Effect of SOD1 overexpression on age- and noise-related hearing loss
Effect of SOD1 overexpression on age- and noise-related hearing loss
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DOI：
10.1016/s0891-5849(02)01439-9
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发表时间：
2003-04-01
影响因子：
7.4
通讯作者：
Lalwani, AK
中科院分区：
文献类型：
--
作者：
Coling, DE;Yu, KCY;Lalwani, AK
活性氧（ROS）与衰老和噪声暴露相关的听力损失有关。超氧化物歧化酶（SODS）形成对抗由超氧阴离子（最常见的ROS）介导的损伤的第一道防线。Cu/Zn SOD（SOD 1）的缺乏已被证明会增强与噪声暴露和年龄相关的听力损失。相反，超氧化物歧化酶1的过度表达可能被假设为提供保护，从年龄和噪音相关的听力损失。这一假设可以使用携带人SOD 1基因的转基因小鼠模型进行测试。与预期相反，在这里，我们报告说，在7个月大的小鼠中没有观察到对年龄相关的听力损失的保护，或者当8周龄的小鼠暴露于宽带噪声（4-45 kHz，110 dB持续1 h）时，没有观察到对噪声诱导的听力损失的保护。线粒体DNA缺失，一个老化的指标，在转基因小鼠的听神经相比，非转基因同窝出生。结果表明，耳蜗中氧化代谢的复杂性比之前假设的要大。(C)2003年爱思唯尔科学公司
Reactive oxygen species (ROS) have been implicated in hearing loss associated with aging and noise exposure. Superoxide dismutases (SODS) form a first line of defense against damage mediated by the superoxide anion, the most common ROS. Absence of Cu/Zn SOD (SOD1) has been shown to potentiate hearing loss related to noise exposure and age. Conversely, overexpression of SOD1 may be hypothesized to afford a protection from age- and noise-related hearing loss. This hypothesis may be tested using a transgenic mouse model carrying the human SOD1 gene. Contrary to expectations, here, we report that no protection against age-related hearing loss was observed in mice up to 7 months of age or from noise-induced hearing loss when 8 week old mice were exposed to broadband noise (4-45 kHz, 110 dB for 1 h). Mitochondrial DNA deletion, an index of aging, was elevated in the acoustic nerve of transgenic mice compared to nontransgenic littermates. The results indicate the complexity of oxidative metabolism in the cochlea is greater than previously hypothesized. (C) 2003 Elsevier Science Inc.