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Ototoxicity: mechanisms of cochlear impairment and its prevention

K Tabuchi1, B Nishimura, M Nakamagoe

  • 1Department of Otolaryngology, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, 305-8575, Japan. ktabuchi@md.tsukuba.ac.jp

Current Medicinal Chemistry
|September 17, 2011
PubMed

Insights

Aminoglycosides and cisplatin can cause permanent hearing loss by inducing outer hair cell apoptosis via reactive oxygen species (ROS). Non-steroidal anti-inflammatory drugs (NSAIDs) may cause temporary hearing issues but also show potential therapeutic benefits for cochlear injuries.

Area of Science:

  • Pharmacology
  • Ototoxicology
  • Cell Biology

Background:

  • Aminoglycosides, cisplatin, and NSAIDs are common drugs with potential ototoxic side effects.
  • Ototoxicity can manifest as transient or permanent hearing loss and tinnitus.
  • Recent animal studies have elucidated the mechanisms of drug-induced ototoxicity.

Purpose of the Study:

  • To review recent findings from animal studies on the ototoxicity of aminoglycosides, cisplatin, and NSAIDs.
  • To focus on the underlying mechanisms of ototoxicity induced by these agents.

Main Methods:

  • Review of recent animal studies on drug-induced ototoxicity.
  • Analysis of mechanisms involving reactive oxygen species (ROS) and cell-death pathways.

Main Results:

  • Aminoglycosides and cisplatin induce permanent hearing loss primarily through outer hair cell apoptosis, mediated by ROS activating JNK and MAPK pathways.
  • NSAID abuse can lead to transient tinnitus and hearing loss by impairing outer hair cell function and affecting auditory neurons.
  • NSAIDs also show potential as therapeutic agents against cochlear injuries.

Conclusions:

  • The mechanisms of ototoxicity for aminoglycosides, cisplatin, and NSAIDs involve distinct pathways affecting cochlear hair cells and auditory neurons.
  • Understanding these mechanisms is crucial for managing and potentially preventing drug-induced hearing loss.
  • NSAIDs present a dual role, with potential for both ototoxicity and therapeutic intervention in cochlear injuries.

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