Experimental germanium myopathy.

Abstract

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.

• Authors: I Higuchi, K Takahashi, K Nakahara, S Izumo, M Nakagawa, M Osame
• Journal: Acta neuropathologica (Acta Neuropathol) Vol. 82 Issue 1 Pg. 55-9 ( 1991) ISSN: 0001-6322 [Print] Germany
• PMID: 1950478 (Publication Type: Journal Article)

Chemical References

• Germanium
• germanium oxide

Topics

• Animals
• Germanium (toxicity)
• Male
• Microscopy, Electron
• Muscles (drug effects, pathology, ultrastructure)
• Muscular Diseases (chemically induced, pathology)
• Rats
• Rats, Inbred Strains
• Time Factors
• Vacuoles (ultrastructure)