scholarly journals Effect of Phlorofucofuroeckol A and Dieckol Extracted from Ecklonia cava on Noise-induced Hearing Loss in a Mouse Model

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Radical Scavenging ◽  
Threshold Shift ◽  
Ecklonia Cava ◽  
Control Group ◽  
Noise Induced Hearing Loss ◽  
Antioxidant Agents ◽  
Brainstem Response

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects.

scholarly journals Inhibition of Cochlear HMGB1 Expression Attenuates Oxidative Stress and Inflammation in an Experimental Murine Model of Noise-Induced Hearing Loss

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 810
Author(s):  
Cheng-Ping Shih ◽  
Chao-Yin Kuo ◽  
Yuan-Yung Lin ◽  
Yi-Chun Lin ◽  
Hang-Kang Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Noise Exposure ◽  
Outer Hair Cells ◽  
Control Group ◽  
Noise Induced Hearing Loss ◽  
Post Exposure ◽  
Nadph Oxidase 4 ◽  
Brainstem Response ◽  
Ros Formation

Noise-induced hearing loss (NIHL) is a common inner ear disease but has complex pathological mechanisms, one of which is increased oxidative stress in the cochlea. The high-mobility group box 1 (HMGB1) protein acts as an inflammatory mediator and shows different activities with redox modifications linked to the generation of reactive oxygen species (ROS). We aimed to investigate whether manipulation of cochlear HMGB1 during noise exposure could prevent noise-induced oxidative stress and hearing loss. Sixty CBA/CaJ mice were divided into two groups. An intraperitoneal injection of anti-HMGB1 antibodies was administered to the experimental group; the control group was injected with saline. Thirty minutes later, all mice were subjected to white noise exposure. Subsequent cochlear damage, including auditory threshold shifts, hair cell loss, expression of cochlear HMGB1, and free radical activity, was then evaluated. The levels of HMGB1 and 4-hydroxynonenal (4-HNE), as respective markers of reactive nitrogen species (RNS) and ROS formation, showed slight increases on post-exposure day 1 and achieved their highest levels on post-exposure day 4. After noise exposure, the antibody-treated mice showed markedly less ROS formation and lower expression of NADPH oxidase 4 (NOX4), nitrotyrosine, inducible nitric oxide synthase (iNOS), and intercellular adhesion molecule-1 (ICAM‑1) than the saline-treated control mice. A significant amelioration was also observed in the threshold shifts of the auditory brainstem response and the loss of outer hair cells in the antibody-treated versus the saline-treated mice. Our results suggest that inhibition of HMGB1 by neutralization with anti-HMGB1 antibodies prior to noise exposure effectively attenuated oxidative stress and subsequent inflammation. This procedure could therefore have potential as a therapy for NIHL.

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.

Noise

2020 ◽  
pp. 1671-1673
Author(s):  
David Koh ◽  
Tar-Ching Aw
Keyword(s):  
Cardiovascular Disease ◽  
Hearing Loss ◽  
Sleep Disturbance ◽  
Cognitive Performance ◽  
Noise Exposure ◽  
Threshold Shift ◽  
Temporary Threshold Shift ◽  
Noise Induced Hearing Loss ◽  
Occupational Setting ◽  
Human Ear

Noise can affect hearing in the occupational setting but can have other effects where exposures are non-occupational. For clinical purposes, noise is measured in decibels weighted according to the sensitivity of the human ear (dB(A)). Regardless of source, the effects of overexposure to noise are similar. Initially there is a temporary threshold shift, where reversibility of hearing loss is possible with removal away from further noise. Noise-induced hearing loss occurs following prolonged or intense exposure, with poor prospects for improvement of hearing. The classical audiogram for noise-induced hearing loss shows a 4 kHz dip. Non-auditory effects of prolonged noise exposure include annoyance, sleep disturbance, hypertension, and cardiovascular disease, stress, and impaired cognitive performance. Prevention of noise-induced hearing loss is by reducing exposure to noise at source minimizing exposure time, using hearing protection, and participating in surveillance.

