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

Abstract

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.

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Correspondence to Walter Araújo Zin.

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This study was supported by the Brazilian Council for Scientific and Technological Development (CNPq), Carlos Chagas Filho Rio de Janeiro State Research Supporting Foundation (FAPERJ), and the Ministry of Science and Technology (MCT).

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Mazzoli-Rocha, F., Fernandes, S., Einicker-Lamas, M. et al. Roles of oxidative stress in signaling and inflammation induced by particulate matter. Cell Biol Toxicol 26, 481–498 (2010). https://doi.org/10.1007/s10565-010-9158-2

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  • DOI: https://doi.org/10.1007/s10565-010-9158-2

Keywords

  • Air pollution
  • Cell signaling
  • Free radicals
  • Inflammation
  • Oxidative stress
  • Particulate matter