OBJECTIVE:The possible preventive effect of N-acetylcysteine (NAC) in gentamicin ototoxicity was studied with auditory brain stem responses (ABRs), otoacoustic emissions (OAEs), and histopathological investigation of the cochlea. MATERIALS and METHODS:This study is conducted on 36 rats in three groups. Gentamicin, gentamicin plus NAC, and NAC alone were intraperitoneally administered for 15 days. The rats were sacrificed to study the cochleas after testing hearing levels. RESULTS:ABR thresholds and OAEs were attenuated in the gentamicin group, in which apoptosis was detected with histopathological investigation. The group that received NAC in addition to gentamicin had better ABR thresholds and better OAEs. The histopathological evidence of apoptosis in was considerably less in this group. CONCLUSION:Gentamicin ototoxicity can be detected by ABR and OAE testing in rats, and NAC may protect the cochlear cells from apoptosis.

The aim of this study was to investigate the potential protective effect of thymoquinone against cisplatin-induced ototoxicity. This study is a prospective, controlled experimental animal study. Experiments were performed on 30 healthy female Sprague-Dawley rats. Thirty animals were divided into three groups of 10 animals each. Group 1 received an intraperitoneal (i.p.) injection of cisplatin 15 mg/kg. Group 2 received i.p. thymoquinone 40 mg/kg/day for 2 days prior to cisplatin injection and third day i.p. cisplatin 15 mg/kg was administered concomitantly. Group 2 continued to receive i.p. thymoquinone until fifth day. Group 3 received i.p. thymoquinone 40 mg/kg/day for 5 days. Pretreatment distortion product otoacoustic emissions (DPOAE) and auditory brain stem responses (ABR) testing from both ears were obtained from the animals in all groups. After the baseline measurements, drugs were injected intraperitonally. After an observation period of 3 days, DPOAE measurements and ABR testing were obtained again and compared with the pretreatment values. There was no statistically significant difference between pre and post-treatment DPOAE responses and ABR thresholds group 2 and 3. However, group 1 demonstrated significant deterioration of the ABR thresholds and DPOAE responses. Our results suggest that DPOAE responses and ABR thresholds were preserved in the cisplatin plus TQ-treated group when compared with the group receiving cisplatin alone. According to these results, cisplatin-induced ototoxicity may be prevented by thymoquinone use in rats.

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