alexa Reduced Phosphorylation of Histone Variant H2Ax in the Organ of Corti is Associated with Otoprotection from Noise Injury
ISSN: 2161-119X

Otolaryngology: Open Access
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Research Article

Reduced Phosphorylation of Histone Variant H2Ax in the Organ of Corti is Associated with Otoprotection from Noise Injury

O’neil W. Guthrie1,2* and Helen Xu2

1Research Service-151, Loma Linda Veterans Affairs Medical Center, Loma Linda, CA 92357, USA

2Department of Otolaryngology and Head & Neck Surgery, School of Medicine, Loma Linda University Medical Center, Loma Linda, CA 92354, USA

Corresponding Author:
Dr. O’neil W. Guthrie
Research Service-151
Loma Linda Veterans Affairs Medical Center
11201 Benton Street, Loma Linda, CA 92357-USA
Tel: 909 825 7084 Extn 4533
Fax: 909 796 4508
E-mail: O’[email protected]

Received date: November 27, 2012; Accepted date: January 10, 2013; Published date: January 16, 2013

Citation: Guthrie OW, Xu H (2013) Reduced Phosphorylation of Histone Variant H2Ax in the Organ Of Corti Is Associated With Otoprotection from Noise Injury. Otolaryngology 3:131. doi:10.4172/2161-119X.1000131

Copyright: © 2013 Guthrie OW, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Research on the molecular bases of noise induced hearing loss has revealed that noise exposure produces multiple independent and complementary biochemical cascades that could damage DNA. The phosphorylation of Ser139 of histone variant H2Ax (γ-H2Ax) occurs within one minute following DNA damage and spans two million DNA bases on either side of the damage. In the current study we investigated whether noise exposure could induce γ-H2Ax within the organ of Corti. Cumulative signal strength was employed to quantify the absolute level of γ-H2Ax in mathematical energy units. The results indicated that noise exposure could increase the level of γ-H2Ax in the organ of Corti. Furthermore, treatment with a DNA repair enhancing chemotype (carboxy alkyl ester) reduced the noise induced increase of γ-H2Ax which was associated with an accelerated rate of functional recovery from the noise exposure. The combined results implicate molecular mechanisms of DNA damage and repair in the pathophysiology of noise induced hearing loss.

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