Roles of oxidative stress in signaling and inflammation induced by particulate matter
Roles of oxidative stress in signaling and inflammation induced by particulate matter
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DOI：
10.1007/s10565-010-9158-2
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发表时间：
2010-10-01
影响因子：
6.1
通讯作者：
Zin, Walter Araujo
中科院分区：
文献类型：
--
作者：
Mazzoli-Rocha, Flavia;Fernandes, Silviane;Zin, Walter Araujo
本文综述了氧化应激在损害暴露于颗粒物（PM）的肺功能中的作用。PM构成了各种类型颗粒的异质混合物，其中许多可能涉及氧化应激诱导和呼吸系统疾病。可能，PM引起氧化应激的能力是PM暴露增加与肺部疾病恶化之间关联的基础。主要是因为它们的大表面积，超细颗粒已被证明在不同的体内和体外研究中引起氧化应激和促炎作用。颗粒组分和表面积可协同作用诱导肺部炎症。在这种情况下，PM暴露后引发的活性氧已被证明激活肺靶细胞中的许多氧化还原反应性信号传导途径和Ca2+内流，这些细胞参与调节对肺部炎症和疾病的相关反应的基因的表达。
This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca2+ influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.