title: Mechanisms of cisplatin ototoxicity: theoretical review.
abstract: BACKGROUND
  Cisplatin is an effective chemotherapeutic agent commonly used in the treatment of malignant tumours, but ototoxicity is a significant side effect.
  
  
  OBJECTIVE
  To discuss the mechanisms of cisplatin ototoxicity and subsequent cell death, and to present the results of experimental studies.
  
  
  METHODS
  We conducted a systematic search for data published in national and international journals and books, using the Medline, SciELO, Bireme, LILACS and PubMed databases.
  
  
  RESULTS
  The nicotinamide adenine dinucleotide phosphate oxidase 3 isoform (also termed NOX3) seems to be the main source of reactive oxygen species in the cochlea. These reactive oxygen species react with other molecules and trigger processes such as lipid peroxidation of the plasma membrane and increases in expression of the transient vanilloid receptor potential 1 ion channel.
  
  
  CONCLUSIONS
  Cisplatin ototoxicity proceeds via the formation of reactive oxygen species in cochlear tissue, with apoptotic cell death as a consequence.
authors: Department of Speech-Language Pathology and Audiology, Federal University of Santa Maria, Porto Alegre, Brazil. maiarasg@yahoo.com.br
authors: M S
authors: MS
authors: Gonçalves
authors: A F
authors: AF
authors: Silveira
authors: A R
authors: AR
authors: Teixeira
authors: M A
authors: MA
authors: Hyppolito
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000633:toxicity*; D017209:Apoptosis / Q000187:drug effects; D002945:Cisplatin / Q000633:toxicity*; D003051:Cochlea / Q000187:drug effects* / Q000378:metabolism; D015834:Cochlear Diseases / Q000139:chemically induced; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D017382:Reactive Oxygen Species; D002945:Cisplatin