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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.
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