歯牙発生過程の口腔領域における塩化メチル水銀-^<203>Hg の組織細胞内分布とその推移

Abstract

Distribution of methylmercury in tissue cells in dental fields of adult and fetal rats during the process of dental development and its time course change were compared and the following results were obtained. 1. Many tissues and cells in the oral cavity could be exposed to methylmercury in various degrees. 2. Intongue, relatively intense deposition of methylmercury was noted in the mucous membrane of the tip and body of the tongue and in the lingual muscles. Especially in the former, the mechanism of excretion of methylmercury along with epithelial desquamation was suggested. 3. Among the perioral tissues, the deposition was not as intense in the epidermis as in lingual mucous membrane, but deposition and accumulation of methylmercury was noted in the hair. In the muscle tissues of the same portion, the deposition was almost as intense as in the lingual muscle. 4. In the parotid gland, marked deposition was noted in the glandular cells and ducts in the initial period of administration. This was followed by a rapid decrease as time progressed. An excretory mechanism via the saliva is suggested indicating recontamination in the oral cavity. 5. The dental tissues of mature rats showed the lowest mercury uptake among the tissues studied. 6. Tissues and cells in the process of dental development, on the other hand, readily take up methylmercury. The main findings included the following : 1) Intense deposition is generally seen in the epidermal tissues of ectodermal origin in the lamina-shaped stage and bud-shaped stage. Along with the formation of the enamel organ, intense deposition is seen in the inner enamel epithelial cells. 2) In tissues of mesodermal origin, marked deposition of methylmercury was noted in the tissue cells of mesenchymal nature along with formation of the dental papilla, and a considerable uptake was noted in the odontoblasts. 7. Through each period of dental development, such findings of deposition of methylmercury gives a suggestion on the pathogenesis of dental developmental anomaly in patients with fetal Minamata disease.