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Proceedings of the National Academy of... Feb 2024Exposure to loud noise triggers sensory organ damage and degeneration that, in turn, leads to hearing loss. Despite the troublesome impact of noise-induced hearing loss...
Exposure to loud noise triggers sensory organ damage and degeneration that, in turn, leads to hearing loss. Despite the troublesome impact of noise-induced hearing loss (NIHL) in individuals and societies, treatment strategies that protect and restore hearing are few and insufficient. As such, identification and mechanistic understanding of the signaling pathways involved in NIHL are required. Biological zinc is mostly bound to proteins, where it plays major structural or catalytic roles; however, there is also a pool of unbound, mobile (labile) zinc. Labile zinc is mostly found in vesicles in secretory tissues, where it is released and plays a critical signaling role. In the brain, labile zinc fine-tunes neurotransmission and sensory processing. However, injury-induced dysregulation of labile zinc signaling contributes to neurodegeneration. Here, we tested whether zinc dysregulation occurs and contributes to NIHL in mice. We found that ZnT3, the vesicular zinc transporter responsible for loading zinc into vesicles, is expressed in cochlear hair cells and the spiral limbus, with labile zinc also present in the same areas. Soon after noise trauma, ZnT3 and zinc levels are significantly increased, and their subcellular localization is vastly altered. Disruption of zinc signaling, either via ZnT3 deletion or pharmacological zinc chelation, mitigated NIHL, as evidenced by enhanced auditory brainstem responses, distortion product otoacoustic emissions, and number of hair cell synapses. These data reveal that noise-induced zinc dysregulation is associated with cochlear dysfunction and recovery after NIHL, and point to zinc chelation as a potential treatment for mitigating NIHL.
Topics: Mice; Animals; Hearing Loss, Noise-Induced; Zinc; Cochlea; Noise; Hearing; Evoked Potentials, Auditory, Brain Stem; Auditory Threshold
PubMed: 38354264
DOI: 10.1073/pnas.2310561121 -
European Journal of Histochemistry : EJH Aug 2023Lots of adrenergic receptors (ARs) are widely present across the auditory pathways and are positioned to affect auditory and vestibular functions. However, noradrenergic...
Lots of adrenergic receptors (ARs) are widely present across the auditory pathways and are positioned to affect auditory and vestibular functions. However, noradrenergic regulation in the cochlea has not been well characterized. In this study, a rat model of noise-induced hearing loss was developed to investigate the expression of α2A-adrenergic receptor (AR) after acoustic trauma, then, we investigated the expression of α2A-AR in the developing rat cochlea using immunofluorescence, qRT-PCR, and Western blotting. We found that the expression of α2A-AR significantly increased in rats exposed to noise compared with controls. Immunofluorescence analysis demonstrated that α2A-AR is localized on hair cells (HCs), spiral ganglion neurons (SGNs), and the stria vascularis (SV) in the postnatal developing cochlea from post-natal day (P) 0 to P28. Furthermore, we observed α2A-AR mRNA reached a maximum level at P14 and P28 when compared with P0, while no significant differences in α2A-AR protein levels at the various stages when compared with P0. This study provides direct evidence for the expression of α2A-AR in HCs, SGNs, and the SV of the cochlea, indicating that norepinephrine might play a vital role in hearing function within the cochlea through α2A-AR.
Topics: Animals; Rats; Cochlea; Norepinephrine; Rats, Sprague-Dawley; Spiral Ganglion; Receptors, Adrenergic, alpha-2
PubMed: 37548252
DOI: 10.4081/ejh.2023.3748 -
Acta Oto-laryngologica Sep 2023Tinnitus, the perception of sound without external stimuli, varies across hearing loss types. The present study compared the acoustic characteristics of tinnitus in...
BACKGROUND
Tinnitus, the perception of sound without external stimuli, varies across hearing loss types. The present study compared the acoustic characteristics of tinnitus in patients with noise-induced hearing loss (NIHL) and in those with hearing loss unrelated to noise exposure.
OBJECTIVE
This study compared the acoustic characteristics of tinnitus in patients with noise-induced and non-noise-induced hearing loss.
