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  • 1995-1999  (3)
  • Aminoglycoside toxicity  (2)
  • Glutamate toxicity  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 254 (1997), S. 153-157 
    ISSN: 1434-4726
    Keywords: Apoptosis ; Labyrinthine vestibule ; Aminoglycoside toxicity ; Zinc toxicity ; Nick-end labeling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We reported that apoptosis occurred in the guinea pig vestibular hair cells after chronic aminoglycoside treatments. In the present study, we used in situ nick-end labeling to determine whether apoptosis was also induced by the acute effects of aminoglycosides in guinea pig ampullar cristae. In addition, we evaluated the effect of zinc supplements upon these ototoxic treatments. After a local application of streptomycin directly to the round window, we found labeled bodies in the vestibular hair cells. The zinc supplement increased the number of labeled bodies resulting in severe hair cell loss. These findings indicate that the acute effects of aminoglycosides also induce apoptosis of the vestibular hair cells, and that zinc enhances aminoglycoside ototoxicity. Consequently, we propose that an interaction with ion channels may play a key mechanism in the processes of apoptosis affecting the vestibular hair cells.
    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 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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