Histochemical Demonstration of Mercury in Human Tissue Cells of Minamata Disease by Use of Autoradiographic Procedure

Sakai, Ken; Okabe, Michio; Eto, Komyo; Takeuchi, Tadao

doi:10.1267/ahc.8.257

Cited by 29 publications

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“…Localization of mercury in the tissues was studied histochemically by our modified method of Sakai et al(21) with a time of development of 6 min. A modification of this method by Tokunaga et al (51) increased sensitivity 5-to 10-fold.…”

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Review Article: Pathology of Minamata Disease

1997

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Minamata disease, or methylmercury poisoning, was first discovered in 1956 around Minamata Bay, Kumamoto Prefecture, Japan. A similar epidemic occurred in 1965 along the Agano River, Niigata Prefecture, Japan. The neuropathology of Minamata disease has been well studied; this review focuses on human cases of Minamata disease in Kumamoto Prefecture. Nervous system lesions associated with Minamata disease have a characteristic distribution. In the cerebral cortex, the calcarine cortex was found to be involved in all cases of Minamata disease, particularly along the calcarine fissure. The destruction of nerve tissue was prominent in the anterior portions of the calcarine cortex. Occasionally, the centrifugal route from the visual and visual association areas (internal sagittal stratum) showed secondary degeneration in prolonged cases after acute onset. Postcentral, precentral, and temporal transverse cortices showed similar changes, though they were less severe. Intense lesions in the precentral cortex caused the development of secondary bilateral degeneration of the pyramidal tracts. In the cerebellum, the lesions occurred deeper in the hemisphere. The granule cell population was most affected. In the peripheral nerves, sensory nerves were more affected than motor nerves. Secondary degeneration of Goll's tracts was occasionally seen in prolonged or chronic cases.

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Review Article: Pathology of Minamata Disease

1997

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“…Selections of brain, kidney, and liver were excised and xed in 10% neutral formalin. These tissues were processed through ethanol and xylol, and then embedded in paraf n. Next, 6-l thick sections were stained with H&E, Klüver-Barrera, Bodian, and Masson's trichrome stains as well as photo-emulsion histochemical stain for inorganic mercury (19). Another animal brain was perfused with 100 ml of buffer formalin through ascending aorta, followed by an injection of 40 ml of methacrylate resin (Mercox CL-2R, produced by Dainippon Inc, Tokyo).…”

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Methylmercury Poisoning in Common Marmosets—A Study of Selective Vulnerability Within the Cerebral Cortex

et al. 2001

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Neuropathologica l lesions found in chronic human Minamata disease tend to be localized in the calcarine cortex of occipital lobes, the pre-and postcentral lobuli, and the temporal gyri. The mechanism for the selective vulnerability is still not clear, though several hypotheses have been proposed. One hypothesi s is vascular and postulates that the lesions are the result of ischemia secondary to compression of sulcal arteries from methylmercuryinduced cerebral edema. To test this hypothesis, we studied common marmosets because the cerebrum of marmosets has 2 distinct deep sulci, the calcarine and Sylvian ssures. MRI analysis, mercury assays of tissue specimens, histologic and histochemical studies of the brain are reported and discussed. Brains sacri ced early after exposure to methylmercury showed high contents of methylmercury and edema of the cerebral white matter. These results may explain the selective cortical degeneration along the deep cerebral ssures or sulci.

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“…of inorganic mercury in organ specimens. 27,28 With the use of the photoemulsion method, mercury deposits were detected mainly in the kidney, liver and the brain. In the kidney, mercury deposits were found in the epithelial cells of proximal convoluted tubules; no demonstrable precipitate was found in the glomerulus.…”

Section: Histochemistry For Mercurymentioning

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Minamata disease

Eto

2000

Neuropathology

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Minamata disease (methylmercury poisoning) was first discovered in 1956 around Minamata Bay, Kumamoto Prefecture, Japan. A second epidemic in Japan occurred in 1965 along the Agano River, Niigata Prefecture. This paper presents a brief review of Minamata disease with an emphasis on the cases found in Kumamoto Prefecture. At autopsy, the most conspicuous destructive lesion in the cerebrum was found in the anterior portions of the calcarine cortex. Less severe but similar lesions may be found in the post-central, pre-central and temporal transverse cortices. Secondary degeneration from primary lesions may be seen in cases with long survival. In the cerebellum, pathological changes occur deep in the hemisphere. The granule cell population was more affected, compared with Purkinje cells. Among peripheral nerves, sensory nerves were more affected than motor nerves. Our recent experimental studies that reveal knowledge of the pathogenesis of methylmercury poisoning will be discussed.

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Histochemical Demonstration of Mercury in Human Tissue Cells of Minamata Disease by Use of Autoradiographic Procedure

Cited by 29 publications

References 9 publications

Review Article: Pathology of Minamata Disease

Review Article: Pathology of Minamata Disease

Methylmercury Poisoning in Common Marmosets—A Study of Selective Vulnerability Within the Cerebral Cortex

Minamata disease

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