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Antioxidants
Special Issues
Oxidative Stress and Hearing Loss
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Oxidative Stress and Hearing Loss

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 May 2023) | Viewed by 16148

Special Issue Editors

Dr. Isabel Varela-Nieto

E-Mail Website
Guest Editor
1. Institute for Biomedical Research "Alberto Sols" (IIBm), Spanish National Research Council-Autonomous University of Madrid (CSIC-UAM), 28029 Madrid, Spain
2. Rare Diseases Networking Biomedical Research Centre (CIBERER), CIBER, Carlos III Institute of Health, 28029 Madrid, Spain
3. La Paz Hospital Institute for Health Research (IdiPAZ), 28046 Madrid, Spain
Interests: apoptosis; autophagy; senescence; Cochlea; Hearing Loss; Age-related HL; Noise-induced HL; deafness; IGF-1; IGF1R; AKT; RAF; p38; JNK
Dr. Francis Rousset

E-Mail Website
Co-Guest Editor
The Inner Ear and Olfaction Lab, Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, CH-1206 Geneva, Switzerland
Interests: (i) the characterization of molecular pathways involved in the pathogenesis of hearing loss, (ii) the regeneration of auditory cells of the cochlea and (iii) the development of genetic tools for gene therapy of hearing loss

Special Issue Information

Dear Colleagues,

Disabling hearing loss affects 466 million people worldwide (WHO, March 2022). It is heterogeneous in its causes, which can be genetic and/or environmental, such as exposure to noise or ototoxics and aging. It irreversible because the cell types fundamental to hearing, which are auditory neurons, hair cells and supporting cells, do not regenerate in mammals. Although the causes are diverse, when considering the biochemical and molecular mechanisms that lead to the death of these specialized cells, common cues are found. Loss of redox balance leading to the oxidation of molecules essential for cell function and survival is one of the main common mechanisms. Nowadays, the implication of oxidative stress in inner ear damage is well established, however, further research is needed to better understand the exact molecular mechanisms and to prevent redox-mediated forms of hearing loss.

In this Special Issue we want to address these basic aspects from a broad perspective. We will welcome reviews on general redox molecular mechanisms, including those focused on hearing physiopathology, plus original manuscripts focused on understanding how the redox balance is maintained and how the redox balance is lost in the hearing organ, as well as those that address preclinical studies of new molecules aimed at the protection and repair of hearing. We will also welcome complementary manuscripts on related sensory and neural structures, such as the olfactory sensory epithelium and the nervous system.

Dr. Isabel Varela-Nieto
Dr. Francis Rousset
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • redox unbalance
  • ageing mechanisms
  • ototoxicity
  • noise
  • neural and sensory cell types
  • cochlea

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Published Papers (6 papers)

