Recent advances in understanding aminoglycoside ototoxicity and its prevention.
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.
Wu
Wei-Jing
WJ
Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, Mich., USA.
Sha
Su-Hua
SH
Schacht
Jochen
J
D000818:Animals; D000900:Anti-Bacterial Agents / Q000009:adverse effects*; D003638:Deafness / Q000139:chemically induced* / Q000378:metabolism; D005839:Gentamicins / Q000009:adverse effects*; D006198:Hair Cells, Auditory / Q000187:drug effects / Q000378:metabolism; D007612:Kanamycin / Q000009:adverse effects*; D051379:Mice; D017382:Reactive Oxygen Species / Q000378:metabolism
D000900:Anti-Bacterial Agents; D005839:Gentamicins; D017382:Reactive Oxygen Species; D007612:Kanamycin