Otoprotection Mechanisms Against Oxidative Stress Caused by Cisplatin

Abstract

Introduction  Cisplatin damages the auditory system and is related to the generation of free radicals. Glutathione peroxidase is an endogenous free radicals remover.

Objective  To investigate the mechanisms involved in otoprotection by N-acetylcysteine through the expression of glutathione peroxidase in outer hair cells from rats treated with cisplatin.

Methods  Male Wistar rats were intraperitoneally injected with cisplatin (8 mg/Kg) and/or received oral administration by gavage of N-acetylcysteine (300 mg/Kg) for 3 consecutive days. On the 4 ^th day, the animals were euthanized and beheaded. The tympanic bullae were removed and prepared for scanning electron microscopy and immunofluorescence.

Results  Among the groups exposed to ototoxic doses of cisplatin, there was an increase in glutathione peroxidase immunostaining in two groups, the one exposed to cisplatin alone, and the group exposed to both cisplatin and N-acetylcysteine.

Conclusion  The expression of glutathione peroxidase in the outer hair cells of rats exposed to cisplatin showed the synthesis of this enzyme under cellular toxicity conditions.