Higuchi I, Takahashi K, Nakahara K, Izumo S, Nakagawa M, Osame M
Third Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
Acta Neuropathol. 1991;82(1):55-9. doi: 10.1007/BF00310923.
The long-term administration of germanium dioxide (GeO2) to rats produced Ge myopathy characterized by the formation of ragged-red fibers. The earliest pathological changes in experimental Ge myopathy were a decrease in cytochrome c oxidase activity and accumulation of high electron-dense materials in mitochondria. These findings suggest that a mitochondrial dysfunction may be most important in the genesis of experimental Ge myopathy, which could be a useful animal model for the investigation of and therapeutic trials for human mitochondrial myopathies.
