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Oxidative stress-induced apoptosis of cochlear sensory cells: otoprotective strategies
1Department of Otolaryngology, Albert Einstein College of Medicine, Bronx, New York, USA.
Abstract:
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.
Insights
Apoptosis removes damaged auditory cells, but can harm inner ear development. Strategies to prevent reactive oxygen species-induced apoptosis may protect hearing and cochlear sensory cells.
Area of Science:
- Oto-neuroscience
- Cellular biology
- Auditory system research
Background:
- Apoptosis is crucial for inner ear development and clearing oxidative-stress damaged cochlear cells.
- Auditory sensory cells face oxidative stressors like trophic factor loss, ischemia-reperfusion, and ototoxins.
- Reactive oxygen species (ROS) and free radicals trigger apoptosis in auditory neurons and hair cells.
Purpose of the Study:
- To explore the role of apoptosis in inner ear sensory cell damage.
- To identify mechanisms by which oxidative stress induces apoptosis in auditory cells.
- To present strategies for preventing apoptosis-induced auditory sensory loss.
Main Methods:
- Investigating the role of reactive oxygen species (ROS) and free radicals in auditory cell apoptosis.
- Analyzing the formation of aldehydic lipid peroxidation products, such as 4-hydroxynonenal (4-HNE).
- Evaluating preventative approaches targeting ROS production, lipid peroxidation neutralization, and apoptotic pathways.
Main Results:
- Oxidative stressors initiate ROS and free radical production in auditory sensory cells.
- Aldehydic lipid peroxidation products, including 4-HNE, mediate apoptosis in auditory neurons and hair cells.
- Multiple strategies can prevent ROS-induced apoptosis and subsequent auditory sensory loss.
Conclusions:
- Apoptosis is a key mechanism in auditory sensory cell loss due to oxidative stress.
- 4-hydroxynonenal is identified as a significant mediator of apoptosis in cochlear cells.
- Preventing ROS formation, neutralizing lipid peroxidation products, and blocking apoptotic pathways are viable strategies for auditory protection.