Oxidative Stress and Noise Induced Cell Death

Document Type : Review Article

Authors

1 Rehabilitation Research Center, Department of Audiology, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran

2 Scientific Member of the Department of Audiology, Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences, PhD Candidate of Audiology in Tehran University of Medical Sciences, Tehran, Iran

3 PhD Candidate of Gas Engineering Department, Petroleum University of Technology, Ahvaz, Iran

4 PhD, Scientific Member of the Department of Audiology, Musculoskeletal Rehabilitation Research Center, Ahvaz Jundishapur University of Medical Sciences

Abstract

Background and Aims: One of the major causes of sensorineural hearing loss is Noise-induced hearing loss. Cochlear damage following noise exposure occurs through two major mechanisms: direct mechanical damage and biochemical pathways. Direct mechanical damage causes hair cell loss through mechanical damage of sterreocilia and direct damage of sensory and protective cells. Cochlear damage following noise exposure through biochemical pathway result in cell death through apoptosis or necrosis. The reason for this is Oxidative Stress and generation of reactive oxygen species following noise exposure. This may remain in the cochlea long after noise exposure has been terminated.
Materials and Methods: In order to review the relationship between Cell death, Oxidative Stress and Noise induce hearing loss, all of the articles in this field published between 1990-2017 in Ovid, ProQuest, and Google Scholar databases were searched.
Conclusion:  This fact shows the importance of preventing apoptosis even after exposure to noise. Understanding noise-induced cochlear damage, especially the importance of free radical expression in the cochlea, can lead to advancements in preserving the hearing.

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References

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The Scientific Journal of Rehabilitation Medicine
Volume 9, Issue 2
July 2020
Pages 311-317

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History

  • Receive Date: 15 July 2019
  • Revise Date: 04 November 2019
  • Accept Date: 13 December 2019
  • First Publish Date: 21 June 2020

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