title: 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.affiliation: Third Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Higuchi
authors.forename: K
authors.initials: K
authors.lastname: Takahashi
authors.forename: K
authors.initials: K
authors.lastname: Nakahara
authors.forename: S
authors.initials: S
authors.lastname: Izumo
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
authors.forename: M
authors.initials: M
authors.lastname: Osame
mesh_terms: D000818:Animals; D005857:Germanium / Q000633:toxicity*; D008297:Male; D008854:Microscopy, Electron; D009132:Muscles / Q000187:drug effects / Q000473:pathology* / Q000648:ultrastructure; D009135:Muscular Diseases / Q000139:chemically induced / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014617:Vacuoles / Q000648:ultrastructure
chemical_list: D005857:Germanium; C040516:germanium oxide