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缺氧增强噪声性听力损失的机制。

Mechanisms of noise-induced hearing loss potentiation by hypoxia.

作者信息

Chen Guang-Di, Liu Yun

机构信息

College of Pharmacy, The University of Oklahoma Health Sciences Center, P.O. Box 26901, 1110 N. Stonewall Avenue, Oklahoma City, OK 73117, USA.

出版信息

Hear Res. 2005 Feb;200(1-2):1-9. doi: 10.1016/j.heares.2004.08.016.

Abstract

Potentiation of noise-induced permanent threshold shift (PTS) by hypoxia has been reported [Hear. Res. 172 (1-2) (2002) 186]. In this study in rats, effects of noise (110 dB SPL), hypoxia (10% O(2)), and their combination have been determined on different cochlear potentials and on the expression of genes coding proteins in the outer hair cell (OHC) membrane skeleton (beta-actin) and in the mitochondrial respiratory chain (SDHa & b). The noise exposure alone caused CAP threshold shift only in the noise-band. The combined exposure to noise and hypoxia caused an about 40-dB PTS at all frequencies within and above the noise band. Loss of the cochlear amplification was not always related to the CM-suppression. SP was only affected at high frequencies by the combined exposure. Gene expression of beta-actin was up-regulated by the noise exposure, which was blocked by hypoxia. Gene expression of SDHa was also up-regulated by the noise and the combined exposure. The data suggest that loss of the cochlear active process, due to damage to the OHC membrane skeleton and to the cellular energy generation system, is related to the noise-induced hearing loss potentiation by hypoxia. Inner hair cell damage may also be involved in the hypoxia potentiation in the basal turn.

摘要

已有报道称缺氧会增强噪声诱发的永久性阈移(PTS)[《听觉研究》172 (1 - 2) (2002) 186]。在这项针对大鼠的研究中,已确定噪声(110 dB SPL)、缺氧(10% O₂)及其组合对不同的耳蜗电位以及外毛细胞(OHC)膜骨架(β - 肌动蛋白)和线粒体呼吸链(SDHa和b)中编码蛋白质的基因表达的影响。单独的噪声暴露仅在噪声频段引起复合动作电位(CAP)阈移。噪声和缺氧的联合暴露在噪声频段及以上的所有频率处导致约40 dB的PTS。耳蜗放大功能的丧失并不总是与耳蜗微音电位(CM)抑制相关。总和电位(SP)仅在高频时受联合暴露影响。β - 肌动蛋白的基因表达因噪声暴露而上调,但缺氧可阻止这种上调。SDHa的基因表达也因噪声和联合暴露而上调。数据表明,由于OHC膜骨架和细胞能量产生系统受损导致的耳蜗主动过程丧失,与缺氧增强噪声诱发的听力损失有关。内毛细胞损伤可能也参与了基底转的缺氧增强作用。

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