Age, drugs, and noise are major causes of acquired hearing loss. The involvement of reactive oxygen species (ROS) in hair cell death has long been discussed, but there is considerably less information available as to the mechanisms underlying ROS formation. Most cellular ROS arise in mitochondria and this review will evaluate evidence for mitochondrial pathology in general and dysfunction of the mitochondrial respiratory chain in particular in acquired hearing loss. We will discuss evidence that different pathways can lead to the generation of ROS and that oxidative stress might not necessarily be causal to all three pathologies. Finally, we will detail recent advances in exploiting knowledge of aminoglycoside–mitochondria interactions for the development of non-ototoxic antibacterials.
This article is part of a Special Issue entitled “Annual Reviews 2013”.Highlights
▸ Mitochondria play a major role in cochlear function and dysfunction. ▸ Noise may affect mitochondrial metabolism by calcium influx. ▸ Presbycusis correlates with distinct mitochondrial lesions but not necessarily with oxidative stress. ▸ Aminoglycosides inhibit the respiratory chain via targeting mitochondrial function. ▸ Non-ototoxic aminoglycosides can be developed by eliminating their activity against the mitochondrial ribosome.