Department of Occupational Health and Safety Engineering, School of public health, Tehran University of Medical Sciences, Tehran, Iran.
Department of Medical Parasitology and Mycology, School of public health, Tehran University of Medical Sciences, Tehran, Iran.
Mol Biol Rep. 2022 Aug;49(8):7219-7229. doi: 10.1007/s11033-022-07291-7. Epub 2022 Jul 9.
Noise-induced hearing loss (NIHL) is one the major causes of acquired hearing loss in developed countries. Noise can change the pattern of gene expression, inducing sensorineural hearing impairment. There is no investigation on the effects of noise frequency on the expression of GJB2 and SLC26A4 genes involved in congenital hearing impairment in cochlear tissue. Here we investigated the impacts of white and purple noise on gene expression and pathologic changes of cochlear tissue.
In this study, 32 adult male Westar rats were randomly divided into experimental groups: WN, animals exposed to white noise with a frequency range of 100-20000 Hz; PN, animals exposed to purple noise with a frequency range of 4-20 kHz, and control group, without noise. The experimental groups were exposed to a 118-120 dB sound pressure level for 8 h per 3 days and 6 days. 1 h and 1 week after termination of noise exposure, cochlear tissue was prepared for pathology and gene expression analysis.
Both white and purple noises caused permanent damage to the cortical, estrosilica systems of hair cells and ganglion of the hearing nerve. GJB2 and SLC26A4 were downregulated in both groups exposed with white and purple noise by increasing the time of noise exposure. However, differences are notably more significant in purple noise, which is more intensified. Also, 1 weak post noise exposure, the downregulation is remarkably higher than 1 h.
Our findings suggest that downregulation of GJB2 and SLC26A4 genes are associated with pathological injury in response to noise exposure in cochlear tissue. It would be suggested the demand for assessment of RNA and protein expression of genes involved in noise-induced hearing loss and subsequently the practice of hearing protection programs.
噪声性听力损失（NIHL）是发达国家后天性听力损失的主要原因之一。噪声会改变基因表达模式，导致感音神经性听力损伤。目前还没有研究表明噪声频率对参与先天性听力损伤的 GJB2 和 SLC26A4 基因在耳蜗组织中的表达的影响。在此，我们研究了白噪声和紫噪声对耳蜗组织基因表达和病理变化的影响。
本研究中，32 只成年雄性 Westar 大鼠被随机分为实验组：WN 组，暴露于频率范围为 100-20000 Hz 的白噪声中；PN 组，暴露于频率范围为 4-20 kHz 的紫噪声中；对照组，无噪声。实验组每天暴露于 118-120 dB 的声压级 3 天，共 6 天。噪声暴露结束后 1 小时和 1 周，制备耳蜗组织进行病理学和基因表达分析。
白噪声和紫噪声均对皮质、雌激素系统的毛细胞和听神经节造成永久性损伤。在两组暴露于白噪声和紫噪声的情况下，GJB2 和 SLC26A4 基因的表达均下调，随着噪声暴露时间的增加，下调更为明显。然而，紫噪声的差异更为显著，其强度更高。此外，在噪声暴露后 1 小时，下调更为显著。
我们的研究结果表明，GJB2 和 SLC26A4 基因的下调与耳蜗组织对噪声暴露的病理损伤有关。建议评估与噪声性听力损失相关的基因的 RNA 和蛋白质表达，并随后实施听力保护计划。
