Induction of free radicals in the cochlea by an aminoglycoside antibiotic

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The Mouse Round-window Approach for Ototoxic Agent Delivery: A Rapid and Reliable Technique for Inducing Cochlear Cell Degeneration
12:21

The Mouse Round-window Approach for Ototoxic Agent Delivery: A Rapid and Reliable Technique for Inducing Cochlear Cell Degeneration

Published on: November 26, 2015

M Takayama1, H Yamane, K Konishi

  • 1Department of Otolaryngology, Osaka City University Medical School, Japan.

Acta Oto-Laryngologica. Supplementum
|January 1, 1997
PubMed

Insights

Kanamycin (KM) administration causes free radical emergence in guinea pig cochlea. These reactive oxygen species appear in outer hair cells, coinciding with KM transport into the inner ear.

Area of Science:

  • Ototoxicity research
  • Free radical biology
  • Auditory system physiology

Background:

  • Free radicals are implicated in biological tissue damage.
  • Kanamycin (KM) is an antibiotic known to potentially cause hearing loss.

Purpose of the Study:

  • To investigate the emergence of free radicals in the guinea pig cochlea following kanamycin administration.
  • To correlate free radical generation with KM transport into the inner ear.

Main Methods:

  • Histochemical methods were employed to detect free radicals.
  • In vitro incubation of guinea pig cochlea with KM.
  • In vivo study involving topical application of KM to the guinea pig round window membrane.

Main Results:

  • Free radicals were observed in guinea pig cochlea incubated with KM (in vitro).
  • In vivo, free radical emergence was detected along the luminal membrane and hair bundles of outer hair cells.
  • The timing of free radical appearance and disappearance correlated with KM transport into the inner ear.

Conclusions:

  • Kanamycin administration is suggested to induce free radical emergence in the cochlea.
  • This oxidative stress may contribute to kanamycin-induced ototoxicity.
  • Further research is warranted to elucidate the precise mechanisms.

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