scholarly journals Protective Effect of Yang Mi Ryung® Extract on Noise-Induced Hearing Loss in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-11
Author(s):  
Min Soo Kim ◽  
SeongAe Kwak ◽  
Heumyoung Baek ◽  
Zewu Li ◽  
Seong-Kyu Choe ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Protective Effect ◽  
Hair Cells ◽  
Noise Exposure ◽  
Preventive Intervention ◽  
Apoptotic Cell ◽  
Quantitative Polymerase Chain Reaction ◽  
Control Group ◽  
Mrna Levels ◽  
Noise Induced Hearing Loss

Noise-induced hearing loss (NIHL) results from the damage of the delicate hair cells inside the ear after excessive stimulation of noise. Unlike certain lower animals such as amphibians, fishes, and birds, in humans, hair cells cannot be regenerated once they are killed or damaged; thus, there are no therapeutic options to cure NIHL. Therefore, it is more important to protect hair cells from the noise before the damage occurs. In this study, we report the protective effect of Yang Mi Ryung extract (YMRE) against NIHL; this novel therapeutic property of YMRE has not been reported previously. Our data demonstrates that the hearing ability damaged by noise is markedly restored in mice preadministrated with YMRE before noise exposure, to the level of normal control group. Our study also provides the molecular mechanism underlying the protective effect of YMRE against NIHL by showing that YMRE significantly blocks noise-induced apoptotic cell death and reduces reactive oxygen species (ROS) production in cochleae. Moreover, quantitative polymerase chain reaction (qPCR) analysis demonstrates that YMRE has anti-inflammatory properties, suppressing the mRNA levels of TNFα and IL-1β induced by noise exposure. In conclusion, YMRE could be a useful preventive intervention to prevent hearing impairment induced by the exposure to excessive noise.

scholarly journals Effect of Specific Retinoic Acid Receptor Agonists on Noise-Induced Hearing Loss

2019 ◽  
Vol 16 (18) ◽  
pp. 3428 ◽  
Author(s):  
Sang Hyun Kwak ◽  
Gi-Sung Nam ◽  
Seong Hoon Bae ◽  
Jinsei Jung
Keyword(s):  
Hearing Loss ◽  
Retinoic Acid ◽  
Noise Exposure ◽  
Retinoic Acid Receptor ◽  
Protective Effects ◽  
Noise Induced Hearing Loss ◽  
Acid Receptor ◽  
Significant Difference ◽  
Brainstem Response ◽  
Selective Agonists

Noise is one of the most common causes of hearing loss in industrial countries. There are many studies about chemical agents to prevent noise-induced hearing loss (NIHL). However, there is no commercially available drug yet. Retinoic acid is an active metabolite of Vitamin A; it has an anti-apoptic role in NIHL. This study aims to verify the differences among selective agonists of retinoic acid receptors (RARs) in NIHL. All-trans retinoic acid (ATRA), AM80 (selective retinoic acid receptor α agonist), AC261066 (Selective retinoic acid receptor β1 agonist), and CD1530 (Selective retinoic acid λ agonist) were injected to 6–7 weeks old CJ5BL/6 mice before noise (110 dB for 3 h) exposure. In the auditory brainstem response test pre-, post 1, 3, and 7 days after noise exposure, not only ATRA but all kinds of selective RAR agonists showed protective effects in hearing threshold and wave I amplitude. Though there was no significant difference in the level of protective effects between agonists, α agonist showed the most prominent effect in preserving hearing function as well as outer hair cells after noise exposure. In conclusion, selective agonists of RAR demonstrate comparable protective effects against NIHL to retinoic acid. Given that these selective RAR agonists have less side effects than retinoic acid, they may be promising potential drugs against NIHL.

scholarly journals Effects of D-methionine in mice with noise-induced hearing loss mice

