Localization of mercury in CNS of the rat. IV. The effect of selenium on orally administered organic and inorganic mercury.
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.
Møller-Madsen
B
B
Department of Neurobiology, University of Aarhus, Denmark.
Danscher
G
G
D000818:Animals; D002490:Central Nervous System / Q000737:chemistry* / Q000648:ultrastructure; D008297:Male; D008628:Mercury / Q000493:pharmacokinetics* / Q000633:toxicity; D008767:Methylmercury Compounds / Q000493:pharmacokinetics / Q000633:toxicity; D008854:Microscopy, Electron; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000494:pharmacology*
D008767:Methylmercury Compounds; D008628:Mercury; D012643:Selenium