Role of glutathione in protection against noise-induced hearing loss

Yamasoba, Tatsuya; Nuttall, Alfred L.; Harris, Craig; Raphael, Yehoash; Miller, Josef M.

doi:10.1016/s0006-8993(97)01156-6

Cited by 158 publications

(104 citation statements)

References 48 publications

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“…Asterisks indicate statistically reliable differences relative to salinetreated control. Adapted from Yamasoba et al (1998).…”

Section: Discussionmentioning

confidence: 99%

“…This treatment rendered them more susceptible to noise-induced sensory cell death and NIHL (Yamasoba et al, 1998). In contrast, animals treated with 2-oxothiazolidine-4-carboxylate (OTC), a pro-cysteine drug which promotes rapid restoration of GSH, were less susceptible to noise-induced trauma (Yamasoba et al, 1998). Protective effects of OTC were evident as reductions in PTS, with no change in earlier hearing loss, as shown in Figure 1.…”

Section: Endogenous Antioxidant Defense Against Nihlmentioning

confidence: 99%

“…To test that hypothesis, guinea pigs were treated with L-buthionine-[S, R]-sulfoximine (BSO), which inhibits endogenous GSH synthesis. This treatment rendered them more susceptible to noise-induced sensory cell death and NIHL (Yamasoba et al, 1998). In contrast, animals treated with 2-oxothiazolidine-4-carboxylate (OTC), a pro-cysteine drug which promotes rapid restoration of GSH, were less susceptible to noise-induced trauma (Yamasoba et al, 1998).…”

Section: Endogenous Antioxidant Defense Against Nihlmentioning

confidence: 99%

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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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“…Asterisks indicate statistically reliable differences relative to salinetreated control. Adapted from Yamasoba et al (1998).…”

Section: Discussionmentioning

confidence: 99%

Section: Endogenous Antioxidant Defense Against Nihlmentioning

confidence: 99%

Section: Endogenous Antioxidant Defense Against Nihlmentioning

confidence: 99%

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

et al. 2007

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“…Upregulation of the endogenous antioxidant glutathione reduces NIHL and cell pathology [44,45], whereas the opposite is observed with reduced endogenous antioxidants [20,22,23,44]. That exogenous antioxidant agents reduce sensory cell death and NIHL has been well demonstrated in animal studies using a variety of free radical scavengers [24,[44][45][46][47][48][49][50][51][52][53][54][55][56], including several studies with dietary antioxidants [50,[57][58][59][60]. Magnesium supplements also reduce NIHL [61][62][63][64][65][66][67][68][69].…”

Section: Nih Public Accessmentioning

confidence: 99%

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

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

201

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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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“…Over-production of TXs and LTs is reported to be toxic to the cochlea (Jung et al 1992;Umemura 1993); and it is possible that NSAIDs protect the cochlea against acoustic injury by inhibiting overproduction of these metabolites. Regarding the anti-oxidant action, accumulated evidence suggests that reactive oxygen species (ROS) are produced by acoustic overexposure and that ROS play key roles in acoustic injury (Yamane et al 1995;Yamasoba et al 1998;Ohlemiller et al 1999). Although the mechanisms generating ROS in the cochlea after acoustic overexposure have not been clarified.…”

Section: Discussionmentioning

confidence: 99%