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Oxidative Stress and Inflammation in Deafness: Current and Future Therapy

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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 June 2021) | Viewed by 16720

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Special Issue Editors

Dr. Anna Rita Fetoni

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Guest Editor

Department of Otolaryngology Head and Neck Surgery, Fondazione Policlinico Universitario A. Gemelli, IRCCS, Università Cattolica Sacro Cuore, Rome, Italy
Interests: mechanisms of noise induce hearing loss; aging; drug ototoxicity; auditory cortex dysfunction induced by exogenous insults; translational approaches therapy for sensory-neural hearing loss induced by exogenous factors

Dr. Jing Wang

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Guest Editor

INSERM - UMR 1051, Institut des Neurosciences de Montpellier, 80 rue Augustin Fliche, 34295 Montpellier, France
Interests: mitochondrial dynamics and mitophagy; mitochondrial DNA mutations and dysfunction; interralation of oxidative stress and inflammation in cochlear aging; antioxidant therapy

Special Issue Information

Dear Colleagues,

We would like to invite you to contribute to a Special Issue of Antioxidants that we are planning as Guest Editors.

Hearing loss is the most common form of sensory impairment in humans. Although approximately 1 in 500 children are born with impaired hearing, sudden or progressive forms of hearing loss can manifest at any age. Hearing impairment following cochlear damage due to noise trauma, ototoxicity or age‐related cochlear degeneration has been linked to a common pathogenesis involving the formation of reactive oxygen species (ROS). Identification of oxidative stress and improved knowledge of how cells die has been particularly significant for the development of novel therapeutic agents to reduce disability.

The main objective of this Special Issue is to improve knowledge of overall exogenous-factor--related degeneration of the auditory system, focusing particularly on the roles of oxidative stress, DNA damage and repair, and mitochondrial dysfunction in the pathophysiology of hearing.

In addition to oxidative stress, inflammatory responses in the cochlea following exposure to injury lead to the upregulation of pro-inflammatory mediators and rapid recruitment of inflammatory cells from the vascular system.

We are particularly interested in articles describing new insights into the pathophysiological mechanisms underlying the responses of sensory organs to aging. Special emphasis will be placed on findings that could lead to new diagnostic and therapeutic approaches. We cordially invite researchers to contribute their original articles and reviews to our Special Issue.

Potential topics include but are not limited to the following:

The model systems used to study hearing loss;
Environmental and genetic factors contributing to hearing loss;
The role of mitochondrial dysfunctions in the pathophysiology of hearing loss;
Role of reactive oxygen species in cell death and senescence of sensory cells;
MtDNA and nuclear DNA damage and DNA repair in sensory nervous cell degeneration;
Cross-talk between oxidative stress and inflammation;
Biomarkers of redox unbalance and inflammation;
Pharmacological approaches such as antioxidant, mitochondrial metabolic reprogramming to restore hearing loss;
Regenerative medicine for restoring the sensory inputs;
Clinical applications.

Dr. Anna Rita Fetoni
Dr. Jing Wang
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
Molecular basis
Cell death
Hearing loss
Therapies

Published Papers (5 papers)

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Research

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17 pages, 5567 KiB

Open AccessArticle

Impulse Noise Induced Hidden Hearing Loss, Hair Cell Ciliary Changes and Oxidative Stress in Mice

by Paul Gratias, Jamal Nasr, Corentin Affortit, Jean-Charles Ceccato, Florence François, François Casas, Rémy Pujol, Sylvie Pucheu, Jean-Luc Puel and Jing Wang

Antioxidants 2021, 10(12), 1880; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10121880 - 25 Nov 2021

