Vestibular damage in chronic ototoxicity: a mini-review

Area of Science:

• Oto-neuroscience
• Toxicology
• Cell Biology

Background:

• Ototoxicity, caused by drugs and chemicals, leads to hearing and balance loss.
• Hair cells (HCs) in auditory and vestibular systems are primary targets, but neurons can also be affected.
• Known mechanisms include apoptosis via pathways like c-jun N-terminal kinase (JNK).

Purpose of the Study:

• To investigate the mechanisms of ototoxicity, particularly under chronic low-dose exposure.
• To understand the effects on hair cells and associated neurons in the vestibular system.
• To elucidate pathways involved in sensory cell demise and neuronal damage.

Main Methods:

• Review of human and rodent data on ototoxicity.
• Analysis of cellular responses including apoptosis, necrosis, and extrusion.
• Examination of signaling pathways such as JNK and excitotoxicity.

Main Results:

• Chronic low-dose ototoxicity in rodents shows HC extrusion as a primary cell death mechanism.
• Afferent terminals, especially calyx units, are increasingly involved.
• Excitotoxic phenomena mediated by glutamate may contribute to neuronal damage.

Conclusions:

• Chronic ototoxicity involves unique mechanisms like HC extrusion and excitotoxicity.
• Understanding these processes is crucial for addressing sensory loss from long-term exposure and aging.
• Further research is needed on chronic low-dose exposure effects.