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Audiol > Volume 7(2); 2011 > Article
Audiology 2011;7(2): 124-132.
Published online: December 31, 2011.
doi: http://dx.doi.org/10.21848/audiol.2011.7.2.124
소음성 난청과 치료의 메커니즘
최철희1,2
1대구가톨릭대학교 언어청각치료학과
2생체모방감각제어연구소
Mechanisms of Noise-Induced Hearing Loss and Treatment
Chul-Hee Choi1,2
1Department of Audiology and Speech-Language Pathology, College of Medical Sciences, Catholic University of Daegu, Kyung-Buk, Korea
2Research Institute of Biomimetic Sensory Control, Catholic University of Daegu, Kyung-Buk, Korea
Correspondence  Chul-Hee Choi ,Tel: (053) 850-3185, Fax: (053) 850-3383, Email: cchoi@cu.ac.kr
Received: November 30, 2011;  Accepted: December 6, 2011.  Published online: December 31, 2011.
ABSTRACT
Noise-induced hearing loss (NIHL) means hearing loss or cochlear damage induced by either a short exposure to an intense impulse sounds from 100 to 150 dB SPL or continuous exposure to loud sounds at or above 85 dB SPL over relatively long period of time. Noise exposure results in oxidative stress destroying the antioxidant defense mechanism in the cochlea by over-production of reactive oxygen species (ROS), reactive nitrogen species (RNS), and other free radicals. The purpose of this study is to explain the basic mechanisms of NIHL and to review a target and the site of action of treatment in terms of free radical formation. Oxidative stress begins immediately after noise exposure and continues up to 21 days after the exposure. Cell death process progresses after noise exposure. A primary cell death pathway following noise exposure is called apoptosis. Pharmacological approaches for prevention or treatment of NIHL have been developed with both oxygen-based antioxidant drugs inhibiting the generation of ROS and nitrogen-based antioxidant drugs inhibiting the production of RNS. There are synergistic effects of combined antioxidant drugs because each antioxidant drug may target different treatment mechanism. When one antioxidant drug was used in combination with other antioxidant drugs, the amount of reduction was analyzed and described. In addition, the optimal timing of therapeutic effects of antioxidant drugs depends on the time of initial treatment and the length of treatment before and after noise exposure. The maximal effect of treatment was observed in treatment for 9 days with injection starting at 24 h after noise exposure. The treatment of antioxidant drugs extending up to 10 days after noise exposure can reduce cumulative cochlear damage resulting from the delayed formation of free radicals. However, the relationship between free radical formation and the optimal timing of treatment is still unclear. Further studies on the relationship should be continually performed because of clinical usefulness and its importance.
Key Words: Noise-induced hearing loss (NIHL), Oxidative stress, Reactive oxygen species (ROS), Reactive nitrogen species (RNS), Antioxidant drugs, Oxygen-based antioxidant drug, Nitrogen-based antioxidant drugs, Apoptosis, Necrosis, Synergistic effect, Secondary oxidative burst, Biomarkers, 4-hydroxy-2-nonenal (4-HNE), Nitrotyrosine (NT).
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