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Apoptosis in the OC-k3 immortalized cell line treated with different agents

L Bertolaso1, A Martini, D Bindini

  • 1Center of Bioacoustics, Ferrara University, Italy.

Audiology : Official Organ of the International Society of Audiology
|January 10, 2002
PubMed

Insights

Cisplatin and gentamicin induce inner ear cell death through apoptosis, driven by increased reactive oxygen species (ROS). Antioxidants effectively prevent this ototoxicity, suggesting ROS plays a key role in hearing loss.

Area of Science:

  • Ototoxicity research
  • Cellular apoptosis mechanisms
  • Inner ear drug side effects

Background:

  • Cochlear cells are vulnerable to drug-induced damage.
  • Ototoxic drugs like cisplatin and gentamicin cause significant side effects.
  • Understanding cell death mechanisms is crucial for mitigating hearing loss.

Purpose of the Study:

  • To elucidate the mechanisms of cochlear cell death induced by ototoxic drugs.
  • To investigate the role of reactive oxygen species (ROS) and glutathione (GSH) in drug-induced apoptosis.
  • To evaluate the protective effects of antioxidants against ototoxicity.

Main Methods:

  • Utilized an immortalized OC-k3 cell line derived from mouse organ of Corti.
  • Exposed cells to varying concentrations of cisplatin and gentamicin over 48 hours.
  • Assessed cell viability, ROS production, GSH levels, and apoptosis markers (nuclear fragmentation).

Main Results:

  • Cisplatin and gentamicin induced dose- and time-dependent apoptosis in cochlear cells.
  • Apoptosis was characterized by nuclear fragmentation with intact cell membranes and mitochondria.
  • Early treatment showed increased ROS production and decreased GSH levels, linked to protein kinase C alpha activation.

Conclusions:

  • Reactive oxygen species (ROS) generation is a key mechanism in drug-induced inner ear cell apoptosis.
  • Antioxidants (N-acetylcysteine, GSH, vitamin C) significantly rescued cells from apoptosis.
  • ROS may contribute to age-related hearing decline.

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