Thiol-Disulfide Homeostasis in Noise-Induced Hearing Loss in Rats.

Background: This study was designed to assess if thiol-disulfide homeostasis could be used as diagnostic biomarker in noise-induced hearing loss (NIHL) in a laboratory animal model.

Methods: The study was carried out with a total of 28 female albino rats in 4 groups: group 1 (control group) included rats that were not exposed to noise or any study treatment; in group 2, following noise exposure, rats received 2 mg of dexamethasone per kilogram of body weight via the intramuscular route for 5 days; in Group 3, rats were exposed to noise and received a saline solution for 5 days, in a volume (0.15 cc) matched to that of dexamethasone administered in group 2; and in group 4, rats were exposed to noise, and blood samples were collected during the early phase to assess thiol-disulfide homeostasis without administering any treatment. Rats in groups 2, 3, and 4 were exposed to 120 dB noise in the 4 kHz octave band for 4 hours. The auditory brainstem response (ABR) test was performed in all groups on day 1 after noise exposure and was repeated in groups 1, 2, and 3 on day 5. Auditory brainstem response thresholds were recorded at 8, 12, 16, 20, and 32 kHz frequencies. Groups 1, 2, and 3 rats were sacrificed on day 5, and group 4 rats were sacrificed by exsanguination on day 1 after noise exposure. Venous blood samples collected from the caudal vena cava were centrifuged and sent to the corresponding laboratory for thiol-disulfide homeostasis studies. After sacrificing the rats, the right and left temporal bones of each rat were removed and stained with hematoxylin eosin for histological studies to explore any pyknotic changes in spiral ganglion cells.

Results: Intergroup comparisons by frequency on day 5 of noise exposure showed statistically significantly lower responses in ABR measurements at 8 kHz, 12 kHz, and 16 kHz in group 2 compared to group 3 (P = .003, P=.006, and P=.002). Improvements were observed with dexamethasone administered for therapeutic purposes, particularly if the hearing loss was induced by low-frequency noise. In the assessment of the parameters of thiol-disulfide homeostasis, disulfide/native thiol and disulfide/total thiol ratios and ischemia-modified albumin (IMA) levels were higher in group 4 than in other groups, although only the differences between group 1 and group 4 reached statistical significance.

Conclusion: According to this study, thiol-disulfide homeostasis and IMA can be shown as diagnostic biomarkers in NIHL, especially in the early period. The results from our study suggest that these markers may be used as adjunctive diagnostic tools in NIHL, in addition to audiological studies. However, this issue can be clarified with further clinical studies.