线粒体毒素诱导突发性耳聋模型血管纹损伤机制的研究

THE INJURY MECHANISM OF STRIA VASCULARIS IN THE SUDDEN-ONSET SENSORINEURAL HEARING LOSS MODEL INDUCED BY MITOCHONDRIAL TOXIN

目的研究线粒体毒素诱导豚鼠突发性耳聋模型血管纹损伤的机制。方法20只杂色豚鼠随机分为3-硝基丙酸(3-NP)组和磷酸盐缓冲液(PBS)对照组,分别经圆窗膜给予0.3 mmol/L 3-NP或PBS 10min。分别检测两组豚鼠的听性脑干反应测听(ABR),血管纹丙二醛(MDA)、超氧化物歧化酶(SOD)及边缘细胞超微结构变化。结果与PBS对照组相比较,3-NP组ABR阈移增大、幅值减小;血管纹MDA含量增高(P<0.05),SOD活性降低(P<0.05);边缘细胞超微结构改变,尤以线粒体肿胀,空泡变最为显著。结论线粒体毒素通过氧化应激反应损伤突发性耳聋豚鼠的血管纹。

Objective To investigate the injury mechanism of stria vascularis in the sudden-onset sensori-neural hearing loss model induced by mitochondrial toxin. Methods 3-nitropropionic acid （3-NP） was placed on the round window membrane and kept for 10 min in 10 guinea pigs at the dose of 0. 3 mmol/L. Ten control guinea pigs were tested by placing phosphate buffered saline （PBS） on the round window for the same duration. ABR, SOD, MDA and ultrastructure of the stria vascularis were detected. Results All animals demonstrated from profound hearing loss to total ABRs loss after 3-NP exposure. MDA concertration in the stria vascularis of the 3-NP group was significantly higher than that in the PBS group （P 〈0.05）, while SOD level was much lower than that in the PBS group （P〈0.05） . The ultrastructure of the marginal cells changed, especially swelling and vacuolization in mitochondria. Conclusion Mitochondrial oxidative stress is one of the mechanisms of the stria vascularis injury patterns.