Post-exposure treatment attenuates noise-induced hearing loss

Yamashita, Daisuke; Jiang, Hong; Prell, Colleen G. Le; Schacht, Jochen; Miller, Josef M.

doi:10.1016/j.neuroscience.2005.04.015

Cited by 135 publications

(139 citation statements)

References 46 publications

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“…Using 4-hydroxynonenal and nitryotyrosine, Yamashita et al [86] confirmed that peak ROS and RNS production in cells in the organ of Corti occurs 7-10 days post-noise, and that noise-induced hair cell death is similarly delayed. As a consequence of delayed ROS production, ROS and RNS scavengers reduce NIHL not only when administered prior to noise, but also when treatment begins on days 1 or 3 post-noise [85]. Treatment delayed 5 days relative to noise insult was not effective, suggesting the therapeutic "window of opportunity" for successful antioxidant-based intervention against NIHL occurs within the first three days post-noise.…”

Section: Efficacy Of Delayed Treatment?mentioning

confidence: 99%

“…This noise exposure is routinely used in our laboratory [85,86]. As in those investigations animals were exposed, two at a time in separate cages, in a ventilated sound exposure chamber.…”

Section: Noise Exposurementioning

confidence: 99%

“…and placed on a heating pad in one of two sound-isolated chambers (Industrial Acoustics Company, Bronx, New York, or C-A Tegnér, Bromma, Sweden). The external ear canals and tympanic membranes were inspected using an operating microscope to assure the ear canal was free of wax, there was no canal deformity, no inflammation of tympanic membrane, and no effusion of the middle ear [as in 85], then needle electrodes were placed subcutaneously below the test ear, at the vertex, and below the contralateral ear.…”

Section: Auditory Brainstem Responsesmentioning

confidence: 99%

“…Thus, it is possible that the most efficacious treatment window, assuming oral administration for all agents, will be somewhat longer than 1 hour prenoise exposure. Indeed, treatments based on other antioxidant combinations are the most effective when treatment begins several days prior to noise exposure [85]. Although increasing total daily doses of single agents might reduce the need for lengthy pre-treatment, clinical strategies tested in human subjects must not exceed the upper limits established by the Institute of Medicine's Food and Nutrition Board.…”

Section: Individual Effectsmentioning

confidence: 99%

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Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

201

188

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Free radical formation in the cochlea plays a key role in the development of noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant formation of both reactive oxygen species and reactive nitrogen species 7-10 days following noise exposure. Reduction in cochlear blood flow as a result of free radical formation has also been described. Here we report that the antioxidant agents, vitamins A, C, and E, act in synergy with magnesium to effectively prevent noise-induced trauma. Neither the antioxidant agents nor magnesium reliably reduced NIHL or sensory cell death with the doses we used when these agents were delivered alone. In combination, however, they were highly effective in reducing both hearing loss and cell death even with treatment initiated just one hour prior to noise exposure. This study supports roles for both free radical formation and noise-induced vasoconstriction in the onset and progression of NIHL. Identification of this safe and effective antioxidant intervention that attenuates NIHL provides a compelling rationale for human trials in which free radical scavengers are used to eliminate this single major cause of acquired hearing loss. Keywords cochlea; free radical; noise; hearing; antioxidant; vasodilation Mechanical destruction of cells in the organ of Corti was once assumed to be the primary cause of noise-induced hearing loss (NIHL) [1][2][3][4][5][6][7][8], with perhaps some effect of reduced blood flow to the inner ear [9][10][11][12][13][14][15][16][17][18]. We now know that another key factor is intense metabolic activity that results in production of excess free radicals [19][20][21][22][23] and lipid peroxidation products [24]. Noise-induced production of reactive oxygen species (ROS) in the cochlea has now been well characterized, and several recent reviews are available [25][26][27]. Mitochodrial dysfunction and ROS production have been implicated in numerous neurodegenerative syndromes and diseases [28-34, see 35,36]. The use of antioxidant agents holds significant therapeutic promise for many neurodegenerative processes [32,33,[37][38][39][40][41][42], and there is some suggestion that Correspondence to: C. G. Le Prell, Kresge Hearing Research Institute, University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506, USA. Tel: +1-734-763-5104; fax +1-734-764-0014. E-mail address: colleeng@umich.edu. Disclosure. Dr. Miller is a founding member and Chairman of the Board of Directors at OtoMedicine, Inc., a company that has an option to license the intellectual property described in this report. Dr. Le Prell is a paid consultant to OtoMedicine, Inc. Drs. Miller and Le Prell have disclosed these relationships to the Medical School Conflict of Interest Board at the University of Michigan; conflict management plans including semi-annual review by the Board are in place.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publicatio...

