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Disruption of ion-trafficking system in the cochlear spiral ligament prior to permanent hearing loss induced by exposure to intense noise: possible involvement of 4-hydroxy-2-nonenal as a mediator of oxidative stress.
Disruption of ion-trafficking system in the cochlear spiral ligament prior to permanent hearing loss induced by exposure to intense noise: possible involvement of 4-hydroxy-2-nonenal as a mediator of oxidative stress.
- Source :
-
PloS one [PLoS One] 2014 Jul 11; Vol. 9 (7), pp. e102133. Date of Electronic Publication: 2014 Jul 11 (Print Publication: 2014). - Publication Year :
- 2014
-
Abstract
- Noise-induced hearing loss is at least in part due to disruption of endocochlear potential, which is maintained by various K(+) transport apparatuses including Na(+), K(+)-ATPase and gap junction-mediated intercellular communication in the lateral wall structures. In this study, we examined the changes in the ion-trafficking-related proteins in the spiral ligament fibrocytes (SLFs) following in vivo acoustic overstimulation or in vitro exposure of cultured SLFs to 4-hydroxy-2-nonenal, which is a mediator of oxidative stress. Connexin (Cx)26 and Cx30 were ubiquitously expressed throughout the spiral ligament, whereas Na(+), K(+)-ATPase α1 was predominantly detected in the stria vascularis and spiral prominence (type 2 SLFs). One-hour exposure of mice to 8 kHz octave band noise at a 110 dB sound pressure level produced an immediate and prolonged decrease in the Cx26 expression level and in Na+, K(+)-ATPase activity, as well as a delayed decrease in Cx30 expression in the SLFs. The noise-induced hearing loss and decrease in the Cx26 protein level and Na(+), K(+)-ATPase activity were abolished by a systemic treatment with a free radical-scavenging agent, 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl, or with a nitric oxide synthase inhibitor, N(ω)-nitro-L-arginine methyl ester hydrochloride. In vitro exposure of SLFs in primary culture to 4-hydroxy-2-nonenal produced a decrease in the protein levels of Cx26 and Na(+), K(+)-ATPase α1, as well as Na(+), K(+)-ATPase activity, and also resulted in dysfunction of the intercellular communication between the SLFs. Taken together, our data suggest that disruption of the ion-trafficking system in the cochlear SLFs is caused by the decrease in Cxs level and Na(+), K(+)-ATPase activity, and at least in part involved in permanent hearing loss induced by intense noise. Oxidative stress-mediated products might contribute to the decrease in Cxs content and Na(+), K(+)-ATPase activity in the cochlear lateral wall structures.
- Subjects :
- Aldehydes antagonists & inhibitors
Animals
Cell Communication drug effects
Connexin 26
Connexin 30
Connexins antagonists & inhibitors
Connexins genetics
Connexins metabolism
Free Radicals antagonists & inhibitors
Free Radicals metabolism
Gene Expression Regulation
Hearing Loss, Noise-Induced etiology
Hearing Loss, Noise-Induced genetics
Hearing Loss, Noise-Induced metabolism
Ion Transport drug effects
Male
Mice
Mice, Transgenic
Nitric Oxide Synthase Type I antagonists & inhibitors
Nitric Oxide Synthase Type I genetics
Nitric Oxide Synthase Type I metabolism
Noise adverse effects
Oxidative Stress drug effects
Primary Cell Culture
Signal Transduction
Sodium-Potassium-Exchanging ATPase antagonists & inhibitors
Sodium-Potassium-Exchanging ATPase genetics
Sodium-Potassium-Exchanging ATPase metabolism
Spiral Ligament of Cochlea drug effects
Spiral Ligament of Cochlea pathology
Stria Vascularis drug effects
Stria Vascularis metabolism
Stria Vascularis pathology
Aldehydes pharmacology
Free Radical Scavengers pharmacology
Hearing Loss, Noise-Induced prevention & control
NG-Nitroarginine Methyl Ester pharmacology
Piperidines pharmacology
Spiral Ligament of Cochlea metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 9
- Issue :
- 7
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 25013956
- Full Text :
- https://doi.org/10.1371/journal.pone.0102133