Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

Hear Res. 2007 Apr;226(1-2):22-43. doi: 10.1016/j.heares.2006.10.006. Epub 2006 Dec 4.


Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Antioxidants / therapeutic use
  • Auditory Threshold
  • Calcium / metabolism
  • Cell Death
  • Cochlea / metabolism
  • Dexamethasone / pharmacology
  • Free Radicals / metabolism
  • Glutamic Acid / pharmacology
  • Hearing Loss, Noise-Induced / etiology*
  • Hearing Loss, Noise-Induced / pathology
  • Hearing Loss, Noise-Induced / physiopathology
  • Hearing Loss, Noise-Induced / prevention & control*
  • Humans
  • Models, Biological
  • Nerve Growth Factors / physiology
  • Reactive Nitrogen Species / metabolism
  • Vasodilation


  • Antioxidants
  • Free Radicals
  • Nerve Growth Factors
  • Reactive Nitrogen Species
  • Glutamic Acid
  • Dexamethasone
  • Calcium