Pathology of Minamata disease. With special reference to its pathogenesis.
On the basis of pathological studies of the Minamata disease induced by consumption of large amounts of fish and shellfish contaminated with methylmercury, the neuropathological and metal-histochemical changes in the human body were discussed. Methylmercuric compounds accumulated in the seafoods were absorbed by the human body following oral intake, and distributed widely and accumulated in various organs and tissues. The distribution of the pathological lesions could thus include the nervous system, particularly the brain with a characteristics preference. There were apparently two major mechanisms of destruction of the brain cortex. One was the neurotoxic effect of methylmercury on the neurons which was stronger than its cytotoxic effect on the epithelial and parenchymatous cells in general, and the other was a hypoxemic or anoxemic effect on the brain in its intracranial anatomical situation following disturbance of the blood circulation, resulting in edema of the perivascular space, particularly in the water-shed regions of the brain cortex. Such a vascular mechanism probably exerted a greater influence in acute and subacute severe cases, whereas the neurotoxic effect was functionally more active in chronic onset cases.[1]References
- Pathology of Minamata disease. With special reference to its pathogenesis. Takeuchi, T. Acta Pathol. Jpn. (1982) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg