Abstract
Objective: It was aimed to display ascorbic acid’s protective efficiency in preventing ototoxicity caused by cisplatin use with electrophysiological tests (Transient Evoked Otoacoustic Emission and Auditory Brainstem Responses) and ultrastructural study (light and electron microscopic).
Methods: As a result of electrophysiological tests, 30 ears of 15 guinea pigs with detected normal hearing threshold and emission have been taken into the scope of this survey and they have been randomly divided into 3 groups. One of these three groups have been planned as the control group (Group I), the other two (Group II and III) as working groups. The guinea pigs of the working group, Group II and Group III, have been intraperitoneally administered single dose of 1,5 mg/kg/day cisplatin and, additionally in Group III 300 mg/day Vitamin C administered intraperitoneally for a period of 8 days. Electrophysiological tests for 20 ears of 10 guinea pigs in Group II and III, who have been intraperitoneally drug administered, have been repeated. Internal and inter-group statistical comparisons of data acquired before and after intraperitoneal drug administration have been performed. Temporal bones have been prepared after the measurements, for ultrastructural examinations (for light and electron microscope).
Results: No statistically significant differences in emission parameters (reproductibility, response and Signal/Noise rate) and auditory brainstem responses between the working group and control group before drug administration have been identified. The difference between otoacoustic emission parameters and auditory brainstem responses before and after drug administration in Group II (working group) have been identified as statistically significant (p<0.05). When reproductibility, response values of total of 10 guinea pigs in Group III (working group) before and after drug administration are compared, the decrease have been identified statistically significant (p<0.05). On the other hand when Signal/Noise rates and auditory brainstem response measures are evaluated, the difference before and after the administration is not identified as statistically significant (p>0.05). In working groups II and III when emission parameters after the treatment are compared, difference between reproductibility rates have been identified as statistically significant whereas when response values, Signal/Noise rates and auditory brainstem response thresholds are evaluated, despite lower deterioration compared to those in Group II, this difference is not statistically significant (p>0.05).
In light and electron microscope findings of our works, normal cochlear structures have been observed in control group. After drug administration in working group II, clear dystrophic changes, hyper functions and activation of organelles have been observed both in light and electron microscopic images. No clear dystrophic changes have been identified in either light or electron microscopic images of receptor and support cells in Group III after drug administration.
Conclusions: We may claim that use of ascorbic acid in preventing ototoxicity developing as a result of cisplatin use has a protective efficiency in line with electrophysiological and ultrastructural findings.

Key words: cisplatin, ascorbic acid, ototoxicity