Background and Aim: N-acetylcysteine, a glutathione precursor and reactive oxygen species scavenger, is reported to be effective in reducing noise-induced hearing loss. Many workers in industry are exposed simultaneously to noise and chemical pollutants such as carbon monoxide. We investigated effectiveness of N-acetylcysteine in protecting the cochlea from simultaneous noise and carbon monoxide damages.
Methods: Twelve rabbits were exposed simeltaneously to 100 dB sound pressure level of broad band noise and carbon monoxide 8 hours a day for 5 days. One hour before exposure, experimental group received 325 mg/kg of N-acetylcysteine while normal saline was administered for the control group. The protective effect of N-acetylcysteine was evaluated 3 weeks after exposure by histological assessment of the hair cells.
Results: Simultaneous exposure to noise and carbon monoxide resulted in a considerable damage to the outer hair cells however, the inner hair cells and the pillar cells remained intact. Use of N-acetylcysteine in the experimental group significantly reduced the extent of outer hair cell loss.
Conclusion: N-acetylcysteine attenuates simultaneous noise and carbon monoxide induced hair cell damage in rabbits.
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Background and Aim: One of the chemical pollutions which is frequently common in industry-other than noise is carbon monoxide. The present study aimed to assess the putative protective effect of N-acetylcysteine on the function of outer hair cells of rabbits exposed simultaneously to noise and carbon monoxide.
Methods: 24 male rabbits are entered in this interventional study. After obtaining baseline distortion product otoacoustic emissions, rabits were randomely devided into four groups. The groups Included: exposed with noise and received saline, exposed with noise and carbon monoxide and received saline, exposed with noise and received N-acetylcysteine, and exposed with noise and carbon monoxide and received N-acetylcysteine. Subsequently, they were evaluated again with distortion product otoacoustic emissions in two stages (two hours and one week after the exposure). Data were recorded and analyzed using paired and independent sample t-tests.
Results: Exposure to noise, and also simultaneous exposure to noise and carbon monoxide, and moreover using N-acetylcysteine in both groups, produced significant changes in distortion product otoacoustic emissions amplitudes (p<0.005).
Conclusion: The findings of the present research reveal that simultaneous exposure to noise and carbon monoxide may potentiate noise induced hearing loss. In addition, utilizing N-acetylcysteine can be used as a preventive agent for noise induced hearing loss and to avoid its potentiation with carbon monoxide.