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Mechanisms of cisplatin ototoxicity: theoretical review

Published online by Cambridge University Press:  07 May 2013

M S Gonçalves*
Affiliation:
Department of Speech-Language Pathology and Audiology, Federal University of Santa Maria, Porto Alegre, Brazil
A F Silveira
Affiliation:
Department of Morphology/Health Sciences Center, Federal University of Santa Maria, Porto Alegre, Brazil
A R Teixeira
Affiliation:
Department of Developmental Psychology and Personality, Federal University of Rio Grande do Sul, Porto Alegre, Brazil
M A Hyppolito
Affiliation:
Department of Ophthalmology, Otorhinolaryngology and Head and Neck Surgery, Ribeirão Preto Medical School, University of São Paulo, Brazil
*
Address for correspondence: Dr Maiara S Gonçalves, Avenida Evaldo Behr, 02 Parque Residencial Novo Horizonte, Bairro Camobi, Santa Maria, RS 97110-801, Brazil Fax: +55 55 3301 1166 E-mail: maiarasg@yahoo.com.br

Abstract

Introduction:

Cisplatin is an effective chemotherapeutic agent commonly used in the treatment of malignant tumours, but ototoxicity is a significant side effect.

Objectives:

To discuss the mechanisms of cisplatin ototoxicity and subsequent cell death, and to present the results of experimental studies.

Material and 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.

Conclusion:

Cisplatin ototoxicity proceeds via the formation of reactive oxygen species in cochlear tissue, with apoptotic cell death as a consequence.

Type
Review Articles
Copyright
Copyright © JLO (1984) Limited 2013 

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