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

Cell Biol Toxicol. 2010 Oct;26(5):481-98. doi: 10.1007/s10565-010-9158-2. Epub 2010 Mar 27.


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 Ca(2+) influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Air Pollution
  • Antioxidants / metabolism
  • Calcium / metabolism
  • Catalase / metabolism
  • Free Radicals / metabolism
  • Inflammation / etiology
  • Inflammation / physiopathology*
  • Lung / physiopathology*
  • Lung Diseases / etiology
  • Lung Diseases / physiopathology*
  • Macrophages, Alveolar / physiology
  • Oxidation-Reduction
  • Oxidative Stress*
  • Particulate Matter / toxicity*
  • Reactive Oxygen Species / metabolism
  • Signal Transduction*
  • Superoxide Dismutase / metabolism


  • Antioxidants
  • Free Radicals
  • Particulate Matter
  • Reactive Oxygen Species
  • Catalase
  • Superoxide Dismutase
  • Calcium