Higuchi I, Izumo S, Kuriyama M, Suehara M, Nakagawa M, Fukunaga H, Osame M, Ohtsubo S, Miyata K
Third Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
Acta Neuropathol. 1989;79(3):300-4. doi: 10.1007/BF00294665.
Pathological examinations were carried out on the skeletal muscle of a patient with germanium intoxication. The prominent histochemical finding was vacuolar myopathy with lipid excess, increased acid phosphatase activity and decreased cytochrome c oxidase activity. Ultrastructural lesions revealed a mitochondrial abnormality, autophagic vacuoles and accumulation of high electron-dense materials in deformed mitochondria and at the periphery of lipid droplets. Furthermore, the toxic effect of germanium on skeletal muscle was confirmed by the experimentally induced germanium myopathy, which showed autophagic degeneration, decreased cytochrome c oxidase activity and a mitochondrial abnormality with high electron-dense materials.
对一名锗中毒患者的骨骼肌进行了病理检查。显著的组织化学发现是伴有脂质过多的空泡性肌病、酸性磷酸酶活性增加和细胞色素c氧化酶活性降低。超微结构病变显示线粒体异常、自噬空泡以及在变形线粒体和脂滴周边有高电子密度物质的积累。此外，通过实验诱导的锗肌病证实了锗对骨骼肌的毒性作用，该肌病表现出自噬性变性、细胞色素c氧化酶活性降低以及伴有高电子密度物质的线粒体异常。