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Research

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21 pages, 9346 KiB  
Article
Oxidative Stress Plays an Important Role in Glutamatergic Excitotoxicity-Induced Cochlear Synaptopathy: Implication for Therapeutic Molecules Screening
by Anissa Rym Saidia, Florence François, François Casas, Ilana Mechaly, Stéphanie Venteo, Joseph T. Veechi, Jérôme Ruel, Jean-Luc Puel and Jing Wang
Antioxidants 2024, 13(2), 149; https://doi.org/10.3390/antiox13020149 - 25 Jan 2024
Cited by 2 | Viewed by 1880
Abstract
The disruption of the synaptic connection between the sensory inner hair cells (IHCs) and the auditory nerve fiber terminals of the type I spiral ganglion neurons (SGN) has been observed early in several auditory pathologies (e.g., noise-induced or ototoxic drug-induced or age-related hearing [...] Read more.
The disruption of the synaptic connection between the sensory inner hair cells (IHCs) and the auditory nerve fiber terminals of the type I spiral ganglion neurons (SGN) has been observed early in several auditory pathologies (e.g., noise-induced or ototoxic drug-induced or age-related hearing loss). It has been suggested that glutamate excitotoxicity may be an inciting element in the degenerative cascade observed in these pathological cochlear conditions. Moreover, oxidative damage induced by free hydroxyl radicals and nitric oxide may dramatically enhance cochlear damage induced by glutamate excitotoxicity. To investigate the underlying molecular mechanisms involved in cochlear excitotoxicity, we examined the molecular basis responsible for kainic acid (KA, a full agonist of AMPA/KA-preferring glutamate receptors)-induced IHC synapse loss and degeneration of the terminals of the type I spiral ganglion afferent neurons using a cochlear explant culture from P3 mouse pups. Our results demonstrated that disruption of the synaptic connection between IHCs and SGNs induced increased levels of oxidative stress, as well as altered both mitochondrial function and neurotrophin signaling pathways. Additionally, the application of exogenous antioxidants and neurotrophins (NT3, BDNF, and small molecule TrkB agonists) clearly increases synaptogenesis. These results suggest that understanding the molecular pathways involved in cochlear excitotoxicity is of crucial importance for the future clinical trials of drug interventions for auditory synaptopathies. Full article
(This article belongs to the Special Issue Oxidative Stress and Hearing Loss)
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21 pages, 2325 KiB  
Article
Pharmacological Modulation of Energy and Metabolic Pathways Protects Hearing in the Fus1/Tusc2 Knockout Model of Mitochondrial Dysfunction and Oxidative Stress
by Winston J. T. Tan, Joseph Santos-Sacchi, Jane Tonello, Anil Shanker and Alla V. Ivanova
Antioxidants 2023, 12(6), 1225; https://doi.org/10.3390/antiox12061225 - 6 Jun 2023
Cited by 2 | Viewed by 1943
Abstract
Tightly regulated and robust mitochondrial activities are critical for normal hearing. Previously, we demonstrated that Fus1/Tusc2 KO mice with mitochondrial dysfunction exhibit premature hearing loss. Molecular analysis of the cochlea revealed hyperactivation of the mTOR pathway, oxidative stress, and altered mitochondrial morphology and [...] Read more.
Tightly regulated and robust mitochondrial activities are critical for normal hearing. Previously, we demonstrated that Fus1/Tusc2 KO mice with mitochondrial dysfunction exhibit premature hearing loss. Molecular analysis of the cochlea revealed hyperactivation of the mTOR pathway, oxidative stress, and altered mitochondrial morphology and quantity, suggesting compromised energy sensing and production. Here, we investigated whether the pharmacological modulation of metabolic pathways using rapamycin (RAPA) or 2-deoxy-D-glucose (2-DG) supplementation can protect against hearing loss in female Fus1 KO mice. Additionally, we aimed to identify mitochondria- and Fus1/Tusc2-dependent molecular pathways and processes critical for hearing. We found that inhibiting mTOR or activating alternative mitochondrial energetic pathways to glycolysis protected hearing in the mice. Comparative gene expression analysis revealed the dysregulation of critical biological processes in the KO cochlea, including mitochondrial metabolism, neural and immune responses, and the cochlear hypothalamic–pituitary–adrenal axis signaling system. RAPA and 2-DG mostly normalized these processes, although some genes showed a drug-specific response or no response at all. Interestingly, both drugs resulted in a pronounced upregulation of critical hearing-related genes not altered in the non-treated KO cochlea, including cytoskeletal and motor proteins and calcium-linked transporters and voltage-gated channels. These findings suggest that the pharmacological modulation of mitochondrial metabolism and bioenergetics may restore and activate processes critical for hearing, thereby protecting against hearing loss. Full article
(This article belongs to the Special Issue Oxidative Stress and Hearing Loss)
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23 pages, 3376 KiB  
Article
IGF-1 Controls Metabolic Homeostasis and Survival in HEI-OC1 Auditory Cells through AKT and mTOR Signaling
by Ángela García-Mato, Blanca Cervantes, Lourdes Rodríguez-de la Rosa and Isabel Varela-Nieto
Antioxidants 2023, 12(2), 233; https://doi.org/10.3390/antiox12020233 - 19 Jan 2023
Cited by 7 | Viewed by 3186
Abstract
Insulin-like growth factor 1 (IGF-1) is a trophic factor for the nervous system where it exerts pleiotropic effects, including the regulation of metabolic homeostasis. IGF-1 deficiency induces morphological alterations in the cochlea, apoptosis and hearing loss. While multiple studies have addressed the role [...] Read more.
