Manganese superoxide dismutase influences the extent of noise-induced hearing loss in mice.
Manganese superoxide dismutase influences the extent of noise-induced hearing loss in mice.
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锰超氧化物歧化酶影响小鼠噪音引起的听力损失的程度。
DOI：
10.1016/j.neulet.2017.02.003
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发表时间：
2017
期刊：
影响因子：
2.5
通讯作者：
Yamasoba T
中科院分区：
文献类型：
--
作者：
Tuerdi A;Kinoshita M;Kamogashira T;Fujimoto C;Iwasaki S;Shimizu T;Yamasoba T
活性氧(ROS)的产生是噪声性耳聋的发病机制之一。锰超氧化物歧化酶(Mn-SOD)是线粒体内的一种抗氧化酶，它将有毒的超氧化物转化为过氧化氢。通过检测噪声暴露后C57BL/6野生型(WT)小鼠和杂合子敲除(HET)小鼠听力损失和毛细胞损伤的程度，探讨了Mn-SOD在NIHL中的作用。将HET和WT小鼠暴露于4 kHz倍频程噪声下，声压级为120分贝，持续4h，分别于噪声暴露前、暴露后1h、1h、3d、7d和14d进行听性脑干反应(ABR)检测。噪声暴露14天后处死小鼠，进行耳蜗病理学检查。在噪声暴露后1h，两组小鼠在所有频率的平均ABR阈值都有类似的升高，但HET小鼠在噪声暴露后第7天和第14天的平均ABR阈值明显低于WT小鼠，尤其是在4 kHz时。与WT小鼠相比，HET小鼠的外毛细胞损伤在所有的耳蜗圈中都明显更大。综上所述，这些发现表明，锰-超氧化物歧化酶在保护耳蜗免受噪声损伤方面起着重要作用。
Reactive oxygen species (ROS) generation is one of the mechanisms underlying noise-induced hearing loss (NIHL). Manganese superoxide dismutase (Mn-SOD), an antioxidant enzyme acting within the mitochondria, converts toxic superoxide to hydrogen peroxide. We investigated the role of Mn-SOD in NIHL by examining the extent of hearing loss and hair cell damage after noise exposure in C57BL/6 wild-type (WT) mice and Mn-SOD heterozygous knockout (HET) mice (n = 6 each). Both HET and WT mice were exposed to 120 dB sound pressure level at 4 kHz octave band noise for 4 h. Auditory brainstem responses (ABRs) were used to evaluate hearing thresholds before noise exposure, and at 1 h, and 1, 3, 7, and 14 days after exposure. The mice were euthanized 14 days after noise exposure for examination of the cochlear pathology. Mean ABR thresholds were similarly elevated at all frequencies in both groups 1 h after noise exposure, but were significantly worse, particularly at 4 kHz, on post-noise exposure days 7 and 14 in HET mice compared with WT mice. Outer hair cell damage was significantly greater in all cochlear turns in HET mice compared with WT mice. Collectively, these findings suggest that Mn-SOD plays an important role in protecting the cochlea from noise-induced damage.