Cited by 5 | Viewed by 3120

Abstract

Recent studies demonstrated that reversible continuous noise exposure may induce a temporary threshold shift (TTS) with a permanent degeneration of auditory nerve fibers, although hair cells remain intact. To probe the impact of TTS-inducing impulse noise exposure on hearing, CBA/J Mice were exposed to noise impulses with peak pressures of 145 dB SPL. We found that 30 min after exposure, the noise caused a mean elevation of ABR thresholds of ~30 dB and a reduction in DPOAE amplitude. Four weeks later, ABR thresholds and DPOAE amplitude were back to normal in the higher frequency region (8–32 kHz). At lower frequencies, a small degree of PTS remained. Morphological evaluations revealed a disturbance of the stereociliary bundle of outer hair cells, mainly located in the apical regions. On the other hand, the reduced suprathreshold ABR amplitudes remained until 4 weeks later. A loss of synapse numbers was observed 24 h after exposure, with full recovery two weeks later. Transmission electron microscopy revealed morphological changes at the ribbon synapses by two weeks post exposure. In addition, increased levels of oxidative stress were observed immediately after exposure, and maintained for a further 2 weeks. These results clarify the pathology underlying impulse noise-induced sensory dysfunction, and suggest possible links between impulse-noise injury, cochlear cell morphology, metabolic changes, and hidden hearing loss. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Deafness: Current and Future Therapy)

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20 pages, 7330 KiB

Open AccessArticle

Role of Oxidative Stress in the Senescence Pattern of Auditory Cells in Age-Related Hearing Loss

by Luz del Mar Rivas-Chacón, Sofía Martínez-Rodríguez, Raquel Madrid-García, Joaquín Yanes-Díaz, Juan Ignacio Riestra-Ayora, Ricardo Sanz-Fernández and Carolina Sánchez-Rodríguez

Antioxidants 2021, 10(9), 1497; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10091497 - 21 Sep 2021

Cited by 12 | Viewed by 2882

Abstract

Age-related hearing loss (ARHL) is an increasing and gradual sensorineural hearing dysfunction. Oxidative stress is an essential factor in developing ARHL; additionally, premature senescence of auditory cells induced by oxidative stress can produce hearing loss. Hydrogen peroxide (H₂O₂) represents a method commonly used to generate cellular senescence in vitro. The objective of the present paper is to study H₂O₂-induced senescence patterns in three auditory cell lines (House Ear Institute-Organ of Corti 1, HEI-OC1; organ of Corti, OC-k3, and stria vascularis, SV-k1 cells) to elucidate the intrinsic mechanisms responsible for ARHL. The auditory cells were exposed to H₂O₂ at different concentrations and times. The results obtained show different responses of the hearing cells concerning cell growth, β-galactosidase activity, morphological changes, mitochondrial activation, levels of oxidative stress, and other markers of cell damage (Forkhead box O3a, FoxO3a, and 8-oxoguanine, 8-oxoG). Comparison between the responses of these auditory cells to H₂O₂ is a helpful method to evaluate the molecular mechanisms responsible for these auditory cells’ senescence. Furthermore, this in vitro model could help develop anti-senescent therapeutic strategies for the treatment of AHRL. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Deafness: Current and Future Therapy)

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23 pages, 9375 KiB

Open AccessArticle

Dual-Specificity Phosphatase 1 (DUSP1) Has a Central Role in Redox Homeostasis and Inflammation in the Mouse Cochlea

by Jose M. Bermúdez-Muñoz, Adelaida M. Celaya, Ángela García-Mato, Daniel Muñoz-Espín, Lourdes Rodríguez-de la Rosa, Manuel Serrano and Isabel Varela-Nieto

Antioxidants 2021, 10(9), 1351; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10091351 - 25 Aug 2021

Cited by 8 | Viewed by 3038

Abstract

Stress-activated protein kinases (SAPK) are associated with sensorineural hearing loss (SNHL) of multiple etiologies. Their activity is tightly regulated by dual-specificity phosphatase 1 (DUSP1), whose loss of function leads to sustained SAPK activation. Dusp1 gene knockout in mice accelerates SNHL progression and triggers inflammation, redox imbalance and hair cell (HC) death. To better understand the link between inflammation and redox imbalance, we analyzed the cochlear transcriptome in Dusp1^−/− mice. RNA sequencing analysis (GSE176114) indicated that Dusp1^−/− cochleae can be defined by a distinct profile of key cellular expression programs, including genes of the inflammatory response and glutathione (GSH) metabolism. To dissociate the two components, we treated Dusp1^−/− mice with N-acetylcysteine, and hearing was followed-up longitudinally by auditory brainstem response recordings. A combination of immunofluorescence, Western blotting, enzymatic activity, GSH levels measurements and RT-qPCR techniques were used. N-acetylcysteine treatment delayed the onset of SNHL and mitigated cochlear damage, with fewer TUNEL⁺ HC and lower numbers of spiral ganglion neurons with p-H2AX foci. N-acetylcysteine not only improved the redox balance in Dusp1^−/− mice but also inhibited cytokine production and reduced macrophage recruitment. Our data point to a critical role for DUSP1 in controlling the cross-talk between oxidative stress and inflammation. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Deafness: Current and Future Therapy)

