Effect of SOD1 overexpression on age- and noise-related hearing loss

被引:51
作者
Coling, DE
Yu, KCY
Somand, D
Satar, B
Bai, U
Huang, TT
Seidman, MD
Epstein, CJ
Mhatre, AN
Lalwani, AK
机构
[1] Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, Oncol Mol Lab, Epstein Labs, San Francisco, CA 94143 USA
[2] Henry Ford Hosp, Dept Otolaryngol Head & Neck Surg, Detroit, MI 48202 USA
[3] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA
关键词
superoxide dismutase; oxygen radical; hearing loss; presbyacusis; aging; noise exposure; transgenic mice; free radicals;
D O I
10.1016/S0891-5849(02)01439-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:873 / 880
页数:8
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