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Section: Efficacy Of Delayed Treatment?mentioning

confidence: 99%

“…This noise exposure is routinely used in our laboratory [85,86]. As in those investigations animals were exposed, two at a time in separate cages, in a ventilated sound exposure chamber.…”

Section: Noise Exposurementioning

confidence: 99%

Section: Auditory Brainstem Responsesmentioning

confidence: 99%

Section: Individual Effectsmentioning

confidence: 99%

See 2 more Smart Citations

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

201

188

View full text Add to dashboard Cite

show abstract

“…Les connaissances les plus récentes de la physiologie et de la physiopathologie cochléaire ont permis de développer des voies thérapeu-tiques par voie locale ou systémique [18][19][20]. L'utilisation des antioxydants fait l'objet de travaux récents [21,22]. Leur administration, avant et après un traumatisme sonore, limiterait les lésions cellulaires et la perte auditive après un traumatisme sonore.…”

Section: Thérapeutiqueunclassified

Effets des nuisances sonores sur l’oreille interne

2006

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Pre‐conditioning with near infrared photobiomodulation reduces inflammatory cytokines and markers of oxidative stress in cochlear hair cells

Bartos

Grondin

Bortoni

et al. 2016

Journal of Biophotonics

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Hearing loss is a serious occupational health problem worldwide. Noise, aminoglycoside antibiotics and chemotherapeutic drugs induce hearing loss through changes in metabolic functions resulting in sensory cell death in the cochlea. Metabolic sequelae from noise exposure increase production of nitric oxide (NO) and Reactive Oxygen Species (ROS) contributing to higher levels of oxidative stress beyond the physiologic threshold levels of intracellular repair. Photobiomodulation (PBM) therapy is a light treatment involving endogenous chromophores commonly used to reduce inflammation and promote tissue repair. Near infrared light (NIR) from Light Emitting Diodes (LED) at 810 nm wavelength were used as a biochemical modulator of cytokine response in cultured HEI-OC1 auditory cells placed under oxidative stress. Results reported here show that NIR PBM at 810 nm, 30 mW/cm , 100 seconds, 1.0 J, 3 J/cm altered mitochondrial metabolism and oxidative stress response for up to 24 hours post treatment. We report a decrease of inflammatory cytokines and stress levels resulting from NIR applied to HEI-OC1 auditory cells before treatment with gentamicin or lipopolysaccharide. These results show that cells pretreated with NIR exhibit reduction of proinflammatory markers that correlate with inhibition of mitochondrial superoxide, ROS and NO in response to continuous oxidative stress challenges. Non-invasive biomolecular down regulation of proinflammatory intracellular metabolic pathways and suppression of oxidative stress via NIR may have the potential to develop novel therapeutic approaches to address noise exposure and ototoxic compounds associated with hearing loss.

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Post-exposure treatment attenuates noise-induced hearing loss

Cited by 135 publications

References 46 publications

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Effets des nuisances sonores sur l’oreille interne

Pre‐conditioning with near infrared photobiomodulation reduces inflammatory cytokines and markers of oxidative stress in cochlear hair cells

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