METHODS
A total of 403 patients with tinnitus were divided into those with noise-induced and non-noise-induced hearing loss. Patients were evaluated by pure tone audiometry (PTA), tinnitogram, transient evoked otoacoustic emission (TEOAE), distortion product otoacoustic emission (DPOAE), and auditory brainstem evoked response (ABR) tests.
RESULTS
Patients with NIHL exhibited significantly higher hearing thresholds across all frequencies (125-8000 Hz) ( < .05) and reported significantly higher tinnitus intensity ( < .05). Otoacoustic emission tests showed that response rates were significantly lower ( < .05), and ABR tests found that latency periods were significantly more prolonged ( < .05), in patients with NIHL.
CONCLUSIONS
Tinnitus differs acoustically between patients with NIHL and those with non-noise-induced hearing loss, with specific patterns of intensity and auditory responses. These findings emphasize the need for tailoring the management of tinnitus according to the underlying type of hearing loss.
Topics: Humans; Hearing Loss, Noise-Induced; Tinnitus; Auditory Threshold; Otoacoustic Emissions, Spontaneous; Evoked Potentials, Auditory, Brain Stem; Deafness; Audiometry, Pure-Tone; Acoustics
PubMed: 37897331
DOI: 10.1080/00016489.2023.2266471 -
Hearing Research Jun 2024Understanding the complex pathologies associated with hearing loss is a significant motivation for conducting inner ear research. Lifelong exposure to loud noise,... (Review)
Review
Understanding the complex pathologies associated with hearing loss is a significant motivation for conducting inner ear research. Lifelong exposure to loud noise, ototoxic drugs, genetic diversity, sex, and aging collectively contribute to human hearing loss. Replicating this pathology in research animals is challenging because hearing impairment has varied causes and different manifestations. A central aspect, however, is the loss of sensory hair cells and the inability of the mammalian cochlea to replace them. Researching therapeutic strategies to rekindle regenerative cochlear capacity, therefore, requires the generation of animal models in which cochlear hair cells are eliminated. This review discusses different approaches to ablate cochlear hair cells in adult mice. We inventoried the cochlear cyto- and histo-pathology caused by acoustic overstimulation, systemic and locally applied drugs, and various genetic tools. The focus is not to prescribe a perfect damage model but to highlight the limitations and advantages of existing approaches and identify areas for further refinement of damage models for use in regenerative studies.
Topics: Animals; Hair Cells, Auditory; Disease Models, Animal; Regeneration; Mice; Cochlea; Humans; Hearing; Hearing Loss, Noise-Induced; Hearing Loss; Acoustic Stimulation
PubMed: 38703432
DOI: 10.1016/j.heares.2024.109021 -
American Journal of Audiology Jun 2024The purpose of this study was to map the strategies used in hearing health education with military personnel during the Hearing Preservation Program (HPP). (Review)
Review
PURPOSE
The purpose of this study was to map the strategies used in hearing health education with military personnel during the Hearing Preservation Program (HPP).
METHOD
This study is a scoping review, with electronic searches conducted in online databases and gray literature: Latin American and Caribbean Literature in Health Sciences, PubMed/Medline, Scopus, Web of Science, ASHAWire, Google Scholar, and ProQuest Dissertation & Theses. Only studies describing, analyzing, or evaluating the application of the HPP to active duty or training military personnel were included.
RESULTS
A total of 3,478 references were retrieved, and 12 studies met the inclusion criteria. The strategies were classified into five categories: focus group aimed at exploring knowledge and perceptions regarding hearing health (five studies), training on the proper fitting of hearing protection devices (four studies), the utilization of audiovisual materials (seven studies), questionnaires administrated before and after educational intervention (five studies), and feedback survey concerning the implemented hearing health education (three studies).
CONCLUSION
There are five strategies that aimed at assessing knowledge and attitudes, improving hearing health education, facilitating information access, and evaluating the applied actions.
SUPPLEMENTAL MATERIAL
https://doi.org/10.23641/asha.25219589.
Topics: Humans; Military Personnel; Health Knowledge, Attitudes, Practice; Ear Protective Devices; Health Education; Hearing Loss; Hearing Loss, Noise-Induced
PubMed: 38386287
DOI: 10.1044/2024_AJA-23-00160 -
Environmental Science and Pollution... Aug 2023Hearing loss induced by noise and combinations of factors is a common occupational disease among workers. This study aimed to investigate the impact of acute exposure to...
