Elevation of superoxide dismutase increases acoustic trauma from noise exposure
Elevation of superoxide dismutase increases acoustic trauma from noise exposure
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DOI：
10.1016/j.freeradbiomed.2004.11.008
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发表时间：
2005-02-15
影响因子：
7.4
通讯作者：
Ito, J
中科院分区：
文献类型：
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作者：
Endo, T;Nakagawa, T;Ito, J
超氧化物的产生被认为是过度噪音导致耳蜗损伤的原因之一。铜/锌超氧化物歧化酶（SODI）通常可以防止超氧化物介导的组织损伤，但这种酶对噪声损伤的保护作用存在争议。本研究评估了过表达 SODI 或用卵磷脂化 SODI (PC-SODI) 治疗的 C57BL/6 小鼠的听觉功能。与生理盐水处理的动物相比，噪声暴露导致 PC-SODI 处理的动物的阈值变化明显更高。与盐水处理的动物相比，PC-SODI处理的动物的耳蜗组织表现出SOD活性水平显着升高，但过氧化氢酶活性水平没有显着升高。同样，过度表达 SOD I 的转基因小鼠往往比非转基因同窝小鼠因噪声暴露而遭受更高的阈值变化。研究结果表明，增加 SODI 会加剧噪音暴露后的听觉功能障碍。 (C) 2004 Elsevier Inc. 保留所有权利。
The generation of superoxide has been implicated as a cause of cochlear damage from excessive noise. Cu/Zn superoxide dismutase (SODI) generally will protect against superoxide-mediated tissue injury but protection by this enzyme against noise trauma is controversial. This study assessed auditory function in C57BL/6 mice overexpressing SODI or treated with lecithinized SODI (PC-SODI). Noise exposure caused significantly higher threshold shifts in PC-SODI-treated animals than physiological saline-treated animals. Cochlear tissues of PC-SODI-treated animal, exhibited significant elevation of the levels in the SOD activity, not in the catalase activity, in comparison with those of saline-treated animals. Likewise, transgenic mice overexpressing SOD I tended to suffer higher threshold shifts than nontransgenic littermates from noise exposure. The findings indicate that increasing SODI enhances auditory dysfunction following noise exposure. (C) 2004 Elsevier Inc. All rights reserved.