scholarly journals Involvement of Cholesterol Metabolic Pathways in Recovery from Noise-Induced Hearing Loss

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Na Sai ◽  
Xi Shi ◽  
Yan Zhang ◽  
Qing-qing Jiang ◽  
Fei Ji ◽  
...  

The objective of this study was to explore the molecular mechanisms of acute noise-induced hearing loss and recovery of steady-state noise-induced hearing loss using miniature pigs. We used miniature pigs exposed to white noise at 120 dB (A) as a model. Auditory brainstem response (ABR) measurements were made before noise exposure, 1 day and 7 days after noise exposure. Proteomic Isobaric Tags for Relative and Absolute Quantification (iTRAQ) was used to observe changes in proteins of the miniature pig inner ear following noise exposure. Western blot and immunofluorescence were performed for further quantitative and qualitative analysis of proteomic changes. The average ABR-click threshold of miniature pigs before noise exposure, 1 day and 7 days after noise exposure, were 39.4 dB SPL, 67.1 dB SPL, and 50.8 dB SPL, respectively. In total, 2,158 proteins were identified using iTRAQ. Both gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) database analyses showed that immune and metabolic pathways were prominently involved during the impairment stage of acute hearing loss. During the recovery stage of acute hearing loss, most differentially expressed proteins were related to cholesterol metabolism. Western blot and immunofluorescence showed accumulation of reactive oxygen species and nuclear translocation of NF-κB (p65) in the hair cells of miniature pig inner ears during the acute hearing loss stage after noise exposure. Nuclear translocation of NF-κB (p65) may be associated with overexpression of downstream inflammatory factors. Apolipoprotein (Apo) A1 and Apo E were significantly upregulated during the recovery stage of hearing loss and may be related to activation of cholesterol metabolic pathways. This is the first study to use proteomics analysis to analyze the molecular mechanisms of acute noise-induced hearing loss and its recovery in a large animal model (miniature pigs). Our results showed that activation of metabolic, inflammatory, and innate immunity pathways may be involved in acute noise-induced hearing loss, while cholesterol metabolic pathways may play an important role in recovery of hearing ability following noise-induced hearing loss.

2020 ◽  
Vol 21 (12) ◽  
pp. 1216-1224
Author(s):  
Fatemeh Forouzanfar ◽  
Samira Asgharzade

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.


Author(s):  
David C. Byrne ◽  
Thais C. Morata

Exposure to industrial noise and the resulting effect of occupational hearing loss is a common problem in nearly all industries. This chapter describes industrial noise exposure, its assessment, and hearing disorders that result from overexposure to noise. Beginning with the properties of sound, noise-induced hearing loss and other effects of noise exposure are discussed. The impact of hearing disorders and the influence of other factors on hearing loss are described. Typically, noise-induced hearing loss develops slowly, and usually goes unnoticed until a significant impairment has occurred. Fortunately, occupational hearing loss is nearly always preventable. Therefore, this chapter gives particular attention to recommendations for measures to prevent occupational hearing loss such as engineering noise controls and hearing protection devices.


Author(s):  
Feifan Chen ◽  
Zuwei Cao ◽  
Emad M. Grais ◽  
Fei Zhao

Abstract Purpose Noise-induced hearing loss (NIHL) is a global issue that impacts people’s life and health. The current review aims to clarify the contributions and limitations of applying machine learning (ML) to predict NIHL by analyzing the performance of different ML techniques and the procedure of model construction. Methods The authors searched PubMed, EMBASE and Scopus on November 26, 2020. Results Eight studies were recruited in the current review following defined inclusion and exclusion criteria. Sample size in the selected studies ranged between 150 and 10,567. The most popular models were artificial neural networks (n = 4), random forests (n = 3) and support vector machines (n = 3). Features mostly correlated with NIHL and used in the models were: age (n = 6), duration of noise exposure (n = 5) and noise exposure level (n = 4). Five included studies used either split-sample validation (n = 3) or ten-fold cross-validation (n = 2). Assessment of accuracy ranged in value from 75.3% to 99% with a low prediction error/root-mean-square error in 3 studies. Only 2 studies measured discrimination risk using the receiver operating characteristic (ROC) curve and/or the area under ROC curve. Conclusion In spite of high accuracy and low prediction error of machine learning models, some improvement can be expected from larger sample sizes, multiple algorithm use, completed reports of model construction and the sufficient evaluation of calibration and discrimination risk.


Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  

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.


