Survival-fixation of the cochlea: a technique for following time-dependent degeneration and repair in noise-exposed chinchillas

Bohne, Barbara A.; Harding, Gary W.; Nordmann, Amy S.; Tseng, Charles J.; Liang, Griffith E.; Bahadori, Robert S.

doi:10.1016/s0378-5955(99)00082-9

Cited by 26 publications

(16 citation statements)

References 24 publications

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“…In the central saccule, maximum bundle loss was observed after 3-5·days of recovery from noise, indicating ongoing degeneration following cessation of noise. Progressive post-exposure development of noise-induced morphological damage has also been noted in other teleost fishes and in the mammalian cochlea (Hastings et al, 1996;Bohne et al, 1999;McCauley et al, 2003;Yamashita et al, 2004). Significant apoptosis was only detected for 2·days after noise exposure, suggesting that some dying hair cells in the central saccule may have retained their bundles for one or more days before the bundle degenerated.…”

Section: Discussionmentioning

confidence: 58%

Anatomical and functional recovery of the goldfish (Carassius auratus) ear following noise exposure

Smith

Coffin

Miller

et al. 2006

Journal of Experimental Biology

129

128

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Many vertebrates, including fishes and marine mammals, rely on acoustic signals for communication. In aquatic environments, where sound propagates five times faster than in air, acoustic signals are particularly important for communication over long distances or in low-light environments. Research on a variety of fishes, however, demonstrates sensitive hearing capabilities even in nonvocalizing fishes, leading to the hypothesis that hearing in fishes evolved for analysis of the complete auditory scene, including both biotic (e.g.

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Section: Discussionmentioning

confidence: 58%

Anatomical and functional recovery of the goldfish (Carassius auratus) ear following noise exposure

Smith

Coffin

Miller

et al. 2006

Journal of Experimental Biology

129

128

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“…Ohlemiller et al [21] were among the first to suggest oxidative stress begins early and becomes substantial over time. Free radical insult that builds over time would explain hair cell death that continues up to 14 days post-noise [106]. 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.…”

Section: Efficacy Of Delayed Treatment?mentioning

confidence: 99%

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

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

198

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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“…Free radical insult that builds over time would potentially explain observations of hair cell death that accelerates with time after exposure for a period of up to 14 days (Bohne et al, 1999;Yamashita et al, 2004). Using 4-hydroxynonenal (4-HNE) to mark ROS byproducts and nitryotyrosine (NT) to mark RNS byproducts, Yamashita et al (2004) demonstrated peak ROS and RNS production occurs in cells in the organ of Corti 7-10 days following noise insult (see Figure 4).…”

Section: Enhancing Antioxidant Defense Attenuates Nihlmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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Survival-fixation of the cochlea: a technique for following time-dependent degeneration and repair in noise-exposed chinchillas

Cited by 26 publications

References 24 publications

Anatomical and functional recovery of the goldfish (Carassius auratus) ear following noise exposure

Anatomical and functional recovery of the goldfish (Carassius auratus) ear following noise exposure

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

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

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