Abstract
Epidemiological studies have shown that particulate air pollutants, such as diesel exhaust particles (DEPs) are implicated in the increased incidence of allergic airway disorders. DEPs induce and exaggerate allergic airway inflammation in vitro and in vivo. Studies of molecular mechanisms have focused on the role of reactive oxygen species (ROS) generated directly and indirectly by exposure to DEPs. The ROS play an important role in proinflammatory reaction in airways. Nuclear erythroid 2 P45-related factor 2 (Nrf2) is a key transcription factor that regulates host antioxidant and contributes to regulate airway inflammation and exacerbation of allergic inflammation induced by DEPs. The authors demonstrated that DEPs-induced oxidants stress and resultant inflammatory changes were blocked by antioxidants such as N-acetyl cysteine (NAC). Therefore, chemoprevention against DEPs health effects in susceptible individuals may become a choice for future environmental protection policy.
Keywords: Diesel exhaust particles, oxidative stress, antioxidant enzyme, airway inflammation, allergy and asthma, chemoprevention, reactive oxygen species, Nuclear erythroid 2, N-acetyl cysteine (NAC), polycyclic aromatic hydrocarbons (PAHs), interleukin-8, intercellular adhesion molecule (ICAM)-1, granulocyte-macrophage colony-stimulating factor, (GM-CSF), leucine, bronchoalveolar lavage (BAL), ovalbumin (OVA), anaphylaxis, selenium, Erythromycin (EM), scleroderma fibroblasts, Particulate matter of diameter, <, 2.5 μm, Nuclear erythroid 2 P45-related factor 2, Intercellular adhesion molecule, Regulated on activation, normal T-cell expressed and secreted, Mitogen activated protein kinase, Bronchoalveolar lavage, Reduced glutathione/oxidized glutathione, Ovalbumin, Erythromycin
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