2017 ◽  
Vol 26 (3S) ◽  
pp. 352-368 ◽  
Author(s):  
Vincent Nadon ◽  
Annelies Bockstael ◽  
Dick Botteldooren ◽  
Jérémie Voix

Purpose In spite of all the efforts to implement workplace hearing conservation programs, noise-induced hearing loss remains the leading cause of disability for North American workers. Nonetheless, an individual's susceptibility to noise-induced hearing loss can be estimated by monitoring changes in hearing status in relation to the level of ambient noise exposure. The purpose of this study was to validate an approach that could improve workplace hearing conservation practices. The approach was developed using a portable and robust system designed for noisy environments and consisted of taking continuous measurements with high temporal resolution of the health status of the inner ear using otoacoustic emissions (OAEs). Method A pilot study was conducted in a laboratory, exposing human subjects to industrial noise recordings at realistic levels. In parallel, OAEs were measured periodically using the designed OAE system as well as with a commercially available OAE system, used as a reference. Results Variations in OAE levels were analyzed and discussed along with the limitations of the reference and designed systems. Conclusions This study demonstrates that the monitoring of an individual's OAEs could be useful in monitoring temporary changes in hearing status induced by exposure to ambient noise and could be considered as a new tool for effective hearing conservation programs in the workplace.


2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Holly J. Beaulac ◽  
Felicia Gilels ◽  
Jingyuan Zhang ◽  
Sarah Jeoung ◽  
Patricia M. White

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.


2021 ◽  
Vol 100 (9) ◽  
pp. 947-952
Author(s):  
Elena A. Preobrazhenskaia ◽  
Anna V. Sukhova ◽  
Elena N. Kriuchkova

Introduction. The high incidence of noise-induced hearing loss (NIHL) makes it possible to attribute the problem of prevention and prediction of the risk of NIHL to the number of socially significant ones. The aim of the study is to conduct a comparative assessment of the potential risk of hearing loss caused by noise according to GOST R ISO 1999-2017, and the actual risk of NIHL in workers of “noise” industries according to epidemiological research. Materials and methods. The calculation of the potential risk of hearing loss according to GOST R ISO 1999-2017 included assessing age, noise and total hearing loss at noise exposure with 85, 90, 95 and 100 dBA. The actual risk of NIHL was evaluated on survey data of 600 miners and 600 workers of processing plants. Results. The calculation of the probable risk according to GOST R ISO 1999-2017 and the assessment of the actual risk according to epidemiological studies showed that the risk of NIHL depends on both noise exposure and age. As the levels of noise affecting an employee increase, the risk of an NIHL becomes more determined by the effect of noise. At noise levels 85, 90 and 95 dBA, the probable risk calculated under GOST R ISO 1999-2017 coincides with the actual risk established according to epidemiological studies. At the same time, for miners exposed to high-intensity noise 100 dBА, the real risk was not as high as could be assumed from the calculated data. Conclusion. The results obtained allow stating that the GOST ISO 1999-2017 standard with a high degree of potential risk allows predicting the group risk of hearing loss due to noise exposure, to quantify the degree of risk and can be used for the formation of risk groups for NIHL and the development of programs for the preservation of hearing.


1985 ◽  
Vol 121 (4) ◽  
pp. 501-514 ◽  
Author(s):  
ELELYN TALBOTT ◽  
JAMES HELMKAMP ◽  
KARAN MATHEWS ◽  
LEWIS KULLER ◽  
ERIC COTTINGTON ◽  
...  

2020 ◽  
pp. 1671-1673
Author(s):  
David Koh ◽  
Tar-Ching Aw

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.


2020 ◽  
Vol 10 (10) ◽  
pp. 732
Author(s):  
Tang-Chuan Wang ◽  
Ta-Yuan Chang ◽  
Richard Tyler ◽  
Ying-Ju Lin ◽  
Wen-Miin Liang ◽  
...  

Long-term noise exposure often results in noise induced hearing loss (NIHL). Tinnitus, the generation of phantom sounds, can also result from noise exposure, although understanding of its underlying mechanisms are limited. Recent studies, however, are shedding light on the neural processes involved in NIHL and tinnitus, leading to potential new and innovative treatments. This review focuses on the assessment of NIHL, available treatments, and development of new pharmacologic and non-pharmacologic treatments based on recent studies of central auditory plasticity and adaptive changes in hearing. We discuss the mechanisms and maladaptive plasticity of NIHL, neuronal aspects of tinnitus triggers, and mechanisms such as tinnitus-associated neural changes at the cochlear nucleus underlying the generation of tinnitus after noise-induced deafferentation. We include observations from recent studies, including our own studies on associated risks and emerging treatments for tinnitus. Increasing knowledge of neural plasticity and adaptive changes in the central auditory system suggest that NIHL is preventable and transient abnormalities may be reversable, although ongoing research in assessment and early detection of hearing difficulties is still urgently needed. Since no treatment can yet reverse noise-related damage completely, preventative strategies and increased awareness of hearing health are essential.


Sign in / Sign up

Export Citation Format

Share Document