Attenuation of cochlear damage from noise trauma by an iron chelator, a free radical scavenger and glial cell line-derived neurotrophic factor in vivo

Yamasoba, Tatsuya; Schacht, Jochen; Shoji, Fumi; Miller, Josef M.

doi:10.1016/s0006-8993(98)01100-7

Cited by 169 publications

(101 citation statements)

References 39 publications

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“…Free radical formation has been implicated in all. Interventions can be directed at preventing initial ROS formation and maintaining cochlear blood flow (as reported here and by others); alternative therapeutic interventions and strategies include neurotrophic growth factors [119][120][121][122], steroids [123,124], calcineurin inhibitors [125,126], caspase inhibitors [127][128][129][130][131][132], and Src protein tyrosine kinase (Src-PTK) inhibitors [133]. Each of these are at least partially effective in prevention of hearing loss and hair cell death; none of these strategies have alone been sufficiently effective.…”

Section: Discussionmentioning

confidence: 94%

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: Discussionmentioning

confidence: 94%

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

“…For example, vitamin D, which increases GDNF production, protects against damage of dopaminergic neurons induced by both 6-hydroxydopamine and H 2 O 2 (Son et al, 1999;Wang et al, 2001). GDNF also has protective effects against the consequences of ROS damage for cochlear cells (Yamasoba et al, 1999). In cultured motor neurons, GDNF was found to inhibit both the formation of ROS and ROS-induced biochemical reactions (Irie and Hirabayashi, 1999).…”

Section: Discussionmentioning

confidence: 99%

An In Vitro Model of Human Dopaminergic Neurons Derived from Embryonic Stem Cells: MPP+ Toxicity and GDNF Neuroprotection

Zeng

Chen

Deng

et al. 2006

Neuropsychopharmacol

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Human embryonic stem cells (hESCs) can proliferate indefinitely yet also differentiate in vitro, allowing normal human neurons to be generated in unlimited numbers. Here, we describe the development of an in vitro neurotoxicity assay using human dopaminergic neurons derived from hESCs. We showed that the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP + ), which produces features of Parkinson's disease in humans, was toxic for hESC-derived dopaminergic neurons. Treatment with glial cell line-derived neurotrophic factor protected tyrosine hydroxylase-positive neurons against MPP + -induced apoptotic cell death and loss of neuronal processes as well as against the formation of intracellular reactive oxygen species. The availability of human dopaminergic neurons, derived from hESCs, therefore allows for the possibility of directly examining the unique features of human dopaminergic neurons with respect to their responses to pharmacological agents as well as environmental and chemical toxins.

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“…First, pharmacological studies have documented the ability of antioxidant drugs or prodrugs to block or reduce NIHL (e.g., Seidman et al 1993;Yamasoba et al 1999;Henderson et al 1999). Second, genetic studies have demonstrated that laboratory animal models with reduced antioxidant buffering capacity are more vulnerable to NIHL than are wild-type subjects (e.g., Ohlemiller et al 1999aOhlemiller et al , 2000.…”

Section: Introductionmentioning

confidence: 99%

Acrylonitrile Potentiates Noise-Induced Hearing Loss in Rat

Fechter

Gearhart

Shirwany

2004

JARO - Journal of the Association for Research in Otolaryngolog

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Acrylonitrile, one of the 50 most commonly produced industrial chemicals, has recently been identified as a promoter of noise-induced hearing loss (NIHL). This agent has the potential to produce oxidative stress through multiple pathways. We hypothesize that acrylonitrile potentiates NIHL as a consequence of oxidative stress. The objectives of this study were to characterize acrylonitrile exposure conditions that promote permanent NIHL in rats and determine the ability of this nitrile to produce auditory dysfunction by itself. Additionally, we sought to determine whether a spin-trap agent that can form adducts with ROS would protect against the effects of acrylonitrile. Acrylonitrile administration produced significant elevation in NIHL detected as a loss in compound action potential sensitivity. The effect was particularly robust for high-frequency tones and particularly when acrylonitrile and noise were given on repeated occasions. Acrylonitrile by itself did not disrupt threshold sensitivity. Administration of the spin-trap agent phenyl-N-tert-butylnitrone (PBN), given to rats prior to acrylonitrile and noise, did block the elevation of NIHL by acrylonitrile. However, PBN at the dose and time interval given was ineffective in protecting auditory function in subjects exposed to noise alone. The results suggest that oxidative stress may play a role in the promotion of NIHL by acrylonitrile.

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Attenuation of cochlear damage from noise trauma by an iron chelator, a free radical scavenger and glial cell line-derived neurotrophic factor in vivo

Cited by 169 publications

References 39 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

An In Vitro Model of Human Dopaminergic Neurons Derived from Embryonic Stem Cells: MPP+ Toxicity and GDNF Neuroprotection

Acrylonitrile Potentiates Noise-Induced Hearing Loss in Rat

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