Effects of ascorbic acid on oxidative system and transient evoked otoacoustic emissions in rabbits exposed to noise

Abstract

Objectives/hypothesis: The objective was to investigate the effects of both noise exposure and ascorbic acid on oxidative status and hearing thresholds of rabbits.

Study design: Randomized prospective animal study comparing oxidative parameters and otoacoustic emissions in two rabbit groups exposed to noise. One group was given ascorbic acid, the other group was not given any treatment.

Methods: Two groups of rabbits were used in the study; each group had six rabbits. The six rabbits in the first group were not given any treatment, whereas 500 mg intramuscular ascorbic acid twice daily for 2 1/2 days was given to the six rabbits in the second group. Transient evoked otoacoustic emissions were recorded in all animals before and after noise exposure. Total protein sulfhydryl groups, carbonyl contents, and malondialdehyde levels, as well as erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels, were measured in all rabbits. All the rabbits were exposed to noise (100 dB sound pressure level, 1000 Hz, 1 h), and transient evoked otoacoustic emissions were recorded again.

Results: When oxidative parameters before noise exposure were compared, erythrocyte glutathione and catalase enzyme levels were detected to be higher in the second group (P <.05). In the first group of rabbits after noise exposure, total protein sulfhydryl groups were found to be reduced (P <.05), whereas plasma carbonyl contents and malondialdehyde levels were elevated significantly (P <.05). In this group, erythrocyte glutathione, superoxide dismutase, and catalase enzyme levels were low (P <.05). In the second group, which was given ascorbic acid, total protein sulfhydryl groups were reduced (P <.05), whereas plasma carbonyl contents and malondialdehyde levels did not change (P >.05) following noise exposure. In the second group, erythrocyte glutathione and catalase enzyme levels were reduced (P <.05), but superoxide dismutase levels did not change (P >.05). Transient evoked otoacoustic emissions after noise exposure were weak in both groups, but reproducibility and signal-to-noise ratios were higher in the second group (P <.05).

Conclusion: Ascorbic acid treatment inhibited both lipid peroxidation and oxidative damage of proteins in rabbits exposed to noise. The study data suggest, at least, that oxidative status should be included in the physiopathology of noise-induced hearing loss; in addition, a brief application of ascorbic acid before noise exposure appeared to play a protective role for cochlea.