Oxidative Stress in Hearing Loss

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: 30 September 2024 | Viewed by 1102

Special Issue Editors


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Guest Editor
School of Medicine, Yale University, New Haven, CT, USA
Interests: ear; outer hair cell; inner ear

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Guest Editor
School of Medicine, Yale University, New Haven, CT, USA
Interests: hair cells; auditory; ear; inner; neurosciences; otolaryngology; physiology

Special Issue Information

Dear Colleagues,

The topics of this Special Issue are oxidative stress and hearing loss. As we all know, increased oxidative stress in the inner ear is one of the most dominant etiologies of genetical or environmental hearing loss. In the last two decades or so, hearing loss caused by oxidative stress has continued to be a prominent topic in hearing research, involving both basic research and clinical applications. As most of the research articles are spread out in various journals, this Special Issue will collate the efforts of our colleagues. We hope this Special Issue will lead to strong research on this topic. 

Our objective is to invite authors from multidiscipline research fields to submit relevant research papers and reviews.

Dr. Lei Song
Prof. Dr. Joseph Santos-Sacchi
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

  • ear
  • outer hair cell
  • inner ear

Published Papers (1 paper)

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Research

14 pages, 3993 KiB  
Article
Lercanidipine’s Antioxidative Effect Prevents Noise-Induced Hearing Loss
by Zhaoqi Guo, E Tian, Sen Chen, Jun Wang, Jingyu Chen, Weijia Kong, Debbie C. Crans, Yisheng Lu and Sulin Zhang
Antioxidants 2024, 13(3), 327; https://doi.org/10.3390/antiox13030327 - 07 Mar 2024
Viewed by 815
Abstract
Noise-induced hearing loss (NIHL) is a prevalent form of adult hearing impairment, characterized by oxidative damage to auditory sensory hair cells. Although certain dihydropyridines, the L-type calcium channel blockers, exhibit protective properties against such damage, the ability of third-generation dihydropryidines like lercanidipine to [...] Read more.
Noise-induced hearing loss (NIHL) is a prevalent form of adult hearing impairment, characterized by oxidative damage to auditory sensory hair cells. Although certain dihydropyridines, the L-type calcium channel blockers, exhibit protective properties against such damage, the ability of third-generation dihydropryidines like lercanidipine to mitigate NIHL remains unclear.We utilized glucose oxidase (GO)-treated OC1 cell lines and cochlear explants to evaluate the protective influence of lercanidipine on hair cells. To further investigate its effectiveness, we exposed noise-stimulated mice in vivo and analyzed their hearing thresholds. Additionally, we assessed the antioxidative capabilities of lercanidipine by examining oxidation-related enzyme expression and levels of oxidative stress markers, including 3-nitrotyrosine (3NT) and 4-hydroxynonenal (4HNE). Our findings demonstrate that lercanidipine significantly reduces the adverse impacts of GO on both OC-1 cell viability (0.3 to 2.5 µM) and outer hair cell (OHC) survival in basal turn cochlear explants (7 µM). These results are associated with increased mRNA expression of antioxidant enzyme genes (HO-1, SOD1/2, and Txnrd1), along with decreased expression of oxidase genes (COX-2, iNOS). Crucially, lercanidipine administration prior to, and following, noise exposure effectively ameliorates NIHL, as evidenced by lowered hearing thresholds and preserved OHC populations in the basal turn, 14 days post-noise stimulation at 110 dB SPL. Moreover, our observations indicate that lercanidipine’s antioxidative action persists even three days after simultaneous drug and noise treatments, based on 3-nitrotyrosine and 4-hydroxynonenal immunostaining in the basal turn. Based on these findings, we propose that lercanidipine has the capacity to alleviate NIHL and safeguard OHC survival in the basal turn, potentially via its antioxidative mechanism. These results suggest that lercanidipine holds promise as a clinically viable option for preventing NIHL in affected individuals. Full article
(This article belongs to the Special Issue Oxidative Stress in Hearing Loss)
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