Intense noise induces formation of vasoactive lipid peroxidation products in the cochlea

Citation
Y. Ohinata et al., Intense noise induces formation of vasoactive lipid peroxidation products in the cochlea, BRAIN RES, 878(1-2), 2000, pp. 163-173
Citations number
52
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
878
Issue
1-2
Year of publication
2000
Pages
163 - 173
Database
ISI
SICI code
0006-8993(20000929)878:1-2<163:INIFOV>2.0.ZU;2-M
Abstract
This study investigates the correlation between the formation of reactive o xygen species (ROS) and auditory damage in noise-induced hearing loss. The noise exposure (4-kHz octave band, 115 dB SPL, 5 h) created permanent thres hold shifts at frequencies from 2 to 20 kHz. The lipid peroxidation product , 8-isoprostane, was determined biochemically and histochemically as an ind icator of ROS. Noise exposure increased 8-isoprostane levels in the cochlea in a time-dependent manner. After 5 h of exposure, 8-isoprostane levels we re more than 30-fold greater than baseline, and decreased rapidly after the termination of noise. The immunoreactivity to 8-isoprostane was increased in the stria vascularis, spiral ganglion cells and the organ of Corti. In t he organ of Corti, immunostaining was restricted to the second turn in a re gion 10-12 mm from the apex. This region sustained most of the permanent ha ir cell damage as revealed in surface preparations. Outer hair cells were m ore heavily immunostained than inner hair cells while Hensen's cells showed still less immunostain. These data are consistent with the view that ROS a re involved in noise-induced damage. However, the relationship between ROS formation and tissue damage appears complex. In the organ of Corti, the pat tern of noise-induced lipid peroxidation correlates well with subsequent mo rphological damage. The stria vascularis, however, does not sustain permane nt damage despite intense lipid peroxidation. Differences in endogenous ant ioxidant levels and commitment to different apoptotic or survival pathways may underlie such differential responses. (C) 2000 Elsevier Science B.V. Al l rights reserved.