Occupational noise exposure is one of the leading factors for developing noise-induced hearing loss (NIHL), particularly among workers worldwide. The literature review reveals that beside conventional strategies for preventing NIHL, multiple interventions can be applied to reduce or prevent such disorders. The present study aimed to investigate the preventive effects of normobaric hyperoxia pre- and post-treatment on the development of NIHL in rats.
Four groups of male Wistar rats were exposed to pure oxygen alone, noise alone, or oxygen plus noise for 6 hours a day, 5 days a week for 4 weeks. One group served as the control and received neither noise nor oxygen. Animals in the noise groups were exposed to high-pass white noise of 100 dB SPL, centred at 8 KHz. The treatment protocols were based on inhalation of pure normobaric oxygen (95%) for 3 hours in a chamber either before or after noise exposure. The auditory brainstem responses (ABRs) for click and 4, 6, 8, 12, and 16 kHz stimuli, as well as distortion product otoacoustic emissions (DPOAEs) at 4, 6, 8, and 10 kHz, were recorded to assess the level of hearing impairment before exposure and 4 weeks post-exposure.
The results showed that pre-treatment of rats with 3 hours of normobaric hyperoxia contributed to a significant reduction in ABR threshold shifts, while improving the DPOAE amplitudes (P < 0.01). However, three hours of post-treatment did not produce any comparable results in terms of ABR threshold shifts or DPOAE amplitude improvements. DPOAE amplitudes and ABR threshold shifts remained almost constant during exposure in the control group (P > 0.05).
Pre- and post-treatment with normobaric hyperoxia seem to produce protective effects through either boosting cellular oxygenation or maximizing antioxidant enzyme activities and tolerance against noise-induced ischemia and hypoxia in the cochlea. Therefore, application of normobaric hyperoxia pre- or post-treatment, along with other conventional protective strategies, can be helpful in the fight against NIHL.