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Related Experiment Videos

Trichloroethylene ototoxicity: evidence for a cochlear origin

L D Fechter1, Y Liu, D W Herr

  • 1Toxicology Program, The University of Oklahoma College of Pharmacy, Oklahoma City, Oklahoma, USA.

Toxicological Sciences : an Official Journal of the Society of Toxicology
|May 30, 1998
PubMed
Summary

Trichloroethylene (TCE) exposure causes hearing loss in rats, primarily affecting midfrequencies. This auditory deficit stems from cochlear dysfunction, specifically impacting spiral ganglion cells.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Auditory Science

Background:

  • Trichloroethylene (TCE) exposure is linked to hearing impairment in animals, characterized by midfrequency hearing loss.
  • The precise mechanism of TCE-induced auditory deficit, particularly its origin within the cochlea, requires further investigation.

Purpose of the Study:

  • To investigate whether Trichloroethylene (TCE)-induced auditory deficits result from cochlear dysfunction.
  • To identify specific cellular targets within the cochlea affected by TCE exposure.

Main Methods:

  • Adult Long Evans hooded rats were exposed to 4000 ppm Trichloroethylene (TCE) via inhalation.
  • Auditory thresholds were assessed using reflex modification audiometry (RMA).
  • Cochlear function was evaluated through electrophysiological measurements, including cochlear action potentials (CAP) and cochlear microphonics, followed by cochlear histopathology.

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Main Results:

  • Reflex modification audiometry confirmed a TCE-induced loss in midfrequency hearing sensitivity (8 and 16 kHz).
  • Cochlear action potential (CAP) thresholds were elevated at midfrequencies in TCE-exposed rats, with suppressed N1 amplitude.
  • Cochlear histopathology revealed significant spiral ganglion cell loss in the middle turn, while cochlear microphonics remained unaffected.

Conclusions:

  • The study strongly suggests that Trichloroethylene (TCE)-induced hearing loss is attributable to cochlear impairment.
  • Spiral ganglion cells appear to be a primary target of Trichloroethylene (TCE) toxicity in the cochlea.