Ohinata Y, Yamasoba T, Schacht J, Miller J M
Kresge Hearing Research Institute, University of Michigan, Ann Arbor, MI 48109-0506, USA.
Hear Res. 2000 Aug;146(1-2):28-34. doi: 10.1016/s0378-5955(00)00096-4.
The generation of reactive oxygen species (ROS) is thought to be part of the mechanism underlying noise-induced hearing loss (NIHL). Glutathione (GSH) is an important cellular antioxidant that limits cell damage by ROS. In this study, we investigated the effectiveness of a GSH supplement to protect GSH-deficient animals from NIHL. Pigmented guinea pigs were exposed to a 4 kHz octave band noise, 115 dB SPL, for 5 h. Group 1 had a normal diet, while groups 2, 3 and 4 were fed a 7% low protein diet (leading to lowered tissue levels of GSH) for 10 days prior to noise exposure. One hour before, immediately after and 5 h after noise exposure, subjects received either an intraperitoneal injection of 5 ml/kg body weight of 0.9% NaCl (groups 1 and 2), 0.4 M glutathione monoethyl ester (GSHE; group 3) or 0.8 M GSHE (group 4). Auditory thresholds were measured by evoked brain stem response at 2, 4, 8, 12, 16 and 20 kHz before and after noise exposure. Ten days post exposure, group 1 showed noise-induced threshold shifts of approximately 20 dB at 2, 16 and 20 kHz and 35 to 40 dB at other frequencies. Threshold shifts in group 2 were significantly greater than baseline at 2, 4, 16 and 20 kHz. GSHE supplementation in a dose-dependent fashion attenuated the threshold shifts in the low protein diet animals. Hair cell loss, as evaluated with cytocochleograms, was consistent with the auditory-evoked brainstem response results. Group 2 exhibited significantly more hair cell loss than any of the other groups; hair cell loss in group 3 was similar to that seen in group 1; group 4 showed less loss than group 1. These results indicate that GSH is a significant factor in limiting noise-induced cochlear damage. This is compatible with the notion that ROS generation plays a role in NIHL and that antioxidant treatment may be an effective prophylactic intervention.
活性氧(ROS)的产生被认为是噪声性听力损失(NIHL)潜在机制的一部分。谷胱甘肽(GSH)是一种重要的细胞抗氧化剂,可限制ROS对细胞的损伤。在本研究中,我们调查了补充GSH对保护GSH缺乏的动物免受NIHL影响的有效性。将有色豚鼠暴露于115 dB SPL的4 kHz倍频程带噪声中5小时。第1组给予正常饮食,而第2、3和4组在噪声暴露前10天喂食7%的低蛋白饮食(导致组织中GSH水平降低)。在噪声暴露前1小时、暴露后立即以及暴露后5小时,受试动物分别腹腔注射5 ml/kg体重的0.9%氯化钠(第1和2组)、0.4 M谷胱甘肽单乙酯(GSHE;第3组)或0.8 M GSHE(第4组)。在噪声暴露前后,通过诱发脑干反应测量2、4、8、12、16和20 kHz的听觉阈值。暴露后10天,第1组在2、16和20 kHz处显示出约20 dB的噪声诱发阈值变化,在其他频率处为35至40 dB。第2组在2、4、16和20 kHz处的阈值变化显著大于基线。以剂量依赖方式补充GSHE可减轻低蛋白饮食动物的阈值变化。用细胞耳蜗图评估的毛细胞损失与听觉诱发脑干反应结果一致。第2组表现出比其他任何组都明显更多的毛细胞损失;第3组的毛细胞损失与第1组相似;第4组的损失比第1组少。这些结果表明,GSH是限制噪声性耳蜗损伤的重要因素。这与ROS产生在NIHL中起作用以及抗氧化治疗可能是一种有效的预防性干预措施的观点相一致。