title: Aminoglycoside ototoxicity.
abstract: OBJECTIVE
  To summarize mechanisms of ototoxicity associated with aminoglycoside antibiotics and discuss possible protective strategies.
  
  
  RESULTS
  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 administration 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Head and Neck Institute, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
authors.forename: Mark Douglas
authors.initials: MD
authors.lastname: Rizzi
authors.forename: Keiko
authors.initials: K
authors.lastname: Hirose
mesh_terms: D000617:Aminoglycosides / Q000009:adverse effects* / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000009:adverse effects* / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D020022:Genetic Predisposition to Disease; D006198:Hair Cells, Auditory / Q000187:drug effects; D006319:Hearing Loss, Sensorineural / Q000139:chemically induced*; D006801:Humans; D009154:Mutation; D014012:Tinnitus / Q000139:chemically induced; D015837:Vestibular Diseases / Q000139:chemically induced*