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环境臭氧暴露后鼻灌洗液中的芳香族羟基化作用。

Aromatic hydroxylation in nasal lavage fluid following ambient ozone exposure.

作者信息

Frischer T, Pullwitt A, Kühr J, Meinert R, Haschke N, Studnicka M, Lubec G

机构信息

University Children's Hospital, Vienna, Austria.

出版信息

Free Radic Biol Med. 1997;22(1-2):201-7. doi: 10.1016/s0891-5849(96)00292-4.

Abstract

Ozone at ambient concentrations affects lung function and initiates an inflammatory response of the airways. However, the underlying mechanisms are poorly understood. In vitro studies have shown that ozone reacts with water to give reactive hydroxyl radicals capable of oxidizing a wide range of biomolecules. We conducted a study to determine if in vivo hydroxyl radical attack on human airways occurs under natural exposure to ozone. The relation of orthotyrosine to para-tyrosine as a measure of hydroxyl radical attack was analyzed in nasal lavage samples of 44 primary school children in an epidemiologic study. Repeated nasal lavages were performed between May and October 1991 both following "low" (daily half-hour maximum < 140 micrograms/m3, approximately 70 ppb) and "high" (daily half-hour maximum > 180 micrograms/m3, approximately 90 ppb) ozone exposure. Concomitantly, lung function tests were performed. On average, 11.6 (6-16) nasal lavages were performed for each of 24 study days (10 days following "low" ozone exposure and 14 days following "high" ozone exposure). Average ortho-tyrosine (median; 5-95% percentile) for each child was 0.037 mumol/L (0.016-0.064 mumol/L) and average para-tyrosine was 15.7 mumol/L (9.8-24.1 mumol/L). Ortho-tyrosine (as percentage of tyrosine) was significantly higher following days with "high" ozone exposure (0.18%) vs. days following "low" ozone exposure (0.02%; p = .0001). Ortho-tyrosine showed an inverse relationship with forced vital capacity (p = .01) but was not related to inflammation of the upper airways as assessed by cell counts of polymorphonuclear neutrophils. Hydroxyl radical attack subsequent to ambient ozone occurs in the upper airways of healthy children and is related to lung function decrements.

摘要

环境浓度的臭氧会影响肺功能并引发气道炎症反应。然而,其潜在机制尚不清楚。体外研究表明,臭氧与水反应会生成能够氧化多种生物分子的活性羟基自由基。我们开展了一项研究,以确定在自然暴露于臭氧的情况下,体内羟基自由基是否会攻击人类气道。在一项流行病学研究中,分析了44名小学生鼻腔灌洗样本中作为羟基自由基攻击指标的邻酪氨酸与对酪氨酸的关系。在1991年5月至10月期间,分别在“低”(每日半小时最高值<140微克/立方米,约70 ppb)和“高”(每日半小时最高值>180微克/立方米,约90 ppb)臭氧暴露后进行反复鼻腔灌洗。同时,进行肺功能测试。在24个研究日中,平均每个研究对象进行了11.6次(6 - 16次)鼻腔灌洗(“低”臭氧暴露后10天,“高”臭氧暴露后14天)。每个儿童的平均邻酪氨酸(中位数;第5 - 95百分位数)为0.037微摩尔/升(0.016 - 0.064微摩尔/升),平均对酪氨酸为15.7微摩尔/升(9.8 - 24.1微摩尔/升)。“高”臭氧暴露日后邻酪氨酸(占酪氨酸的百分比)显著高于“低”臭氧暴露日后(0.18%对0.02%;p = 0.0001)。邻酪氨酸与用力肺活量呈负相关(p = 0.01),但与通过多形核中性粒细胞计数评估的上呼吸道炎症无关。环境臭氧暴露后羟基自由基攻击发生在健康儿童的上呼吸道,且与肺功能下降有关。

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