Oxidative stress‐induced apoptosis of cochlear sensory cells: otoprotective strategies

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 fact...

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Published in:International journal of developmental neuroscience 2000-06, Vol.18 (2-3), p.259-270
Main Authors: Huang, Tina, Cheng, Alan G., Stupak, Howard, Liu, Wei, Kim, Ana, Staecker, Hinrich, Lefebvre, Philippe P., Malgrange, Brigitte, Kopke, Richard, Moonen, Gustave, Van De Water, Thomas R.
Format: Article
Language:English
Subjects:
4-hydroxynonenal
Animals
Apoptosis
Apoptosis - physiology
Auditory system
Calpains
Caspases
Cisplatin
Hair cells
Hair Cells, Auditory - cytology
Hair Cells, Auditory - enzymology
Ischemia/hypoxia
Neurons
otoprotection
Oxidative Stress - physiology
Reactive oxygen species
Spiral Ganglion - cytology
Trophic factor withdrawal
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Summary: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.
ISSN:0736-5748
1873-474X
DOI:10.1016/S0736-5748(99)00094-5