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19 pages, 3771 KiB

Open AccessArticle

Noise-Induced Cochlear Damage Involves PPAR Down-Regulation through the Interplay between Oxidative Stress and Inflammation

by Fabiola Paciello, Anna Pisani, Rolando Rolesi, Vincent Escarrat, Jacopo Galli, Gaetano Paludetti, Claudio Grassi, Diana Troiani and Anna Rita Fetoni

Antioxidants 2021, 10(8), 1188; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10081188 - 26 Jul 2021

Cited by 13 | Viewed by 2402

Abstract

The cross-talk between oxidative stress and inflammation seems to play a key role in noise-induced hearing loss. Several studies have addressed the role of PPAR receptors in mediating antioxidant and anti-inflammatory effects and, although its protective activity has been demonstrated in several tissues, less is known about how PPARs could be involved in cochlear dysfunction induced by noise exposure. In this study, we used an in vivo model of noise-induced hearing loss to investigate how oxidative stress and inflammation participate in cochlear dysfunction through PPAR signaling pathways. Specifically, we found a progressive decrease in PPAR expression in the cochlea after acoustic trauma, paralleled by an increase in oxidative stress and inflammation. By comparing an antioxidant (Q-ter) and an anti-inflammatory (Anakinra) treatment, we demonstrated that oxidative stress is the primary element of damage in noise-induced cochlear injury and that increased inflammation can be considered a consequence of PPAR down-regulation induced by ROS production. Indeed, by decreasing oxidative stress, PPARs returned to control values, reactivating the negative control on inflammation in a feedback loop. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Deafness: Current and Future Therapy)

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Review

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14 pages, 916 KiB

Open AccessReview

Oxidative Stress and Inflammation Caused by Cisplatin Ototoxicity

by Vickram Ramkumar, Debashree Mukherjea, Asmita Dhukhwa and Leonard P. Rybak

Antioxidants 2021, 10(12), 1919; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10121919 - 29 Nov 2021

Cited by 43 | Viewed by 4397

Abstract

Hearing loss is a significant health problem that can result from a variety of exogenous insults that generate oxidative stress and inflammation. This can produce cellular damage and impairment of hearing. Radiation damage, ageing, damage produced by cochlear implantation, acoustic trauma and ototoxic drug exposure can all generate reactive oxygen species in the inner ear with loss of sensory cells and hearing loss. Cisplatin ototoxicity is one of the major causes of hearing loss in children and adults. This review will address cisplatin ototoxicity. It includes discussion of the mechanisms associated with cisplatin-induced hearing loss including uptake pathways for cisplatin entry, oxidative stress due to overpowering antioxidant defense mechanisms, and the recently described toxic pathways that are activated by cisplatin, including necroptosis and ferroptosis. The cochlea contains G-protein coupled receptors that can be activated to provide protection. These include adenosine A1 receptors, cannabinoid 2 receptors (CB2) and the Sphingosine 1-Phosphate Receptor 2 (S1PR2). A variety of heat shock proteins (HSPs) can be up-regulated in the cochlea. The use of exosomes offers a novel method of delivery of HSPs to provide protection. A reversible MET channel blocker that can be administered orally may block cisplatin uptake into the cochlear cells. Several protective agents in preclinical studies have been shown to not interfere with cisplatin efficacy. Statins have shown efficacy in reducing cisplatin ototoxicity without compromising patient response to treatment. Additional clinical trials could provide exciting findings in the prevention of cisplatin ototoxicity. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Deafness: Current and Future Therapy)

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