The Role of Oxidative Stress in Noise-Induced Hearing Loss

2006 ◽  
Vol 27 (1) ◽  
pp. 1-19 ◽  
Author(s):  
Donald Henderson ◽  
Eric C. Bielefeld ◽  
Kelly Carney Harris ◽  
Bo Hua Hu
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Noise Induced Hearing Loss

MicroRNAs in Noise-Induced Hearing Loss and their Regulation by Oxidative Stress and Inflammation

2020 ◽  
Vol 21 (12) ◽  
pp. 1216-1224
Author(s):  
Fatemeh Forouzanfar ◽  
Samira Asgharzade
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Cell Damage ◽  
Sensory Cells ◽  
Noise Induced Hearing Loss ◽  
Irreversible Damage ◽  
Open Access Journals

Noise exposure (NE) has been recognized as one of the causes of sensorineural hearing loss (SNHL), which can bring about irreversible damage to sensory hair cells in the cochlea, through the launch of oxidative stress pathways and inflammation. Accordingly, determining the molecular mechanism involved in regulating hair cell apoptosis via NE is essential to prevent hair cell damage. However, the role of microRNAs (miRNAs) in the degeneration of sensory cells of the cochlea during NE has not been so far uncovered. Thus, the main purpose of this study was to demonstrate the regulatory role of miRNAs in the oxidative stress pathway and inflammation induced by NE. In this respect, articles related to noise-induced hearing loss (NIHL), oxidative stress, inflammation, and miRNA from various databases of Directory of Open Access Journals (DOAJ), Google Scholar, PubMed; Library, Information Science & Technology Abstracts (LISTA), and Web of Science were searched and retrieved. The findings revealed that several studies had suggested that up-regulation of miR-1229-5p, miR-451a, 185-5p, 186 and down-regulation of miRNA-96/182/183 and miR-30b were involved in oxidative stress and inflammation which could be used as biomarkers for NIHL. There was also a close relationship between NIHL and miRNAs, but further research is required to prove a causal association between miRNA alterations and NE, and also to determine miRNAs as biomarkers indicating responses to NE.

The role of middle ear muscles in the development of resistance to noise induced hearing loss

1994 ◽  
Vol 74 (1-2) ◽  
pp. 22-28 ◽  
Author(s):  
Donald Henderson ◽  
Malini Subramaniam ◽  
Martin Papazian ◽  
Vlasta P. Spongr
Keyword(s):  
Hearing Loss ◽  
Middle Ear ◽  
Noise Induced Hearing Loss ◽  
Development Of Resistance

scholarly journals Primed to die: an investigation of the genetic mechanisms underlying noise-induced hearing loss and cochlear damage in homozygous Foxo3-knockout mice

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Holly J. Beaulac ◽  
Felicia Gilels ◽  
Jingyuan Zhang ◽  
Sarah Jeoung ◽  
Patricia M. White
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Multiphoton Microscopy ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Noise Induced Hearing Loss ◽  
Knock Out ◽  
Cell Death Pathway ◽  
Cochlear Damage

AbstractThe prevalence of noise-induced hearing loss (NIHL) continues to increase, with limited therapies available for individuals with cochlear damage. We have previously established that the transcription factor FOXO3 is necessary to preserve outer hair cells (OHCs) and hearing thresholds up to two weeks following mild noise exposure in mice. The mechanisms by which FOXO3 preserves cochlear cells and function are unknown. In this study, we analyzed the immediate effects of mild noise exposure on wild-type, Foxo3 heterozygous (Foxo3+/−), and Foxo3 knock-out (Foxo3−/−) mice to better understand FOXO3’s role(s) in the mammalian cochlea. We used confocal and multiphoton microscopy to examine well-characterized components of noise-induced damage including calcium regulators, oxidative stress, necrosis, and caspase-dependent and caspase-independent apoptosis. Lower immunoreactivity of the calcium buffer Oncomodulin in Foxo3−/− OHCs correlated with cell loss beginning 4 h post-noise exposure. Using immunohistochemistry, we identified parthanatos as the cell death pathway for OHCs. Oxidative stress response pathways were not significantly altered in FOXO3’s absence. We used RNA sequencing to identify and RT-qPCR to confirm differentially expressed genes. We further investigated a gene downregulated in the unexposed Foxo3−/− mice that may contribute to OHC noise susceptibility. Glycerophosphodiester phosphodiesterase domain containing 3 (GDPD3), a possible endogenous source of lysophosphatidic acid (LPA), has not previously been described in the cochlea. As LPA reduces OHC loss after severe noise exposure, we treated noise-exposed Foxo3−/− mice with exogenous LPA. LPA treatment delayed immediate damage to OHCs but was insufficient to ultimately prevent their death or prevent hearing loss. These results suggest that FOXO3 acts prior to acoustic insult to maintain cochlear resilience, possibly through sustaining endogenous LPA levels.

