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实验动物和人类中空气污染的毒性:氧化应激的作用。

The toxicity of air pollution in experimental animals and humans: the role of oxidative stress.

作者信息

Menzel D B

机构信息

Department of Community and Environmental Medicine, University of California, Irvine 92717.

出版信息

Toxicol Lett. 1994 Jun;72(1-3):269-77. doi: 10.1016/0378-4274(94)90038-8.

DOI:10.1016/0378-4274(94)90038-8
PMID:8202941
Abstract

Nitrogen dioxide (NO2) and ozone (O3) occur throughout the world as the primary pollutants of urban air. NO2 and O3 oxidize cell membrane lipids and proteins. Inflammatory agents are elaborated from the lung either as a direct result of oxidation or as a consequence of leukocytes recruited into the lung by injury. My hypothesis is that NO2 and O3 initiate or exacerbate chronic lung disease through an inflammatory mechanism which can be reduced by supplementation with greater amounts than those required to alleviate vitamin deficiency symptoms of vitamins C (ascorbic acid) and E (alpha-tocopherol). Children, whose lungs are developing, are the most likely group to benefit from supplementation with vitamins C and E because the adverse effects of inflammation on the developing lung are likely to be greater and the time of exposure is longer than in adults. This hypothesis is in accord with current human and experimental animal data and the chemistry of O3 and NO2 toxicity, and is supported by recent ecological epidemiological studies of persons supplementing their intake of vitamins C and E.

摘要

二氧化氮(NO₂)和臭氧(O₃)作为城市空气的主要污染物在全球范围内存在。NO₂和O₃会氧化细胞膜脂质和蛋白质。炎症介质可直接因氧化作用从肺部产生,也可作为损伤后募集到肺部的白细胞的结果而产生。我的假设是,NO₂和O₃通过一种炎症机制引发或加剧慢性肺病,而补充比缓解维生素C(抗坏血酸)和维生素E(α-生育酚)缺乏症状所需量更多的这两种维生素,可减轻这种炎症机制。肺部正在发育的儿童是最有可能从补充维生素C和E中受益的群体,因为炎症对发育中肺部的不利影响可能更大,且暴露时间比成年人更长。这一假设与当前的人体和实验动物数据以及O₃和NO₂毒性的化学原理相符,并得到了近期补充维生素C和E摄入量人群的生态流行病学研究的支持。

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