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运动期间的实验性木柴烟雾暴露与血液氧化应激。

Experimental Woodsmoke Exposure During Exercise and Blood Oxidative Stress.

机构信息

School of Kinesiology, Auburn University, Auburn, Alabama (Dr Peters, Dr Ballmann, Ms Zehner, Mr McCroskey); Department of Health and Human Performance (Ms Quindry, Dr Dumke, Dr Quindry); Center for Environmental Health Sciences (Mr Ferguson); School of Public and Community Health Sciences (Dr Ward), University of Montana, Missoula, Montana.

出版信息

J Occup Environ Med. 2018 Dec;60(12):1073-1081. doi: 10.1097/JOM.0000000000001437.

Abstract

OBJECTIVES

The current laboratory study quantified blood oxidative stress to woodsmoke exposure.

METHODS

Participants inhaled woodsmoke during three randomized crossover exercise trials (Clean Air [0 μg/m], Low Exposure [250 μg/m], and High Exposure [500 μg/m], Woodsmoke [particulate matter less than 2.5 μm, PM2.5]). Trolox equivalent antioxidant capacity (TEAC), uric acid (UA), 8-isoprostanes (8-ISO), lipid hydroperoxides (LOOH), protein carbonyls (PC), nitrotyrosine (3-NT), 8-isoprostane, and myeloperoxidase (MPO) were quantified in Pre, immediately Post, and 1- (1Hr) hour post blood samples.

RESULTS

UA decreased following Low Exposure, while plasma TEAC levels increased Post and 1Hr. LOOH levels decreased 1Hr Post (High Exposure), while 8-Iso increased following both smoke trials. PC and MPO were unchanged following all trials, while 3-NT increased over Clean Air.

CONCLUSION

Blood oxidative stress occurred largely independent of PM2.5 concentrations. Future studies should employ longer duration smoke and exercise combined with physiologic parameters.

摘要

目的

本实验室研究定量分析了血氧化应激与木柴燃烧烟雾暴露的关系。

方法

参与者在三个随机交叉运动试验(清洁空气[0μg/m]、低暴露[250μg/m]和高暴露[500μg/m]、木柴燃烧烟雾[小于 2.5μm 的颗粒物,PM2.5])中吸入木柴燃烧烟雾。在血液样本采集前(Pre)、吸入后即刻(Immediately Post)和 1 小时(1Hr)后,分别检测 Trolox 等效抗氧化能力(TEAC)、尿酸(UA)、8-异前列腺素(8-ISO)、脂质过氧化物(LOOH)、蛋白羰基(PC)、硝基酪氨酸(3-NT)、8-异前列腺素和髓过氧化物酶(MPO)的水平。

结果

低暴露组 UA 在吸入后即刻下降,而 TEAC 水平在吸入后和 1 小时后增加。高暴露组 1 小时后 LOOH 水平下降,而 8-ISO 在两次烟雾暴露后均增加。PC 和 MPO 在所有试验后均无变化,而 3-NT 在清洁空气组后增加。

结论

血液氧化应激的发生在很大程度上与 PM2.5 浓度无关。未来的研究应采用更长时间的烟雾暴露和运动,并结合生理参数进行研究。

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