Environmentally persistent free radicals induce airway hyperresponsiveness in neonatal rat lungs.
Environmentally persistent free radicals induce airway hyperresponsiveness in neonatal rat lungs.
复制标题
环境持续的自由基在新生大鼠肺中引起气道高反应性。
DOI：
10.1186/1743-8977-8-11
复制
发表时间：
2011-03-09
影响因子：
10
通讯作者：
Cormier SA
中科院分区：
文献类型：
--
作者：
Balakrishna S;Saravia J;Thevenot P;Ahlert T;Lominiki S;Dellinger B;Cormier SA
儿童和婴儿哮喘风险/哮喘恶化的增加与接触超细颗粒物 (PM) 水平升高有关。燃烧源 PM 中存在一类新发现的污染物，即环境持久性自由基 (EPFR)，这表明存在潜在的未被识别的导致哮喘发生和/或恶化的危险因素。新生大鼠（7 日龄）每天暴露于含有 EPFR 的燃烧产生的超细颗粒 (CGUFP)、不含 EPFR 的 CGUFP 或空气中 20 分钟，持续一周。对暴露的大鼠和年龄匹配的对照组的肺功能进行了评估。分离灌洗液并分析细胞结构和细胞因子以及体内氧化应激指标。还进行了肺组织病理学和肺匀浆中差异蛋白表达的表征。暴露于含有 EPFR 的 CGUFP 的新生儿出现了明显的肺部炎症和气道高反应性。这与肺部氧化应激水平升高相关。使用差异二维电泳，我们鉴定了对照组和 CGUFP 暴露组之间的 16 个差异表达蛋白。在暴露于含有 EPFR 的 CGUFP 的大鼠中； peroxiredoxin-6、cofilin1 和annexin A8 上调。新生儿暴露于含有 EPFR 的 CGUFP 会诱发肺氧化应激和肺功能障碍。这与各种蛋白质表达的变化有关，这些蛋白质与氧化应激反应和 T 淋巴细胞中糖皮质激素受体易位的调节有关。
Increased asthma risk/exacerbation in children and infants is associated with exposure to elevated levels of ultrafine particulate matter (PM). The presence of a newly realized class of pollutants, environmentally persistent free radicals (EPFRs), in PM from combustion sources suggests a potentially unrecognized risk factor for the development and/or exacerbation of asthma. Neonatal rats (7-days of age) were exposed to EPFR-containing combustion generated ultrafine particles (CGUFP), non-EPFR containing CGUFP, or air for 20 minutes per day for one week. Pulmonary function was assessed in exposed rats and age matched controls. Lavage fluid was isolated and assayed for cellularity and cytokines and in vivo indicators of oxidative stress. Pulmonary histopathology and characterization of differential protein expression in lung homogenates was also performed. Neonates exposed to EPFR-containing CGUFP developed significant pulmonary inflammation, and airway hyperreactivity. This correlated with increased levels of oxidative stress in the lungs. Using differential two-dimensional electrophoresis, we identified 16 differentially expressed proteins between control and CGUFP exposed groups. In the rats exposed to EPFR-containing CGUFP; peroxiredoxin-6, cofilin1, and annexin A8 were upregulated. Exposure of neonates to EPFR-containing CGUFP induced pulmonary oxidative stress and lung dysfunction. This correlated with alterations in the expression of various proteins associated with the response to oxidative stress and the regulation of glucocorticoid receptor translocation in T lymphocytes.
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DOI：
10.1080/00039896.1993.9936721
发表时间：
1993-09-01
期刊：
ARCHIVES OF ENVIRONMENTAL HEALTH
影响因子：
--
作者：
HOEK, G;BRUNEKREEF, B
通讯作者：
BRUNEKREEF, B
影响因子：
10.4
作者：
Lipsett M;Hurley S;Ostro B
通讯作者：
Ostro B
影响因子：
4.8
作者：
Kang, SW;Baines, IC;Rhee, SG
通讯作者：
Rhee, SG
影响因子：
10
作者：
McGrath, LT;Mallon, P;Elborn, S
通讯作者：
Elborn, S
DOI：
10.1164/ajrccm.160.1.9809140
发表时间：
1999-07-01
影响因子：
24.7
作者：
Montuschi, P;Corradi, M;Barnes, PJ
通讯作者：
Barnes, PJ