Experimental germanium myopathy.
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.
Higuchi
I
I
Third Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
Takahashi
K
K
Nakahara
K
K
Izumo
S
S
Nakagawa
M
M
Osame
M
M
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
D005857:Germanium; C040516:germanium oxide