Abstract

Since late 1953, with its peak in 1956, Minamata disease appeared among those who lived by fishing at Minamata Bay in southern parts of Kumamoto Prefecture. The number of patients reached 111, and 42 of them died. Some of the patients are still suffering from severe sequels with poor prognostic expectation.In 1964, 10 years after the onset of the disease, “second” Minamata disease broke out at near the mouth of the Agano River in Niigata Prefecture. Since that time, this disease began to attract the various fields of medicine and fundamental investigations started.Several years after the first occurrence in Kumamoto Prefecture, the causative agents were suspected to be methyl mercury compounds, because the symptoms were discovered among those who ate at each meal mainly fishes and shellfishes polluted with methyl mercury compounds in waste water. Therefore, it was necessary to investigate the toxicity of low alkyl mercury compounds both from the possibility of poisoning potential and metabolism in the animal body.After oral administrations of foods mixed with various mercury compounds to rats, Sebe et al. followed its Minamata disease-like symptoms and measured the contents of mercury in several organs and hair. However, these were not measured as the form of organic mercury.Miller's method has been used for quantitative measurement of organic mercury, as being employed by Sadakane. For the measurement by this method, some extent of organic mercury was generally thought to be needed.In our laboratory, quantitative analysis of organic mercury using gas chromatography was recently developed and ultra-microanalysis of tissue specimen became possible. Employing this method, the author investigated toxicities of various low alkyl mercury compounds by comparing organic with total inorganized mercuries of the same sample. Some of the results obtained by the author's method are as follows.

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