塩化メチル水銀によるネズミの味蕾障害についての光学顕微鏡的ならびに電子顕微鏡的研究

Abstract

Organic mercury poisoning was caused in rats by inducing methylmercuric chloride with per os administration. Pathological changes of the sensory receptor-apparatus for taste were investigated both light and electron microscopically and the following results were obtained. 1. The methylmercury induced in rats caused disorders of the taste buds as a sensory receptor apparatus for taste. The most characteristic changes were observed on the taste bud cells in which severe exhausion due to cell degeneration occurred resulting a consequential atrophy of the taste buds. 2. Light microscopically, the cells revealed their degenerative appearances such as pyknosis, karyolysis, karyorrhexis and swelling of the cytoplasm. 3. Electron microscopically, it became difficult to differentiate type 1 cells (light cell) from type 2 cells (dark cell), because the difference of density between the two kinds of cells decreased during the degenerative course. In the taste bud cell cytoplasm, a particular change of mitochondrial matrices appeared revealing a wormeating spot-like, translucent lesions. These lesions developed in later stage to vacuolarization of the mitochondria with an additional change of loss of cristae. Similar vacuolarization occurred in endoplasmic reticulum and Golgi element. Therefore, whole cytoplasm was observed being occupied by vacuolated organelles in the end stadium. In contrast, the nuclei of the taste bud cells increased remarkably their densities which were regarded to correspond with pyknosis in the light microscopic changes. Some of the severely affected cells were supposed to come to final cell destruction. 4. The same kind of mitochondrial degeneration as that in the taste bud cells appeared also in the nerve endings. Changes of neurotubules came thereafter. 5. No severe affections were found on the squamous epithelial cells surrounding the taste buds. But slight vacuolarization was detectable in some of the epithelial cell mitochondria. So that, the degenerative appearancte of the taste buds formed a sharp conrast with intact views of the surrounding tissues. We understand that our findings of the disturbance of the taste buds which was caused by methylmercury are important because our results found in this experiment are not only the first presentation of pathological changes which can explain the mechanism of taste disturbance in human Minamata disease, but it will suggest a direction of future investigation for other sensory disturbances in methylmercury poisoning.