Recent Advances in Understanding Aminoglycoside Ototoxicity and Its Prevention
- 3 June 2002
- journal article
- Published by S. Karger AG in Audiology and Neurotology
- Vol. 7 (3) , 171-174
- https://doi.org/10.1159/000058305
Abstract
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 present recent results on the adult mouse as a new animal model of aminoglycoside ototoxicity and its prevention.Keywords
This publication has 7 references indexed in Scilit:
- Aminoglycoside AntibioticsAudiology and Neurotology, 2000
- Attenuation of aminoglycoside-induced cochlear damage with the metabolic antioxidant α-lipoic acidHearing Research, 1999
- Iron Chelators Protect From Aminoglycoside-Induced Cochleo- and Vestibulo-ToxicityFree Radical Biology & Medicine, 1998
- Attenuation of Neomycin Ototoxicity by Iron ChelationThe Laryngoscope, 1998
- Reactive oxygen species in chick hair cells after gentamicin exposure in vitroHearing Research, 1997
- Direct detection of ototoxicant-induced reactive oxygen species generation in cochlear explantsHearing Research, 1996
- Cochlear cultures as a model system for studying aminoglycoside induced ototoxicityHearing Research, 1991