Summary
The pathological features and experimental results of Minamata disease are summarized. This disease is an unusual neurological disorder resulting from eating a large amount of fish and shellfish of Minamata bay in Japan. Minamata disease is a toxic encephalopathy characterized by cerebellar atrophy of granule-cell type, preferential injury of both calcarine regions and degenerative disturbances, to a lesser degree, of other cortical areas. Other parts of the nervous system may occasionally be disturbed. There are little or no remarkable changes in organs other than the nervous system, except for an occasional fatty degeneration of the liver and kidney, erosion in the digestive tract, and hypoplasia of the bone marrow.
This disease affects not only human beings, but also various animals eating seafood from the bay, and it is pathologically demonstrated that even fish in the bay can be affected with the disease. Chemically, an appreciable quantity of mercury is demonstrated in organs of the human and animal autopsy cases. The ratio between the mercury content of the brain and that of the liver and kidney reveals a characteristic pattern of organomercury poisoning. Experimentally, Minamata disease is produced by feeding animals with fish and shellfish from the bay. The identical symptoms and pathological findings have been produced by administering to animals some organic mercury compounds, particularly alkyl-mercuric compounds such as alkylmercuric sulfide.
At the present stage it is assumed that Minamata disease is caused by eating fish and shellfish containing an alkylmercuric compound with the R-Hg-S-group, which is produced under specific circumstances by yet unknown processes.
Zusammenfassung
Die pathologischen Merkmale der Minamata-Krankheit, einer durch den reichlichen Genuß von Fischen und Muscheln aus der Minamatabucht in Japan verursachten, ungewöhnlichen neurologischen Störung, und darauf bezügliche experimentelle Ergebnisse werden zusammengefaßt. Die Minamata-Krankheit ist eine toxische Encephalopathie, die durch Kleinhirnrindenatrophie vom Körnerzelltyp, den bevorzugten Befall der Calcarina und zu einem geringeren Grad durch degenerative Schädigungen anderer Rindengebiete gekennzeichnet ist. Manchmal sind Läsionen auch an anderen Stellen des Nervensystems zu finden. In anderen Organen treten keine oder nur geringfügige Veränderungen auf, außer gelegentlich Zellverfettung in Leber und Niere, Erosionen der Darmschleimhaut und Hypoplasie des Knochenmarkes.
Nicht nur Menschen, sondern auch verschiedene Tiere, die sich von den Meerestieren in der Bucht ernähren, werden von der Krankheit befallen; es wird mit pathologischen Befunden belegt, daß sogar die in der Bucht lebenden Fische erkranken. Chemisch ist bei der Autopsie an Menschen und Tieren eine beträchtliche Menge von Quecksilber in den Organen nachzuweisen. Das Verhältnis des Quecksilbergehaltes im Gehirn zu dem in der Leber und Niere zeigt die Wesenszüge einer organischen Quecksilbervergiftung. Auf experimentellem Wege wird die Minamata-Krankheit durch die Fütterung von Tieren mit Fischen und Muscheln aus der Bucht hervorgerufen. Gleichartige Symptome und pathologische Befunde wurden erzielt, indem Tieren organische Quecksilberverbindungen, besonders Alkylquecksilberverbindungen wie Alkylquecksilbersulfid, verabreicht wurden.
Gegenwärtig wird angenommen, daß die Minamata-Krankheit durch den Genuß von Fischen und Muscheln verursacht wird, welche eine unter besonderen Umständen auf eine bis jetzt noch unbekannte Art und Weise entstandene Alkylquecksilberverbindung mit der R-Hg-S-Gruppe enthalten.
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Takeuchi, T., Morikawa, N., Matsumoto, H. et al. A pathological study of Minamata disease in Japan. Acta Neuropathol 2, 40–57 (1962). https://doi.org/10.1007/BF00685743
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DOI: https://doi.org/10.1007/BF00685743