Møller-Madsen B, Danscher G
Department of Neurobiology, University of Aarhus, Denmark.
Toxicol Appl Pharmacol. 1991 May;108(3):457-73. doi: 10.1016/0041-008x(91)90092-s.
The distribution and exact cellular localization of mercury in the brain and upper cervical spinal cord of the adult male Wistar rat has been determined using the autometallographic silver-enhancement technique. A detailed atlas of mercury-containing nuclei following oral administration of HgCl2 (20 mg x liter-1 or CH3HgCl (20 mg x liter-1) was prepared. The effect of orally administered Na2SeO3 (2 mg x liter-1) on these patterns was investigated. In animals treated with CH3HgCl, sodium selenite induced a conspicuous increase in mercury staining of nerve cell bodies in specific areas of the central nervous system (CNS) including laminae III-VI in the cerebral cortex, thalamus, hypothalamus, and brain stem nuclei. In the cerebellum, the cortical Purkinje cells and nerve cells in the deep nuclei were targets for appreciable mercury accumulations after CH3HgCl. Again, these deposits were increased by coadministration of selenite. In the spinal cord following administration of CH3HgCl alone, staining was limited to the gray matter. The intensity of this staining was increased by selenite and deposits also appeared in the white matter. Mercury accumulations were present in scattered glia cells in the cuneate and gracile fasciculi. Treatment with HgCl2 alone or in combination with selenite yielded no staining of the Purkinje cells, nor did selenite result in an increase in the density of other stained cell bodies throughout the CNS, as was the case with organic mercury. The most intense neuronal staining was seen in sections taken from rats treated with a combination of CH3HgCl and selenite. Lesser staining was seen in neuroglia, ependymal, and choroidal cells. In the latter two cell types, staining intensity was unaffected by selenite treatment. In HgCl2-treated rats the same cell types were targets for mercury deposits although staining was to a significantly lesser degree. Concurrent treatment with selenite had no visible effect on the staining pattern. Ultrastructurally, the bulk of the mercury was located in lysosomes. Administration of CH3HgCl combined with selenite caused mercury to appear in the nuclei of neurons. Selenium treatment delayed the functional toxic effects of CH3HgCl. Sections prepared from animals treated separately with selenium or demineralized water (used as the solvent for all compounds) were devoid of mercury deposits.
利用自动金相银增强技术，已确定成年雄性Wistar大鼠大脑和颈上段脊髓中汞的分布及确切细胞定位。制备了口服氯化汞（20毫克/升）或甲基氯化汞（20毫克/升）后含汞核的详细图谱。研究了口服亚硒酸钠（2毫克/升）对这些模式的影响。在用甲基氯化汞处理的动物中，亚硒酸钠导致中枢神经系统（CNS）特定区域神经细胞体的汞染色显著增加，这些区域包括大脑皮层的III - VI层、丘脑、下丘脑和脑干核。在小脑中，皮质浦肯野细胞和深部核团中的神经细胞是甲基氯化汞处理后汞大量蓄积的靶点。同样，亚硒酸钠共同给药会增加这些沉积物。单独给予甲基氯化汞后，脊髓中的染色仅限于灰质。亚硒酸钠增加了这种染色的强度，并且白质中也出现了沉积物。在楔束和薄束中有散在的胶质细胞存在汞蓄积。单独用氯化汞或与亚硒酸钠联合处理均未使浦肯野细胞染色，亚硒酸钠也未导致整个中枢神经系统中其他染色细胞体的密度增加，而有机汞处理则会出现这种情况。在用甲基氯化汞和亚硒酸钠联合处理的大鼠切片中观察到最强的神经元染色。在神经胶质细胞、室管膜细胞和脉络膜细胞中染色较弱。在后两种细胞类型中，染色强度不受亚硒酸钠处理的影响。在氯化汞处理的大鼠中，相同的细胞类型是汞沉积的靶点，尽管染色程度明显较低。亚硒酸钠同时处理对染色模式没有明显影响。超微结构上，大部分汞位于溶酶体中。甲基氯化汞与亚硒酸钠联合给药导致汞出现在神经元细胞核中。硒处理延迟了甲基氯化汞的功能毒性作用。分别用硒或去离子水（用作所有化合物的溶剂）处理的动物制备的切片没有汞沉积。
