A radical demise. Toxins and trauma share common pathways in hair cell death

R Kopke; K A Allen; D Henderson; M Hoffer; D Frenz; T Van de Water

doi:10.1111/j.1749-6632.1999.tb08641.x

A radical demise. Toxins and trauma share common pathways in hair cell death

Ann N Y Acad Sci. 1999 Nov 28:884:171-91. doi: 10.1111/j.1749-6632.1999.tb08641.x.

Authors

R Kopke¹, K A Allen, D Henderson, M Hoffer, D Frenz, T Van de Water

Affiliation

¹ DoD Spatial Orientation Center, Naval Medical Center, San Diego, California 92134, USA. rdkopke@nmcsd.med.navy.mil

PMID: 10842593
DOI: 10.1111/j.1749-6632.1999.tb08641.x

Abstract

The pathologic similarities noted after ototoxic and/or traumatic injury to the cochlea as well as the key features of the cochlea that make it susceptible to reactive oxygen species (ROS) damage are reviewed. Recent evidence linking ROS to cochlear damage associated with both ototoxins and/or trauma are presented. Mechanisms of generation of ROS in the cochlea and how these metabolites damage the cochlea and impair function are also reviewed. Finally, examples of novel therapeutic strategies to prevent and reverse hearing loss due to noise and/or ototoxins are presented to illustrate the clinical relevance of these new findings.

Publication types

Review

MeSH terms

Aminoglycosides
Animals
Anti-Bacterial Agents / adverse effects
Antineoplastic Agents / adverse effects
Antioxidants / metabolism
Antioxidants / therapeutic use
Cell Death / drug effects
Cell Death / physiology*
Cisplatin / adverse effects
Deafness / chemically induced
Deafness / drug therapy
Deafness / metabolism*
Hair Cells, Auditory / drug effects
Hair Cells, Auditory / physiology*
Hearing Loss, Noise-Induced / drug therapy
Hearing Loss, Noise-Induced / metabolism*
Reactive Oxygen Species / metabolism*

Substances

Aminoglycosides
Anti-Bacterial Agents
Antineoplastic Agents
Antioxidants
Reactive Oxygen Species
Cisplatin