Insulin-like growth factor 1 (IGF-1) is a trophic factor for the nervous system where it exerts pleiotropic effects, including the regulation of metabolic homeostasis. IGF-1 deficiency induces morphological alterations in the cochlea, apoptosis and hearing loss. While multiple studies have addressed the role of IGF-1 in hearing protection, its potential function in the modulation of otic metabolism remains unclear. Here, we report that “House Ear Institute-organ of Corti 1” (HEI-OC1) auditory cells express IGF-system genes that are regulated during their differentiation. Upon binding to its high-affinity receptor IGF1R, IGF-1 activates AKT and mTOR signaling to stimulate anabolism and, concomitantly, to reduce autophagic catabolism in HEI-OC1 progenitor cells. Notably, IGF-1 stimulation during HEI-OC1 differentiation to mature otic cells sustained both constructive metabolism and autophagic flux, possibly to favor cell remodeling. IGF1R engagement and downstream AKT signaling promoted HEI-OC1 cell survival by maintaining redox balance, even when cells were challenged with the ototoxic agent cisplatin. Our findings establish that IGF-1 not only serves an important function in otic metabolic homeostasis but also activates antioxidant defense mechanisms to promote hair cell survival during the stress response to insults. Full article
(This article belongs to the Special Issue Oxidative Stress and Hearing Loss)
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25 pages, 7896 KiB  
Article
Kanamycin and Cisplatin Ototoxicity: Differences in Patterns of Oxidative Stress, Antioxidant Enzyme Expression and Hair Cell Loss in the Cochlea
by Alejandro Gibaja, Juan C. Alvarado, Verena Scheper, Liliana Carles and José M. Juiz
Antioxidants 2022, 11(9), 1759; https://doi.org/10.3390/antiox11091759 - 6 Sep 2022
Cited by 7 | Viewed by 2350
Abstract
Kanamycin and cisplatin are ototoxic drugs. The mechanisms are incompletely known. With subcutaneous kanamycin (400 mg/kg, 15 days), auditory threshold shifts were detected at days 12–13 at 16 and 32 kHz, extending to 8 and 4 kHz at days 14–15. The outer hair [...] Read more.
Kanamycin and cisplatin are ototoxic drugs. The mechanisms are incompletely known. With subcutaneous kanamycin (400 mg/kg, 15 days), auditory threshold shifts were detected at days 12–13 at 16 and 32 kHz, extending to 8 and 4 kHz at days 14–15. The outer hair cell (OHC) loss was concentrated past day 12. The maximum cochlear length showing apoptotic cells, tested with TUNEL, was at day 13. At day 15, 1/5 of the apical cochlea contained preserved OHCs. 3-nitrotyrosine (3-NT) immunolabeling, showing oxidative stress, was found in surviving OHCs and in basal and middle portions of the stria vascularis (SV). The antioxidant Gpx1 gene expression was decreased. The immunocytochemistry showed diminished Gpx1 in OHCs. With intraperitoneal cisplatin (16 mg/kg, single injection), no evoked auditory activity was recorded at the end of treatment, at 72 h. The basal third of the cochlea lacked OHCs. Apoptosis occupied the adjacent 1/3, and the apical third contained preserved OHCs. 3-NT immunolabeling was extensive in OHCs and the SV. Gpx1 and Sod1 gene expression was downregulated. Gpx1 immunostaining diminished in middle and basal SV. More OHCs survived cisplatin than kanamycin towards the apex, despite undetectable evoked activity. Differential regulation of antioxidant enzyme levels suggests differences in the antioxidant response for both drugs. Full article
(This article belongs to the Special Issue Oxidative Stress and Hearing Loss)
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12 pages, 4592 KiB  
Article
Safety and Efficacy of Intratympanic Alpha-Lipoic Acid Injection in a Mouse Model of Noise-Induced Hearing Loss
by Jae Sang Han, Ye Lin Kim, Hyo Jeong Yu, Jung Mee Park, Yeonji Kim, So Young Park and Shi Nae Park
Antioxidants 2022, 11(8), 1423; https://doi.org/10.3390/antiox11081423 - 22 Jul 2022
Cited by 6 | Viewed by 2553
Abstract
Alpha-lipoic acid (ALA) is an antioxidant with oto-protective effects. In the present study, the safety and effectiveness of ALA therapy after noise-induced hearing loss was confirmed based on the administration method. The safety of intratympanic ALA (IT-ALA) was evaluated with oto-endoscopy and middle [...] Read more.
Alpha-lipoic acid (ALA) is an antioxidant with oto-protective effects. In the present study, the safety and effectiveness of ALA therapy after noise-induced hearing loss was confirmed based on the administration method. The safety of intratympanic ALA (IT-ALA) was evaluated with oto-endoscopy and middle ear mucosa morphologic study. Perilymph ALA concentrations according to the administration routes were compared, and the efficacy of ALA was investigated through hearing tests and cochlear histological studies. The middle ear mucosa was swollen 1 week after IT-ALA but completely recovered within 3 weeks. ALA concentration in the perilymph was significantly higher in the IT-ALA group. Recovery of organ of Corti morphology and hearing levels were predominant in the IT-ALA group compared with the intraperitoneal injection group (IP-ALA) and showed similar rescue effects in the IT-dexamethasone group (IT-DEX). Interleukin-1 beta and nuclear factor-kappa B expression was significantly downregulated in the IT-ALA group. IT-ALA showed better cochlear recovery from acoustic trauma with higher inner ear penetration rate than IP-ALA. The rescue effect of IT-ALA after noise-induced hearing loss was similar to IT-DEX; however, the ALA and DEX mechanisms are different. IT-ALA appears to be another safe and effective treatment modality after acoustic trauma and comparable to IT-DEX. Full article
(This article belongs to the Special Issue Oxidative Stress and Hearing Loss)
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Review

