title: Diesel exhaust particles induce cysteine oxidation and s-glutathionylation in house dust mite induced murine asthma.
abstract: BACKGROUND
  Diesel exhaust particle (DEP) exposure enhances allergic inflammation and has been linked to the incidence of asthma. Oxidative stress on the thiol molecules cysteine (Cys) and glutathione (GSH) can promote inflammatory host responses. The effect of DEP on the thiol oxidation/reduction (redox) state in the asthmatic lung is unknown.
  
  
  OBJECTIVE
  To determine if DEP exposure alters the Cys or GSH redox state in the asthmatic airway.
  
  
  METHODS
  Bronchoalveolar lavage fluid was obtained from a house dust mite (HDM) induced murine asthma model exposed to DEP. GSH, glutathione disulfide (GSSG), Cys, cystine (CySS), and s-glutathionylated cysteine (CySSG) were determined by high pressure liquid chromatography.
  
  
  RESULTS
  DEP co-administered with HDM, but not DEP or HDM alone, decreased total Cys, increased CySS, and increased CySSG without significantly altering GSH or GSSG.
  
  
  CONCLUSIONS
  DEP exposure promotes oxidation and S-glutathionylation of cysteine amino acids in the asthmatic airway, suggesting a novel mechanism by which DEP may enhance allergic inflammatory responses.
authors.affiliation: Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
authors.forename: Gerald B
authors.initials: GB
authors.lastname: Lee
authors.forename: Eric B
authors.initials: EB
authors.lastname: Brandt
authors.forename: Chang
authors.initials: C
authors.lastname: Xiao
authors.forename: Aaron M
authors.initials: AM
authors.lastname: Gibson
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Le Cras
authors.forename: Lou Ann S
authors.initials: LA
authors.lastname: Brown
authors.forename: Anne M
authors.initials: AM
authors.lastname: Fitzpatrick
authors.forename: Gurjit K
authors.initials: GK
authors.lastname: Khurana Hershey
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects; D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D001980:Bronchi / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002460:Cell Line; D003545:Cysteine / Q000031:analogs & derivatives* / Q000032:analysis* / Q000276:immunology / Q000378:metabolism; D003553:Cystine / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D005978:Glutathione / Q000031:analogs & derivatives* / Q000032:analysis* / Q000276:immunology / Q000378:metabolism; D019803:Glutathione Disulfide / Q000032:analysis / Q000276:immunology / Q000378:metabolism; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D052638:Particulate Matter / Q000009:adverse effects*; D039981:Pyroglyphidae / Q000276:immunology; D001335:Vehicle Emissions / Q000032:analysis
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D001335:Vehicle Emissions; D003553:Cystine; C031586:cysteine-glutathione disulfide; D005978:Glutathione; D003545:Cysteine; D019803:Glutathione Disulfide
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