Noise-Induced Hearing Loss (NIHL) as a Target of Oxidative Stress-Mediated Damage: Cochlear and Cortical Responses after an Increase in Antioxidant Defense
Noise-Induced Hearing Loss (NIHL) as a Target of Oxidative Stress-Mediated Damage: Cochlear and Cortical Responses after an Increase in Antioxidant Defense
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DOI：
10.1523/jneurosci.2282-12.2013
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发表时间：
2013-02-27
影响因子：
5.3
通讯作者：
Troiani, Diana
中科院分区：
文献类型：
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作者：
Fetoni, Anna Rita;De Bartolo, Paola;Troiani, Diana
本研究探讨了重复噪声暴露大鼠耳蜗氧化损伤与听皮层损伤之间的关系。为了测试增加的抗氧化防御的效果，使用了水溶性辅酶Q（10）类似物（Q（ter））。我们分析了听觉功能、耳蜗氧化应激、听皮质和耳蜗结构的形态学改变以及辅酶Q（9）和Q（10）（分别为CoQ（9）和CoQ（10））水平作为内源性抗氧化能力的指标。我们报告三个主要结果。首先，听力损失和毛细胞和螺旋神经节的损伤是通过噪声诱导的氧化应激来确定的。第二，声损伤改变了听皮质Ⅱ-Ⅲ层和Ⅴ-Ⅵ层锥体神经元的树突形态，减少了锥体神经元的棘数。第三，水溶性辅酶Q（10）类似物的全身给药减少了氧化诱导的耳蜗损伤，听力损失和皮质树突状细胞损伤。耳蜗CoQ（9）和CoQ（10）含量增加。这些研究结果表明，抗氧化剂治疗恢复听觉皮层神经元的形态和听力功能，减少噪音引起的氧化还原失衡的耳蜗和传入神经阻滞的影响上游的声学通路。
This study addresses the relationship between cochlear oxidative damage and auditory cortical injury in a rat model of repeated noise exposure. To test the effect of increased antioxidant defenses, a water-soluble coenzyme Q(10) analog (Q(ter)) was used. We analyzed auditory function, cochlear oxidative stress, morphological alterations in auditory cortices and cochlear structures, and levels of coenzymes Q(9) and Q(10) (CoQ(9) and CoQ(10), respectively) as indicators of endogenous antioxidant capability. We report three main results. First, hearing loss and damage in hair cells and spiral ganglion was determined by noise-induced oxidative stress. Second, the acoustic trauma altered dendritic morphology and decreased spine number of II-III and V-VI layer pyramidal neurons of auditory cortices. Third, the systemic administration of the water-soluble CoQ(10) analog reduced oxidative-induced cochlear damage, hearing loss, and cortical dendritic injury. Furthermore, cochlear levels of CoQ(9) and CoQ(10) content increased. These findings indicate that antioxidant treatment restores auditory cortical neuronal morphology and hearing function by reducing the noise-induced redox imbalance in the cochlea and the deafferentation effects upstream the acoustic pathway.