Oxidative stress-induced apoptosis of cochlear sensory cells: Otoprotective strategies

Tina Huang, Alan G. Cheng, Howard Stupak, Wei Liu, Ana Kim, Hinrich Staecker, Philippe P. Lefebvre, Brigitte Malgrange, Richard Kopke, Gustave Moonen, Thomas R. Van De Water

Research output: Contribution to journalArticlepeer-review

175 Scopus citations


Apoptosis is an important process, both for normal development of the inner ear and for removal of oxidative-stress damaged sensory cells from the cochlea. Oxidative-stressors of auditory sensory cells include: loss of trophic factor support, ischemia-reperfusion, and ototoxins. Loss of trophic factor support and cisplatin ototoxicity, both initiate the intracellular production of reactive oxygen species and free radicals. The interaction of reactive oxygen species and free radicals with membrane phospholipids of auditory sensory cells creates aldehydic lipid peroxidation products. One of these aldehydes, 4-hydroxynonenal, functions as a mediator of apoptosis for both auditory neurons and hair cells. We present several approaches for the prevention of auditory sensory loss from reactive oxygen species-induced apoptosis: 1) preventing the formation of reactive oxygen species; (2) neutralizing the toxic products of membrane lipid peroxidation; and 3) blocking the damaged sensory cells' apoptotic pathway. Copyright (C) 2000 ISDN.

Original languageEnglish (US)
Pages (from-to)259-270
Number of pages12
JournalInternational Journal of Developmental Neuroscience
Issue number2-3
StatePublished - Jun 2000

Bibliographical note

Funding Information:
This work was supported by the Hearing Research Fund of Montefiore Medical Center to TRV, and Albert Einstein College of Medicine Neuropathology Training grant NS07098 support to Tina Huang, Alan G. Cheng, Howard Stupak, and Ana Kim.


  • Apoptosis
  • Auditory system
  • Calpains
  • Caspases
  • Cisplatin
  • Hair cells
  • Ischemia/hypoxia
  • Neurons
  • Reactive oxygen species
  • Trophic factor withdrawal


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