析法测定汞浓度。

结果

我们发现,与年龄匹配的对照组相比,多发性硬化症患者海马体中的汞浓度和汞/硒摩尔比显著降低。然而,在这些组中,其余六个脑区的汞浓度和汞/硒摩尔比未检测到统计学上的显著差异。

结论

由于患有阿尔茨海默病或多发性硬化症的已故受试者脑中的汞浓度并不显著高于对照组,本研究没有提供科学依据支持汞在这些神经系统疾病的发病机制中起重要作用。

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