Hearing loss induced by noise and combinations of factors is a common occupational disease among workers. This study aimed to investigate the impact of acute exposure to white noise and AlO NPs, alone and in combination, on changes in the hearing and structural functions of the cochlea in rats. Thirty-six rats were randomly assigned to one of six groups: Control, acute exposure to white noise, exposure to γ-AlO NPs, exposure to noise plus γ-AlO NPs, exposure to α-AlO NPs, and exposure to the combination of noise plus α-AlO NPs. TTS and PTS were examined using DPOAE, while oxidative index (MDA, GSH-Px), gene expression (NOX3, TGF-ß, CYP1A1), protein expression (ß-Tubulin, Myosin VII), and histopathological changes were examined in the cochlea. The morphology of AlO NPs was examined by TEM. The results of the DPOAE test showed a significant increase in TTS in all groups and an increase in PTS in the groups exposed to noise, γ-AlO NPs, and a combination of noise plus AlO NPs (P < 0.05). In the group exposed to white noise plus AlO NPs, the MDA levels increased, the level of GSH-Px decreased, and the expression percentage of ß-Tubulin and Myosin VII decreased, while the expression of NOX3, TGF-ß, and CYP1A1 (except for the α-AlO NPs group) significantly increased (P < 0.05). Histopathological changes of the cochlea indicated damage to hair and ganglion cells, which was more severe in the combined exposure group. The combined and independent exposure to white noise and AlO NPs damaged hair and ganglion cells for high-frequency perception, affecting the function and structure of the cochlea and leading to TTS and PTS.
Topics: Rats; Animals; Hearing Loss, Noise-Induced; Rats, Wistar; Tubulin; Cytochrome P-450 CYP1A1; Auditory Threshold; Cochlea
PubMed: 37460886
DOI: 10.1007/s11356-023-28745-w -
Journal of Environmental Management Jul 2024As urbanization and population growth escalate, the challenge of noise pollution intensifies, particularly within the aviation industry. This review examines current... (Review)
Review
As urbanization and population growth escalate, the challenge of noise pollution intensifies, particularly within the aviation industry. This review examines current insights into noise-induced hearing loss (NIHL) in aviation, highlighting the risks to pilots, cabin crew, aircraft maintenance engineers, and ground staff from continuous exposure to high-level noise. It evaluates existing noise management and hearing conservation strategies, identifying key obstacles and exploring new technological solutions. While progress in developing protective devices and noise control technologies is evident, gaps in their widespread implementation persist. The study underscores the need for an integrated strategy combining regulatory compliance, technological advances, and targeted educational efforts. It advocates for global collaboration and policy development to safeguard the auditory health of aviation workers and proposes a strategic framework to enhance hearing conservation practices within the unique challenges of the aviation sector.
Topics: Hearing Loss, Noise-Induced; Humans; Aviation; Noise, Occupational; Occupational Exposure; Aircraft
PubMed: 38850921
DOI: 10.1016/j.jenvman.2024.121413 -
Seminars in Hearing Nov 2023Workers rely on hearing protection devices to prevent occupational noise-induced hearing loss. This study aimed to evaluate changes in attenuation over time for properly... (Review)
Review
Workers rely on hearing protection devices to prevent occupational noise-induced hearing loss. This study aimed to evaluate changes in attenuation over time for properly fit devices when worn by workers exposed to hazardous noise. Earplug fit testing was accomplished on 30 workers at a brewery facility with three types of foam and three types of premolded earplugs. The personal attenuation ratings (PARs) were measured before and after a 2-hour work period while exposed to hazardous noise levels. The minimum acceptable initial PAR was 15 dB. Average decreases in PAR ranged from -0.7 to -2.6 dB across all six earplug types. Significant changes in PAR were observed for the Foam-1 ( = 0.009) and Premold-3 ( = 0.004) earplugs. A linear mixed regression model using HPD type and study year as fixed effects and subject as random effect was not significant for either fixed effect ( = 0.05). Ninety-five percent of the final PAR measurements maintained the target attenuation of 15 dB. Properly fitting earplugs can be effective at reducing worker's noise exposures over time. The potential for a decrease in attenuation during the work shift should be considered when training workers and establishing the adequacy of protection from hazardous noise exposures.
