Recent Advances in Understanding Aminoglycoside Ototoxicity and Its Prevention

@article{Wu2002RecentAI,
  title={Recent Advances in Understanding Aminoglycoside Ototoxicity and Its Prevention},
  author={Wei-jing Wu and Su-Hua Sha and Jochen Schacht},
  journal={Audiology and Neurotology},
  year={2002},
  volume={7},
  pages={171 - 174}
}
Studies over the last decade have left little doubt that reactive oxygen species (ROS) participate in the cellular events leading to aminoglycoside-induced hearing loss. The evidence ranges from the demonstration of aminoglycoside-mediated ROS formation in vitro to the prevention of ototoxicity by antioxidants in guinea pig in vivo. Here we review a hypothesis of the mechanism of toxicity, discuss possible causes underlying the gradient in base-to-apex sensitivity of outer hair cells, and… 

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The mechanism by which ototoxicity emerges following drug administration both in a clinical setting and in an in vitro model assay system used for its investigation is described, through use of mouse cochlear cultures.
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Results demonstrate that there was a considerable self-protection phenomenon by gentamicin in guinea pigs with normal hearing.
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TLDR
Comparing the effects of systemic treatment with four different, yet common, aminoglycoside antibiotics in two mouse strains, evaluating their effects on mortality, cochlear morphology and auditory brainstem responses indicates that gentamicin and neomycin caused high mortality in the adult mouse without significantly changing the auditory threshold.
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