Document Detail


Early elevation of cochlear reactive oxygen species following noise exposure.
MedLine Citation:
PMID:  10436315     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reactive oxygen species (ROS) have been implicated in a growing number of neurological disease states, from acute traumatic injury to neurodegenerative conditions such as Alzheimer's disease. Considerable evidence suggests that ROS also mediate ototoxicant- and noise-induced cochlear injury, although most of this evidence is indirect. To obtain real-time assessment of noise-induced cochlear ROS production in vivo, we adapted a technique which uses the oxidation of salicylate to 2,3-dihydroxybenzoic acid as a probe for the generation of hydroxyl radical. In a companion paper we described the development and characterization of this method in cochlear ischemia-reperfusion. In the present paper we use this method to demonstrate early elevations in ROS production following acute noise exposure. C57BL/6J mice were exposed for 1 h to intense broad-band noise sufficient to cause permanent threshold shift (PTS), as verified by auditory brainstem responses. Comparison of noise-exposed animals with unexposed controls indicated that ROS levels increase nearly 4-fold in the period 1-2 h following exposure and do not decline over that time. Our ROS measures extend previous results indicating that noise-induced PTS is associated with elevated cochlear ROS production and ROS-mediated injury. Persistent cochlear ROS elevation following noise exposure suggests a sustained process of oxidative stress which might be amenable to intervention with chronic antioxidant therapy.
Authors:
K K Ohlemiller; J S Wright; L L Dugan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Audiology & neuro-otology     Volume:  4     ISSN:  1420-3030     ISO Abbreviation:  Audiol. Neurootol.     Publication Date:    1999 Sep-Oct
Date Detail:
Created Date:  1999-09-30     Completed Date:  1999-09-30     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9606930     Medline TA:  Audiol Neurootol     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  229-36     Citation Subset:  IM    
Affiliation:
Research Department, Central Institute for the Deaf, Washington University School of Medicine, St. Louis, MO 63110, USA. kohlemiller@cid.wustl.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Chromatography, High Pressure Liquid / methods
Cochlea / chemistry,  metabolism*,  pathology
Evoked Potentials, Auditory, Brain Stem / physiology
Female
Gentisates / analysis,  metabolism*
Hair Cells, Auditory / pathology
Male
Mice
Mice, Inbred C57BL
Noise / adverse effects*
Reactive Oxygen Species / metabolism*
Salicylates / analysis,  metabolism*
Time Factors
Grant Support
ID/Acronym/Agency:
AG00599/AG/NIA NIH HHS; R03 DC92675/DC/NIDCD NIH HHS
Chemical
Reg. No./Substance:
0/Gentisates; 0/Reactive Oxygen Species; 0/Salicylates

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