Evaluation of Oxidative-Stress Pathway and Recovery of Sudden Sensorineural Hearing Loss

Elias, Thaís Gomes Abrahão; Monsanto, Rafael da Costa; Amaral, Jônatas Bussador do; Oyama, Lila Missae; Maza, Paloma Korehisa; Penido, Norma de Oliveira

doi:10.1055/s-0040-1714130

Cited by 11 publications

(3 citation statements)

References 33 publications

(60 reference statements)

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“…In this regard, there are many shortcomings in the study of SSNHL, including a) the pathophysiological mechanisms underlying SSNHL are poorly understood, b) the intracochlear environment is not yet accessible through laboratorial or imaging tests; and c) there is no animal model that categorically emulates the events leading to SSNHL (10,11). Therefore, it is warranted that existing tools are used to determine the clinical phenotypic characteristics of SSNHL to allow an assertive diagnosis and development of diagnosis and treatment guidelines in the future (12).…”

Section: Discussionmentioning

confidence: 99%

Bilateral Sudden Sensorineural Hearing Loss: A Distinct Phenotype Entity

Elias¹,

Monsanto²,

Jean³

et al. 2022

Otology &Amp; Neurotology

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Objective: To investigate the clinical phenotype and hearing prognosis of patients with unilateral and bilateral (simultaneous and nonsimultaneous) sudden sensorineural hearing loss (SSNHL). Study Design: Retrospective cohort. Setting: Otology outpatient clinic of a tertiary university hospital. Patients: Three hundred eighty-five medical records from patients with SSNHL. Main Outcome Measure(s): Comparison of demographic, clinical, and audiometric (pretreatment and posttreatment) data of patients with unilateral and bilateral SSNHL. Results: Our final analysis comprised of 239 medical records of patients with SSNHL. Most patients had unilateral SSNHL (186, 77.82%). We identified a potential underlying cause for the SSNHL in 105 (43.9%) of the cases, being more frequent in cases of bilateral simultaneous SSNHL (100%) as compared with unilateral (45.6%) and nonsimultaneous bilateral SSNHL (22.7%). Cases of simultaneous bilateral SSNHL presented more frequently with severe or profound hearing loss (89%; unilateral SSNHL 50.5%; nonsimultaneous bilateral SSNL, 59.1%) and had a significantly worse hearing recovery prognosis as compared with unilateral or nonsimultaneous bilateral SSNHL ( p ¼ 0.002). Conclusion:We observed a high heterogeneity of clinical presentations of SSNHL, the most common being unilateral SSNHL. Our results demonstrate that the clinical and audiological prognosis of simultaneous bilateral SSNHL differed significantly from unilateral and nonsimultaneous bilateral SSNHL, suggesting that simultaneous cases of bilateral SSNHL may be a part of a different disease process. The presence of a simultaneous, bilateral SSNHL indicates the need to investigate the presence of an underlying systemic disease.

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Section: Discussionmentioning

confidence: 99%

Bilateral Sudden Sensorineural Hearing Loss: A Distinct Phenotype Entity

Elias¹,

Monsanto²,

Jean³

et al. 2022

Otology &Amp; Neurotology

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“…However, when the ability of eliminating ROS declines, oxidative stress will be activated [ 29 ]. There were many research showed that Oxidative stress plays a role in the pathogenesis of noise-related hearing loss, as well as in drug- and aging-related hearing loss [ 9 , 30 , 31 ].MDA is the terminal output of lipid peroxidation induced by the action of oxygen free radicals on polyunsaturated fatty acids on biofilms. The level of MDA reflects the severity of free radical attack and can be used as an indicator to evaluate degree of oxidative stress [ 32–34 ].…”

Section: Discussionmentioning

confidence: 99%

“…The damages on cochlear tissues and cellular structures are finally induced to disrupt the normal functions [ 7 , 8 ]. Therefore, improving the activity of antioxidant enzymes, scavenging ROS, alleviating oxidative stress damage, and maintaining redox balance will be effective methods to mitigate the damage of cochlear cells, which is of great significance for the protection of hearing function [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-106a facilitates the sensorineural hearing loss induced by oxidative stress by targeting connexin-43

Ding

2022

Bioengineered

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Sensorineural hearing loss (SNHL) is a common clinical side effect resulted from the overusing of aminoglycoside antibacterial drugs, such as gentamicin. Oxidative stress is recently evidenced to be an important inducer for SNHL, which is reported to be associated with the knockdown of connexin-43. MiR-106a is recently found as a regulator of connexin-43. The present study aims to investigate whether miR-106a is a vital mediator in the development of SNHL. Firstly, upregulated miR-106a was observed in the peripheral blood sample of SNHL patients. Glucose oxidase (GO) was utilized to induce oxidative injury in isolated rat cochlear marginal cells (MCs), followed by introducing the miR-106a inhibitor. We found that the declined proliferation ability, increased apoptosis, and activated oxidative stress in GO-stimulated MCs were dramatically abolished by the miR-106a inhibitor, accompanied by the upregulation of connexin-43. The targeting correlation between miR-106a and connexin-43 was predicted and confirmed by the dual luciferase gene reporter assay. Furthermore, the regulatory effect of miR-106a inhibitor against the proliferation, apoptosis, and oxidative stress in GO-treated MCs were dramatically abolished by the knockdown of connexin-43. Gentamicin was utilized to establish the SNHL model in rats, followed by the treatments of antagomir-106a and antagomir-106a combined with carbenoxolone, an inhibitor of connexin-43. The alleviated pathological state, reduced apoptosis, and ameliorated oxidative stress in cochlea tissues were observed in antagomir-106a treated SNHL rats, which were dramatically reversed by the co-administration of carbenoxolone. Collectively, miR-106a facilitated the SNHL induced by oxidative stress via targeting connexin-43.

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