scholarly journals Multiphoton NAD(P)H FLIM reveals metabolic changes in individual cell types of the intact cochlea upon sensorineural hearing loss

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Paromita Majumder ◽  
Thomas S. Blacker ◽  
Lisa S. Nolan ◽  
Michael R. Duchen ◽  
Jonathan E. Gale
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Cell Model ◽  
Organ Of Corti ◽  
Cell Types ◽  
Fluorescence Lifetime Imaging ◽  
Noise Induced Hearing Loss ◽  
Label Free ◽  
Age Related ◽  
The Individual

AbstractAn increasing volume of data suggests that changes in cellular metabolism have a major impact on the health of tissues and organs, including in the auditory system where metabolic alterations are implicated in both age-related and noise-induced hearing loss. However, the difficulty of access and the complex cyto-architecture of the organ of Corti has made interrogating the individual metabolic states of the diverse cell types present a major challenge. Multiphoton fluorescence lifetime imaging microscopy (FLIM) allows label-free measurements of the biochemical status of the intrinsically fluorescent metabolic cofactors NADH and NADPH with subcellular spatial resolution. However, the interpretation of NAD(P)H FLIM measurements in terms of the metabolic state of the sample are not completely understood. We have used this technique to explore changes in metabolism associated with hearing onset and with acquired (age-related and noise-induced) hearing loss. We show that these conditions are associated with altered NAD(P)H fluorescence lifetimes, use a simple cell model to confirm an inverse relationship between τbound and oxidative stress, and propose such changes as a potential index of oxidative stress applicable to all mammalian cell types.

The role of glutathione in protection against noise-induced hearing loss*

1997 ◽  
Vol 117 (2) ◽  
pp. P94-P94
Author(s):  
T YAMASOBA ◽  
A NUTTALL ◽  
J MILLE
Keyword(s):  
Hearing Loss ◽  
Noise Induced Hearing Loss

Role of antioxidant supplementation in preventing noise induced hearing loss

2015 ◽  
Vol 13 (4) ◽  
pp. 160-165 ◽  
Author(s):  
Anna Rita Fetoni ◽  
Sara Letizia Maria Eramo ◽  
Fabiola Paciello ◽  
Rolando Rolesi ◽  
Diana Troiani ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Induced Hearing Loss ◽  
Antioxidant Supplementation

scholarly journals Role of PGE-type receptor 4 in auditory function and noise-induced hearing loss in mice

2012 ◽  
Vol 62 (4) ◽  
pp. 1841-1847 ◽  
Author(s):  
Kiyomi Hamaguchi ◽  
Norio Yamamoto ◽  
Takayuki Nakagawa ◽  
Tomoyuki Furuyashiki ◽  
Shuh Narumiya ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Induced Hearing Loss ◽  
Auditory Function ◽  
Type Receptor

scholarly journals The Role of MicroRNAs in Environmental Risk Factors, Noise-Induced Hearing Loss, and Mental Stress

2018 ◽  
Vol 28 (9) ◽  
pp. 773-796 ◽  
Author(s):  
Verónica Miguel ◽  
Julia Yue Cui ◽  
Lidia Daimiel ◽  
Cristina Espinosa-Díez ◽  
Carlos Fernández-Hernando ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hearing Loss ◽  
Environmental Risk ◽  
Mental Stress ◽  
Environmental Risk Factors ◽  
Noise Induced Hearing Loss

scholarly journals Loss of Myh14 Increases Susceptibility to Noise-Induced Hearing Loss in CBA/CaJ Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Xiaolong Fu ◽  
Linqing Zhang ◽  
Yecheng Jin ◽  
Xiaoyang Sun ◽  
Aizhen Zhang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Outer Hair Cell ◽  
Cell Loss ◽  
Acoustic Trauma ◽  
Noise Induced Hearing Loss ◽  
Wild Type ◽  
Auditory Function ◽  
Susceptibility To Noise ◽  
Susceptible Gene

MYH14 is a member of the myosin family, which has been implicated in many motile processes such as ion-channel gating, organelle translocation, and the cytoskeleton rearrangement. Mutations in MYH14 lead to a DFNA4-type hearing impairment. Further evidence also shows that MYH14 is a candidate noise-induced hearing loss (NIHL) susceptible gene. However, the specific roles of MYH14 in auditory function and NIHL are not fully understood. In the present study, we used CRISPR/Cas9 technology to establish a Myh14 knockout mice line in CBA/CaJ background (now referred to as Myh14−/−mice) and clarify the role of MYH14 in the cochlea and NIHL. We found that Myh14−/−mice did not exhibit significant hearing loss until five months of age. In addition, Myh14−/−mice were more vulnerable to high intensity noise compared to control mice. More significant outer hair cell loss was observed in Myh14−/−mice than in wild type controls after acoustic trauma. Our findings suggest that Myh14 may play a beneficial role in the protection of the cochlea after acoustic overstimulation in CBA/CaJ mice.

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