• Marcos Rabelo De Freitas, Aline Almeida Figueiredo, Gerly Anne de Castro Brito, Renata Ferreira de Carvalho Leitao, Jose Valdir de Carvalho Junior, Raimundo Martins Gomes Junior, and RibeiroRonaldo de AlbuquerqueRde A.
• Medical School, Federal University of Ceará.
• Braz J Otorhinolaryngol. 2009 Sep 1; 75 (5): 745-52.

UnlabelledCisplatin is a chemotherapy agent frequently used to treat different types of neoplasia. Ototoxicity is one of the side-effects which cause significant morbidity and limits its use. This study aimed at assessing the role of apoptosis in cisplatin-induced ototoxicity.Designexperimental study.Materials And Methodsmale Wistar rats were treated with intraperitoneal cisplatin, in the doses of 24 and 16 mg/kg. The animals were assessed by means of distortion product evoked otoacoustic emissions (DPEOAE) or brainstem evoked auditory potentials (BEAP) in the third (D3) and fourth (D4) days after drug infusion onset. Following that, their cochleas were removed for immunohistochemical studies of apoptosis - TUNEL method.Resultsthe group treated with 24 mg/kg showed a significant reduction in DPEOAE amplitude, and such fact was not seen with the 16 mg/kg. Both doses caused an increase in BEAP electrophysiological threshold in D3 and D4. Apoptosis was the injury mechanism responsible for the cisplatin-induced ototoxicity - 16 mg/kg dose, when the animals were assessed on D3.Conclusionapoptosis may be involved in the cisplatin-induced ototoxicity, depending on the dose and time of injury assessment.

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