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Dynamic changes following combined treatment with gentamicin and ethacrynic acid with and without acoustic

T Hayashida1, H Hiel, D Dulon

  • 1INSERM Research Unit 229, University of Bordeaux II, France.

Acta Oto-Laryngologica
|November 1, 1989
PubMed

Insights

Sound exposure potentiates gentamicin uptake and toxicity in guinea pig hair cells, particularly in the cochlear base. This study reveals how sound activation influences aminoglycoside ototoxicity.

Area of Science:

  • Ototoxicity research
  • Auditory neuroscience
  • Pharmacology

Background:

  • Gentamicin (GM) is an aminoglycoside antibiotic known to cause ototoxicity.
  • Ethacrynic acid (EA) is a diuretic that can enhance GM ototoxicity.
  • The regional selectivity and mechanisms of GM-induced hair cell damage remain under investigation.

Purpose of the Study:

  • To investigate the regional selectivity of gentamicin ototoxicity in guinea pigs.
  • To examine the influence of sound stimulation on GM uptake and toxicity in cochlear hair cells.

Main Methods:

  • Guinea pigs were treated with gentamicin (GM) and ethacrynic acid (EA).
  • Electrophysiological (CAP thresholds), morphological, autoradiographic, and immunohistological methods were employed.
  • Two groups were studied: one with continuous sound stimulation and one with minimal sound exposure.

Main Results:

  • Sound stimulation (Group I) led to rapid high-frequency threshold elevations and widespread outer hair cell (OHC) destruction within 48 hours.
  • In contrast, minimal sound exposure (Group II) delayed threshold changes beyond 24 hours, despite early GM detection in hair cells.
  • Gentamicin uptake showed an apex-to-base gradient, concentrating in OHCs initially, then inner hair cells (IHCs), particularly in the cochlear base, with sound exposure enhancing this pattern and intracellular toxicity.

Conclusions:

  • Gentamicin appears to penetrate hair cells via the basal body.
  • Sound activation significantly potentiates both gentamicin uptake and its intracellular toxicity.
  • These findings highlight the role of acoustic activity in the regional selectivity of aminoglycoside-induced ototoxicity.

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