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臭氧污染、氧化应激、突触可塑性与神经退行性变。

Ozone pollution, oxidative stress, synaptic plasticity, and neurodegeneration.

作者信息

Bello-Medina P C, Rodríguez-Martínez E, Prado-Alcalá R A, Rivas-Arancibia S

机构信息

Departamento de Fisiología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, México.

Departamento de Neurobiología Conductual y Cognitiva, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, México.

出版信息

Neurologia (Engl Ed). 2022 May;37(4):277-286. doi: 10.1016/j.nrl.2018.10.003. Epub 2019 Mar 8.

Abstract

INTRODUCTION

Overpopulation and industrial growth result in an increase in air pollution, mainly due to suspended particulate matter and the formation of ozone. Repeated exposure to low doses of ozone, such as on a day with high air pollution levels, results in a state of chronic oxidative stress, causing the loss of dendritic spines, alterations in cerebral plasticity and in learning and memory mechanisms, and neuronal death and a loss of brain repair capacity. This has a direct impact on human health, increasing the incidence of chronic and degenerative diseases.

DEVELOPMENT

We performed a search of the PubMed, Scopus, and Google Scholar databases for original articles and reviews published between 2000 and 2018 and addressing the main consequences of ozone exposure on synaptic plasticity, information processing in cognitive processes, and the alterations that may lead to the development of neurodegenerative diseases.

CONCLUSIONS

This review describes one of the pathophysiological mechanisms of the effect of repeated exposure to low doses of ozone, which causes loss of synaptic plasticity by producing a state of chronic oxidative stress. This brain function is key to both information processing and the generation of structural changes in neuronal populations. We also address the effect of chronic ozone exposure on brain tissue and the close relationship between ozone pollution and the appearance and progression of neurodegenerative diseases.

摘要

引言

人口过剩和工业增长导致空气污染加剧,主要原因是悬浮颗粒物和臭氧的形成。反复接触低剂量的臭氧,比如在空气污染严重的日子里,会导致慢性氧化应激状态,造成树突棘丢失、大脑可塑性以及学习和记忆机制改变、神经元死亡和大脑修复能力丧失。这对人类健康有直接影响,增加了慢性和退行性疾病的发病率。

发展

我们在PubMed、Scopus和谷歌学术数据库中搜索了2000年至2018年发表的原创文章和综述,这些文章和综述探讨了臭氧暴露对突触可塑性、认知过程中的信息处理以及可能导致神经退行性疾病发展的改变的主要影响。

结论

本综述描述了反复接触低剂量臭氧影响的一种病理生理机制,即通过产生慢性氧化应激状态导致突触可塑性丧失。这种脑功能对于信息处理和神经元群体结构变化的产生均至关重要。我们还探讨了慢性臭氧暴露对脑组织的影响以及臭氧污染与神经退行性疾病的出现和进展之间的密切关系。

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