Antioxidant enzyme induction: a new protective approach against the adverse effects of diesel exhaust particles
Wan J, Diaz-Sanchez D.
Hart and Louise Lyon Laboratory, Division of Clinical Immunology and Allergy, Department of Medicine, UCLA David Geffen School of Medicine, University of California, Los Angeles, California 90095-1690, USA.
Inhal Toxicol. 2007;19 Suppl 1:177-82.
Exposure to airborne particulate pollutants such as diesel exhaust particles (DEPs) has been associated with allergic respiratory disorders, including asthma and allergic rhinitis. In this communication, we review recent advances in the mechanism by which DEPs elicit their harmful effects and the protective role of antioxidants.
Reactive oxidative species (ROS) are believed to play a key role in cellular damage after exposure to DEPs. Numerous reports demonstrate that both proinflammatory and anti-inflammatory products are induced by DEPs via the activation of transcription factors. DEPs trigger multiple signaling pathways, which lead to DNA damage and cell apoptosis, inflammatory response, and antioxidant defense. Recent studies both in vitro and in mice show that antioxidants could alleviate the allergic inflammatory effects of DEPs. Human in vivo models suggest that the important phase II enzymes GSTM1 and GSTP1 modify the adjuvant effect of diesel exhaust particles on allergic inflammation. We have shown that the induction of phase II enzymes by the chemical sulforaphane can block DEP-induced enhanced immunoglobulin (Ig) E production in B cells and DEP-induced proinflammatory cytokine production in epithelial cells.
These findings suggest that overexpression of antioxidant enzymes could constitute a powerful potential chemopreventive approach against adverse effects induced by oxidant pollutants such as DEPs.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17886065&itool=pubmed_DocSum
PMID: 17886065 [PubMed - in process]
Wan J, Diaz-Sanchez D.
Hart and Louise Lyon Laboratory, Division of Clinical Immunology and Allergy, Department of Medicine, UCLA David Geffen School of Medicine, University of California, Los Angeles, California 90095-1690, USA.
Inhal Toxicol. 2007;19 Suppl 1:177-82.
Exposure to airborne particulate pollutants such as diesel exhaust particles (DEPs) has been associated with allergic respiratory disorders, including asthma and allergic rhinitis. In this communication, we review recent advances in the mechanism by which DEPs elicit their harmful effects and the protective role of antioxidants.
Reactive oxidative species (ROS) are believed to play a key role in cellular damage after exposure to DEPs. Numerous reports demonstrate that both proinflammatory and anti-inflammatory products are induced by DEPs via the activation of transcription factors. DEPs trigger multiple signaling pathways, which lead to DNA damage and cell apoptosis, inflammatory response, and antioxidant defense. Recent studies both in vitro and in mice show that antioxidants could alleviate the allergic inflammatory effects of DEPs. Human in vivo models suggest that the important phase II enzymes GSTM1 and GSTP1 modify the adjuvant effect of diesel exhaust particles on allergic inflammation. We have shown that the induction of phase II enzymes by the chemical sulforaphane can block DEP-induced enhanced immunoglobulin (Ig) E production in B cells and DEP-induced proinflammatory cytokine production in epithelial cells.
These findings suggest that overexpression of antioxidant enzymes could constitute a powerful potential chemopreventive approach against adverse effects induced by oxidant pollutants such as DEPs.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17886065&itool=pubmed_DocSum
PMID: 17886065 [PubMed - in process]
