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.
Copyright 2002 S. Karger AG, Basel