PubMed: 37818150
DOI: 10.1055/s-0043-1769586 -
Biochemical and Biophysical Research... Dec 2023The study aimed to observe the effects of noise exposure on the pericytes of the cochlear stria vascularis (SV) in mice and to investigate its molecular mechanism.
OBJECTIVE
The study aimed to observe the effects of noise exposure on the pericytes of the cochlear stria vascularis (SV) in mice and to investigate its molecular mechanism.
METHOD
Male C57BL/6J mice aged 6-8 weeks were used as the subjects. Auditory Brainstem Response (ABR) was used to assess hearing loss. Hematoxylin and Eosin (HE) staining was conducted to observe morphological alterations in the SV. Immunofluorescence combined with transmission electron microscopy (TEM) was used to scrutinize changes in pericytes following acoustic injury. Western blotting (WB) was used to assess the expression variations of the migration-related protein Osteopontin (OPN). Evans Blue assay was performed to evaluate the permeability of the blood labyrinth barrier (BLB). 4-Hydroxynonenal (4-HNE) staining, in conjunction with measurements of Superoxide Dismutase (SOD), Malondialdehyde (MDA), and Catalase (CAT) content, was used to ascertain whether oxidative stress injury occurred in the SV. WB, combined with immunofluorescence, was used to examine alterations in the expression of proliferator-activated receptor-gamma coactivator 1α (PGC-1α) in the SV and pericytes.
RESULTS
Noise exposure resulted in permanent hearing loss in C57BL/6J mice, accompanied by SV swelling, migration of pericytes from their vascular attachments, BLB leakage, elevated oxidative stress levels in the SV, and reduced expression of PGC-1α on both the SV and migrating pericytes.
CONCLUSION
Noise exposure may potentially increase oxidative stress levels in the SV, downregulate the expression levels of PGC-1α, promote pericytes migration, and subsequently lead to an elevation in BLB permeability.
Topics: Animals; Humans; Male; Mice; Cochlea; Deafness; Ear, Inner; Hearing Loss, Noise-Induced; Mice, Inbred C57BL; Pericytes; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
PubMed: 37931421
DOI: 10.1016/j.bbrc.2023.149172 -
Frontiers in Cellular Neuroscience 2023Noise-induced calcium overload in sensory hair cells has been well documented as an early step in the pathogenesis of noise-induced hearing loss (NIHL). Alterations in...
INTRODUCTION
Noise-induced calcium overload in sensory hair cells has been well documented as an early step in the pathogenesis of noise-induced hearing loss (NIHL). Alterations in cellular calcium homeostasis mediate a series of cellular events, including activation of calcium-dependent protein kinases and phosphatases. Using cell-membrane- and blood-brain-barrier-permeable calpain-1 (μ-calpain) and calpain-2 (m-calpain) inhibitor MDL-28170, we tested the involvement of calpains, a family of calcium-dependent cysteine proteases, and the potential of MDL-28170 in preventing NIHL.
METHODS
CBA/J mice at the age of 12 weeks were exposed to broadband noise with a frequency spectrum from 2-20 kHz for 2 h at 101 dB sound pressure level to induce permanent hearing loss as measured by auditory brainstem response and distortion product otoacoustic emissions. Morphological damage was assessed by quantification of remaining sensory hair cells and inner hair cell synapses 2 weeks after the exposure.
RESULTS
MDL-28170 treatment by intraperitoneal injection significantly attenuated noise-induced functional deficits and cochlear pathologies. MDL-28170 treatment also prevented noise-induced cleavage of alpha-fodrin, a substrate for calpain-1. Furthermore, MDL-28170 treatment prevented reduction of PI3K/Akt signaling after exposure to noise and upregulated p85α and p-Akt (S473) in outer hair cells.
DISCUSSION
These results indicate that noise-induced calpain activation negatively regulates PI3K/Akt downstream signaling, and that prevention of NIHL by treatment with MDL-28170 is associated with upregulation of PI3K/Akt survival signaling pathways.
PubMed: 37484825
DOI: 10.3389/fncel.2023.1199656