2019 ◽  
Vol 47 (8) ◽  
pp. 3874-3885 ◽  
Author(s):  
Yanru Wang ◽  
Yan Qu ◽  
Xuzhen Chen ◽  
Pu Zhang ◽  
Dan Su ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Basement Membrane ◽  
Mouse Model ◽  
Hair Cells ◽  
Noise Exposure ◽  
Stria Vascularis ◽  
Connexin 26 ◽  
Noise Induced Hearing Loss ◽  
Expression Levels ◽  
Brainstem Response

Objective To study the effects of D-methionine in a mouse model of noise-induced hearing loss (NIHL). Methods We investigated changes in auditory function and microscopic cochlear structure in a mouse model of NIHL, and carried out 4-hydroxynonenal (4-HNE) immunostaining and terminal deoxynucleotidyl transferase dUTP nick-end labeling, and examined expression levels of connexins 26 and 30 by western blot. Results The auditory brainstem response threshold was significantly increased by noise exposure. Noise exposure also damaged the inner and particularly the outer hair cells in the cochlear basement membrane, while histochemistry demonstrated only scattered loss of hair cells in the basement membrane in mice treated with D-methionine before or after noise exposure. D-methionine inhibited apoptosis in the cochlear basement membrane, stria vascularis, and spiral ligament. 4-HNE expression in the basement membrane, stria vascularis, and spiral collateral ligament was increased by noise exposure, but this increase was attenuated by D-methionine. Connexin 26 and connexin 30 expression levels were reduced by noise exposure, and this effect was similarly attenuated by D-methionine administered either before or after noise exposure. Conclusion D-methionine administered before or after noise exposure could rescue NIHL by protecting cochlear morphology, inhibiting apoptosis, and maintaining connexin 26 and 30 expression.

scholarly journals Research and Discussion on the Relationships between Noise-Induced Hearing Loss and ATP2B2 Gene Polymorphism

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Suhao Zhang ◽  
Enmin Ding ◽  
Haoyang Yin ◽  
Hengdong Zhang ◽  
Baoli Zhu
Keyword(s):  
Hearing Loss ◽  
Gene Polymorphism ◽  
Noise Exposure ◽  
Venous Blood ◽  
Pure Tone Audiometry ◽  
Control Group ◽  
Case Group ◽  
Noise Induced Hearing Loss ◽  
Cochlear Hair Cells ◽  
Potential Biomarker

Long-term and continuous noise exposure can result in noise-induced hearing loss (NIHL), which is a worldwide problem resulting from the interaction of environmental and genetic factors. The ATP2B2 gene polymorphism can destroy cochlear hair cells and increase the risk of NIHL. A case-control study of 760 Chinese textile workers was conducted to investigate the relationship between ATP2B2 polymorphisms and NIHL susceptibility. Venous blood was collected and questionnaires were conducted by professional physicians. A case group and a control group which were typed by individuals’ pure-tone audiometry test results were set. Three polymorphism sites of ATP2B2 were genotyped by using the PCR technique. Analysis results revealed that the C allele of rs3209637 (95%CI=1.08–2.58, odds ratio OR=1.67, P=0.027) was a dangerous factor and could add to risks of NIHL in the Chinese employees. The data of stratified analysis revealed that individuals who are exposed to noise>95 dB with the rs3209637 C genotype have a higher susceptibility to NIHL (OR=1.34, 95%CI=1.07–1.68). Multifactor dimensionality reduction analysis revealed that the interaction between rs14154 and rs3209637 is linked to increased NIHL risk, and for the interaction among rs14154, smoking and drinking had the same function (OR=1.54 and 1.77, 95%CI=1.15–2.07, 1.33–2.37, and P=0.0037 and P<0.0001, respectively). Our results suggest that genetic polymorphism rs3209637 C within ATP2B2 is a risk factor for NIHL among Chinese employees and rs3209637 C could be a potential biomarker for NIHL patients.

scholarly journals Effect of Workplace Noise on Hearing Ability in Tile and Ceramic Industry Workers in Iran: A 2-Year Follow-Up Study

