Lin Cheng-Yu, Wu Jiunn-Liang, Shih Tung-Sheng, Tsai Perng-Jy, Sun Yih-Min, Guo Yueliang Leon
Department of Otolaryngology, Tainan Municipal Hospital, East District, Tainan City 701, Taiwan.
Hear Res. 2009 Nov;257(1-2):8-15. doi: 10.1016/j.heares.2009.07.008. Epub 2009 Jul 28.
The generation of reactive oxygen species (ROS) is thought to be part of the mechanism underlying noise-induced hearing loss (NIHL). Glutathione is an important cellular antioxidant that limits cell damage by ROS. We aimed to determine the effect of genetic polymorphisms of glutathione S-transferase (GST) T1, GSTM1, and GSTP1, on temporary threshold shift (TTS) in 58 noise-exposed male workers from a steel factory. The pre-shift hearing impairment at high frequency (HF, average of 3, 4, and 6kHz) was 30.7dB HL (S.D.=19.3). The amount of daily noise exposure was 83.0dBA (S.D.=5.0). Noise-induced TTS at HF by pure-tone audiometry (PTA) was related to the daily noise exposure (p<0.05). Based on combinatory analysis, we found that individuals carrying all genotypes with GSTT1 null, GSTM1 null, and GSTP1 Ile(105)/Ile(105) were more susceptible to NIHL. These results suggest that pre-shift hearing impairment and daily noise exposure had impacts on TTS at HF by PTA. In addition, GST genetic polymorphisms may modify the susceptibility to noise-induced TTS.
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。谷胱甘肽是一种重要的细胞抗氧化剂,可限制ROS对细胞的损伤。我们旨在确定谷胱甘肽S-转移酶(GST)T1、GSTM1和GSTP1的基因多态性对一家钢铁厂58名噪声暴露男性工人的暂时性阈移(TTS)的影响。高频(HF,3、4和6kHz平均值)的班前听力损伤为30.7dB HL(标准差=19.3)。每日噪声暴露量为83.0dBA(标准差=5.0)。通过纯音听力计(PTA)测量的高频噪声诱发TTS与每日噪声暴露有关(p<0.05)。基于组合分析,我们发现携带GSTT1缺失、GSTM1缺失和GSTP1 Ile(105)/Ile(105)所有基因型的个体对NIHL更敏感。这些结果表明,班前听力损伤和每日噪声暴露通过PTA对高频TTS有影响。此外,GST基因多态性可能会改变对噪声诱发TTS的易感性。