Differential particulate air pollution induced oxidant stress in human granulocytes, monocytes and alveolar macrophages
Differential particulate air pollution induced oxidant stress in human granulocytes, monocytes and alveolar macrophages
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DOI：
10.1016/s0887-2333(02)00015-2
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发表时间：
2002-06-01
影响因子：
3.2
通讯作者：
Gallagher, JE
中科院分区：
文献类型：
--
作者：
Becker, S;Soukup, JM;Gallagher, JE
已经提出肺中细胞的氧化应激是颗粒污染引起的肺部疾病恶化的潜在机制之一。被认为对颗粒物污染最敏感的人是那些预先存在气道炎症的人，如慢性阻塞性肺病（COPD），肺部感染或哮喘。这些疾病的特征在于气道中存在炎性细胞，包括中性粒细胞（PMN）、嗜酸性粒细胞和单核细胞（Mo），以及肺泡巨噬细胞（AM）数量增加。与肺的其他细胞类型相比，这些细胞具有高的产生氧自由基的能力。为了评估这些各种细胞类型对各种来源的污染颗粒的氧化反应，采用鲁米诺依赖的化学发光。将包括富含过渡金属的渣油飞灰（ROFAs）、煤飞灰、柴油、SiO2、TiO 2和逃逸性粉尘的颗粒与AM、Mo和PMN以10-100 μ g/2 × 10（5）个细胞的剂量范围共培养，并在20分钟相互作用后测定化学发光。AM的强氧化反应仅限于油飞灰，而PMN对含硅酸铝的粉尘最具反应性。在一般情况下，钼的反应是不太积极，但重叠AM和PMN刺激粉尘。然而，在响应SiO2和火山灰的Mo化学发光超过了其他类型的细胞。由AM响应ROFA产生的氧自由基可能依赖于线粒体过程，而PMN中的响应涉及膜NADPH氧化酶复合物，如靶向抑制剂所确定的。AM的各种尺寸的SiO2和TiO 2在从不同的商业来源获得的精细尺寸范围内的响应，是高度可变的，这意味着组合物，而不是大小负责的氧化剂响应。强烈的化学发光反应与反应细胞的细胞毒性并不一致。综上所述，这些结果表明，氧化剂活化的各种来源的颗粒物质是细胞特异性的。因此，发炎的肺可能更容易受到周围空气颗粒物的伤害，因为更广泛的颗粒物造成的氧化应激。(C)出版社：Elsevier Science Ltd.
It has been proposed that oxidant stress of cells in the lung is one of the underlying mechanisms of particulate pollution-induced exacerbation of lung disease. Individuals who are considered most sensitive to particulate pollution are those with pre-existing airways inflammation, such as chronic obstructive pulmonary disease (COPD), lung infection or asthma. These diseases are characterized by a presence of inflammatory cells in the airways including neutrophils (PMN), eosinophils and monocytes (Mo), and increased numbers of alveolar macrophages (AM). These cells have a high capacity for production of oxygen radicals, as compared to other cell types of the lung. To assess the oxidative response of these various cell types to pollution particles of various sources, luminol-dependent chemiluminescence was employed. Particles including transition metal-rich residual oil fly ashes (ROFAs), coal fly ashes, diesel, SiO2, TiO2 and fugitive dusts were co-cultured with AM, Mo and PMN in a dose range of 10-100 mug/2x 10(5) cells and chemiluminescence determined following a 20-min interaction. A strong oxidant response of AM was restricted to oil fly ashes, while the PMN were most reactive to the dusts containing aluminium silicate. In general, the Mo response was less vigorous, but overlapped both AM- and PMN-stimulating dusts. However, in response to SiO2, and volcanic ash the Mo chemiluminescence exceeded that of the other cell types. Oxygen radicals generated in response to ROFA by the AM were likely to be dependent on mitochondrial processes, while the response in PMN involved the membrane NADPH oxidase complex, as determined by targeting inhibitors. The response of AM to SiO2 of various sizes and TiO2 in the fine size range obtained from different commercial sources, was highly variable, implying that composition rather than size was responsible for the oxidant response. A strong chemiluminescence response was not consistently associated with cytotoxicity in the responsive cell. Taken together, these results suggest that oxidant activation by various sources of particulate matter is cell specific. Therefore, the inflamed lung is likely to be more susceptible to harm of ambient air particulates because of the oxidant stress posed by a broader range of particles. (C), 2002 Published by Elsevier Science Ltd.