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Cochlear pathology induced by styrene.

R Lataye1, P Campo, C Barthelemy

  • 1Institut National de Recherche et de Sécurité, Laboratoire de Neurotoxicité, Avenue de Bourgogne, BP 27, Vandoeuvre 54501, France.

Neurotoxicology and Teratology
|March 29, 2001
PubMed
Summary
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Styrene inhalation damages cochlear hair cells and spiral ganglion neurons in rats. Histopathology and electrophysiology suggest distinct injury pathways affecting the organ of Corti and spiral ganglion cells.

Area of Science:

  • Neuroscience
  • Toxicology
  • Otolaryngology

Background:

  • Styrene is a common industrial solvent with potential ototoxic effects.
  • Understanding the specific targets and mechanisms of styrene-induced cochlear damage is crucial for risk assessment.

Purpose of the Study:

  • To investigate the cochlear injury in Long-Evans rats following styrene inhalation.
  • To assess the impact of styrene on hair cells, spiral fibers, and spiral ganglion cells (SGCs).
  • To explore potential differences in intoxication routes affecting the organ of Corti and SGCs.

Main Methods:

  • Cochlear tissues from styrene-treated rats were analyzed histologically to count hair cells, spiral fibers, and SGCs.
  • Electrophysiological recordings of near-field potentials from the inferior colliculus were performed.

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  • Correlation between histopathological findings and electrophysiological data was examined.

    • Main Results:

    • Outer hair cells (OHCs) were identified as primary targets of inhaled styrene.
    • Degeneration of SGCs and spiral fibers was observed, particularly in the middle and mid-basal cochlear turns, with increasing styrene doses.
    • Electrophysiological data reflected SGC and fiber damage but showed weak correlation with organ of Corti histopathology.

    Conclusions:

    • Styrene inhalation causes distinct injuries to the organ of Corti and the spiral ganglion.
    • The findings suggest the existence of at least two separate intoxication routes for styrene within the cochlea.
    • Further research is warranted to elucidate these differential mechanisms of cochlear toxicity.