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  • 1995-1999  (3)
  • Cochlear reperfusion injury  (1)
  • Glutamate toxicity  (1)
  • Hair cell apoptosis  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 255 (1998), S. 127-131 
    ISSN: 1434-4726
    Keywords: Key words Cochlea ; Aminoglycoside toxicity ; Hair cell apoptosis ; Nick-end labeling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although aminoglycosides have been investigated for their cochleotoxicity, it has still not been determined whether apoptosis or necrosis results in cochlear hair cell death following aminoglycoside treatment. To study possible mechanisms of cell death, we used in situ DNA break-labeling to examine guinea pig cochleae affected by kanamycin ototoxicity. Chronic kanamycin treatment induced DNA fragmentation that was detectable in both outer and inner hair cells, suggesting the occurrence of apoptosis. These findings suggest that apoptosis achieves deletion of affected hair cells without disrupting tissue architecture in the organ of Corti.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 256 (1999), S. 323-329 
    ISSN: 1434-4726
    Keywords: Key words Cochlear hair cells ; Glutamate toxicity ; Nitric oxide synthase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to examine the roles of glutamate (GLU) toxicity and involvement of nitric oxide (NO) in the pathogenesis of cochlear degeneration. We examined guinea pig cochleae following chronic exposure to GLU. Trypan blue extrusion and transmission electron microscopy were performed to evaluate degeneration in the organ of Corti. In parallel, nitric oxide synthase (NOS) activity was demonstrated by histochemical staining of NADPH diapholase. GLU treatment caused time-dependent degeneration of outer hair cells (OHCs) in conjunction with a temporal increase of NOS activity in the organ of Corti. This suggests that GLU may be involved in OHC degeneration under toxic conditions, with NO production possibly playing a role in this process.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 252 (1995), S. 504-508 
    ISSN: 1434-4726
    Keywords: Noise trauma ; Superoxide anion radicals ; Strial blood flow ; Cochlear reperfusion injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The emergence of superoxide anion radicals (O2-) in the guinea pig inner ear following acoustic trauma was investigated by histochemical methods. Five minutes after exposure to sound at 120–125 dB SPL for 3 h, an O2- reaction product was detected in the cochlea along the luminal membrane of the marginal cells of the stria vascularis. This reaction product could not be found at 30 min, but reappeared at 2 h. The first appearance of O2- is not explainable by our studies, but the second appearance may be related to recirculation of strial blood flow after blood flow stasis. The present observations raise the possibility that free radicals are produced in the inner ear after acoustic trauma and lead to inner ear damage.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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