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Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss

机译:慢性铅暴露会诱发耳蜗氧化应激并增强噪音引起的听力损失

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摘要

Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8–12 dB and 11–25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18–30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways.
机译:获得性听力损失是由多种环境风险因素(例如铅和噪音水平升高)的复杂相互作用所引起的,而这些因素在城市社区中普遍存在。这项研究描述了铅诱导的听觉功能障碍的潜在机制及其与噪声暴露的潜在相互作用。将年轻的C57BL / 6小鼠暴露于:1)对照条件; 2)在饮用水中加入2 mM乙酸铅28天; 3)90 dB宽带噪声2小时/天,持续两个星期; 4)铅和噪音。通过电感耦合等离子体质谱分析(ICP-MS)测量血铅水平,使用靶向基因阵列评估铅诱导的耳蜗氧化应激信号,并通过记录听觉脑干反应评估听力阈值。慢性铅暴露下调了编码关键抗氧化酶的耳蜗Sod1,Gpx1和Gstk1,并上调了指示细胞凋亡的ApoE,Hspa1a,Ercc2,Prnp,Ccl5和Sqstm1。铅或噪声的隔离暴露分别导致听觉阈值发生8–12 dB和11–25 dB的偏移。组合照射引起18–30 dB的偏移,这明显高于单独照射所观察到的偏移。这项研究表明,长期接触铅可能会通过平行途径诱发耳蜗氧化应激并增强噪声引起的听力障碍。

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