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Mehrdad Mostaghaci ◽  
Seyyed Jalil Mirmohammadi ◽  
Amir Houshang Mehrparvar ◽  
Maryam Bahaloo ◽  
Abolfazl Mollasadeghi ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Hearing Threshold ◽  
Threshold Shift ◽  
Noise Induced Hearing Loss ◽  
Follow Up Study ◽  
Hearing Ability ◽  
The Right ◽  
Ceramic Workers

Introduction. Noise as a common physical hazard may lead to noise-induced hearing loss, an irreversible but preventable disorder. Annual audiometric evaluations help detect changes in hearing status before clinically significant hearing loss develops. This study was designed to track hearing threshold changes during 2-year follow-up among tile and ceramic workers.Methods. This follow-up study was conducted on 555 workers (totally 1110 ears). Subjects were divided into four groups according to the level of noise exposure. Hearing threshold in conventional audiometric frequencies was measured and standard threshold shift was calculated for each ear.Results. Hearing threshold was increased during 2 years of follow-up. Increased hearing threshold was most frequently observed at 4000, 6000, and 3000 Hz. Standard threshold shift was observed in 13 (2.34%), 49 (8.83%), 22 (3.96%), and 63 (11.35%) subjects in the first and second years of follow-up in the right and left ears, respectively.Conclusions. This study has documented a high incidence of noise-induced hearing loss in tile and ceramic workers that would put stress on the importance of using hearing protection devices.

scholarly journals The Physiological Bases of Hidden Noise-Induced Hearing Loss: Protocol for a Functional Neuroimaging Study (Preprint)

2017 ◽  
Author(s):  
Rebecca Susan Dewey ◽  
Deborah A Hall ◽  
Hannah Guest ◽  
Garreth Prendergast ◽  
Christopher J Plack ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Noise Exposure ◽  
Functional Neuroimaging ◽  
Nerve Fibers ◽  
High Threshold ◽  
Hearing Level ◽  
Noise Induced Hearing Loss ◽  
Brainstem Response ◽  
Neuroimaging Study ◽  
Hidden Hearing Loss

BACKGROUND Rodent studies indicate that noise exposure can cause permanent damage to synapses between inner hair cells and high-threshold auditory nerve fibers, without permanently altering threshold sensitivity. These demonstrations of what is commonly known as hidden hearing loss have been confirmed in several rodent species, but the implications for human hearing are unclear. OBJECTIVE Our Medical Research Council–funded program aims to address this unanswered question, by investigating functional consequences of the damage to the human peripheral and central auditory nervous system that results from cumulative lifetime noise exposure. Behavioral and neuroimaging techniques are being used in a series of parallel studies aimed at detecting hidden hearing loss in humans. The planned neuroimaging study aims to (1) identify central auditory biomarkers associated with hidden hearing loss; (2) investigate whether there are any additive contributions from tinnitus or diminished sound tolerance, which are often comorbid with hearing problems; and (3) explore the relation between subcortical functional magnetic resonance imaging (fMRI) measures and the auditory brainstem response (ABR). METHODS Individuals aged 25 to 40 years with pure tone hearing thresholds ≤20 dB hearing level over the range 500 Hz to 8 kHz and no contraindications for MRI or signs of ear disease will be recruited into the study. Lifetime noise exposure will be estimated using an in-depth structured interview. Auditory responses throughout the central auditory system will be recorded using ABR and fMRI. Analyses will focus predominantly on correlations between lifetime noise exposure and auditory response characteristics. RESULTS This paper reports the study protocol. The funding was awarded in July 2013. Enrollment for the study described in this protocol commenced in February 2017 and was completed in December 2017. Results are expected in 2018. CONCLUSIONS This challenging and comprehensive study will have the potential to impact diagnostic procedures for hidden hearing loss, enabling early identification of noise-induced auditory damage via the detection of changes in central auditory processing. Consequently, this will generate the opportunity to give personalized advice regarding provision of ear defense and monitoring of further damage, thus reducing the incidence of noise-induced hearing loss.

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