Oral magnesium intake reduces permanent hearing loss induced by noise exposure

Attias, Joseph; Weisz, Giora; Almog, Shlomo; Shahar, Amir; Wiener, Michael; Joachims, Z.; Netzer, Abraham; Ising, H; Rebentisch, E.; Guenther, Theodor

doi:10.1016/0196-0709(94)90036-1

Cited by 115 publications

(77 citation statements)

References 15 publications

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“…Another agent that may reduce NIHL via protection against noise-induced decreases in cochlear blood flow and oxygenation is magnesium (Altura et al, 1992;Haupt and Scheibe, 2002). As a consequence of its effects on blood flow, other biochemical mechanisms (described below), or some combination of effects, magnesium supplements protect against NIHL in humans (Joachims et al, 1993;Attias et al, 1994;2004), guinea pigs (Scheibe et al, 2000;Haupt and Scheibe, 2002;Scheibe et al, 2002;Attias et al, 2003;Haupt et al, 2003), and rats (Joachims et al, 1983). In contrast, magnesium deficient diets increase susceptibility to NIHL in rats (Joachims et al, 1983) and guinea pigs (Ising et al, 1982;Scheibe et al, 2000).…”

Section: Vasodilation and 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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Section: Vasodilation and Nihlmentioning

confidence: 99%

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

et al. 2007

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“…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].…”

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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“…Thiamine levels can also be affected by ingestion of antibiotics, sulfa drugs, caffeine, antacids, and oral contraceptives. A diet high in carbohydrates can also increase the need for B 1 .…”

Section: Vitamin B 1 (Thiamine)mentioning

confidence: 99%

“…This cation is also required for cellular energy metabolism and has an important role in membrane stabilization, nerve conduction, and ion transport. Deficiency can result in a variety of metabolic abnormalities and clinical consequences, including tinnitus [1].…”

Section: Magnesiummentioning

confidence: 99%