PURPOSE OF REVIEW: To summarize mechanisms of ototoxicity associated with aminoglycoside antibiotics and discuss possible protective strategies. RECENT FINDINGS: Studies in the past 15 years have demonstrated that aminoglycoside ototoxicity is mediated by an apoptotic form of cell death which employs caspase-dependent pathways. Reactive oxygen species have been demonstrated in the sensory epithelium after aminoglycoside adminstration and methods of blocking reactive oxygen species in the cochlea have been attempted, but not found to be uniformly effective in protecting against cell loss or threshold shift. Aspirin has recently been studied in a human chemoprevention trial in China, and while data suggest the possibility of protection, there was a significant increase in gastrointestinal bleeds associated with aspirin use. SUMMARY: There are currently no recommendations for pretreatment or posttreatment therapies to attenuate ototoxicity associated with aminoglycoside antibiotics. Our understanding of the mechanisms of ototoxicity has improved and apoptotic pathways are clearly responsible for hair cell demise. Further studies are necessary before significant improvement in hearing outcome can be expected after use of ototoxic antibiotics.
|Number of pages||6|
|Journal||Current Opinion in Otolaryngology and Head and Neck Surgery|
|State||Published - Oct 2007|
- Hair cell
- Reactive oxygen