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17 pages, 647 KiB  
Review
A Narrative Review of Lifestyle Risk Factors and the Role of Oxidative Stress in Age-Related Hearing Loss
by Diana Tang, Yvonne Tran, Piers Dawes and Bamini Gopinath
Antioxidants 2023, 12(4), 878; https://doi.org/10.3390/antiox12040878 - 4 Apr 2023
Cited by 17 | Viewed by 3278
Abstract
Age-related hearing loss affects a significant proportion of adults aged 60 years and above, with a prevalence of 65%. This condition has a negative impact on both physical and mental well-being, and while hearing interventions can help alleviate the effects of hearing loss, [...] Read more.
Age-related hearing loss affects a significant proportion of adults aged 60 years and above, with a prevalence of 65%. This condition has a negative impact on both physical and mental well-being, and while hearing interventions can help alleviate the effects of hearing loss, they cannot completely restore normal hearing or halt the progression of age-related hearing loss. Oxidative stress and inflammation have been identified as potential contributors to this condition. By addressing modifiable lifestyle risk factors that exacerbate oxidative stress, there may be an opportunity to prevent hearing loss. Therefore, this narrative review provides an overview of the major modifiable lifestyle risk factors associated with age-related hearing loss, that is, exposure to noise and ototoxic chemicals, smoking, diet, physical activity, and the presence of chronic lifestyle diseases, and offers an overview of the role of oxidative stress in the pathophysiology of this condition. Full article
(This article belongs to the Special Issue Oxidative Stress and Hearing Loss)
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