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噪声作为神经退行性疾病的病因:分子和细胞机制。

Noise as a cause of neurodegenerative disorders: molecular and cellular mechanisms.

机构信息

Department of Medical Chemistry, Yerevan State Medical University after M. Heratsi, Koryun 2, 0025, Yerevan, Armenia.

出版信息

Neurol Sci. 2022 May;43(5):2983-2993. doi: 10.1007/s10072-022-05948-6. Epub 2022 Feb 15.

Abstract

Noise as an environmental stressor becomes of increasing importance in our industrialized world, and especially traffic noise from the environment represents a potential novel neurodegenerative risk factor, as well as for hearing loss. A significant number of studies have been suggested that the overproduction of reactive oxygen species (ROS) has a complex role in stimulation of pathologic events. Experimental studies upon molecular pathways of traffic noise exposure proposed that it increased the level of stress hormones and mediated the inflammatory and oxidative stress (OS) pathways resulting in endothelial and neuronal dysfunction. Studies have shown that neurons are especially sensitive to OS due to high polyunsaturated fatty acids content in membranes, high oxygen uptake, and weak antioxidant defense. However, OS induces the necrotic and apoptotic cell deaths in the cochlea. Chronic noise is one of the many overall reasons of obtained sensorineural hearing loss which destroys cognitive functions in human and animals, as well as suppresses neurogenesis in the hippocampus. Nevertheless, behavioral disorders caused by noise are mainly accompanied with oxidative stress, but the clear molecular mechanism of neurodegeneration due to disruption of the pro- and antioxidant systems is still not fully understood. This paper aims to highlight the down-stream pathophysiology of noise-induced mental disorders, including hearing loss, annoyance, anxiety, depression, memory loss, and Alzheimer's disease, describing the underlying mechanisms of induction of inflammation and oxidative stress.

摘要

噪声作为一种环境应激源,在我们这个工业化世界中变得越来越重要,特别是环境中的交通噪声,它不仅代表了一种潜在的新型神经退行性风险因素,也是听力损失的一个潜在因素。大量研究表明,活性氧(ROS)的过度产生在刺激病理事件中具有复杂的作用。关于交通噪声暴露的分子途径的实验研究表明,它会增加应激激素的水平,并介导炎症和氧化应激(OS)途径,导致内皮和神经元功能障碍。研究表明,由于细胞膜中含有大量的多不饱和脂肪酸、高耗氧量和较弱的抗氧化防御,神经元对 OS 特别敏感。然而,OS 会导致耳蜗中的细胞坏死和凋亡。慢性噪声是导致获得性感音神经性听力损失的众多原因之一,它会破坏人类和动物的认知功能,并抑制海马体中的神经发生。然而,噪声引起的行为障碍主要伴随着氧化应激,但由于抗氧化和促氧化剂系统的破坏而导致神经退行性变的明确分子机制仍未完全清楚。本文旨在强调噪声引起的精神障碍的下游病理生理学,包括听力损失、烦恼、焦虑、抑郁、记忆力减退和阿尔茨海默病,描述诱导炎症和氧化应激的潜在机制。

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