Roles of oxidative stress in signaling and inflammation induced by particulate matter

被引:137
|
作者
Mazzoli-Rocha, Flavia [2 ]
Fernandes, Silviane [2 ]
Einicker-Lamas, Marcelo [3 ]
Zin, Walter Araujo [1 ,2 ]
机构
[1] Univ Fed Rio de Janeiro, CCS, Inst Biofis Carlos Chagas Filho, Ilha Fundao, BR-21941902 Rio De Janeiro, Brazil
[2] Univ Fed Rio de Janeiro, Lab Fisiol Resp, BR-21941902 Rio De Janeiro, Brazil
[3] Univ Fed Rio de Janeiro, Lab Fisicoquim Biol Aida Hasson Voloch, Inst Biofis Carlos Chagas Filho, BR-21941902 Rio De Janeiro, Brazil
关键词
Air pollution; Cell signaling; Free radicals; Inflammation; Oxidative stress; Particulate matter; NF-KAPPA-B; DIESEL EXHAUST PARTICLES; BRONCHIAL EPITHELIAL-CELLS; AMBIENT AIR-POLLUTION; ENVIRONMENTAL TOBACCO-SMOKE; CYTOCHROME P450 REDUCTASE; ULTRAFINE CARBON-BLACK; TUMOR-NECROSIS-FACTOR; LONG-TERM EXPOSURE; S-TRANSFERASE P1;
D O I
10.1007/s10565-010-9158-2
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:481 / 498
页数:18
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