Abstract | CONTEXT: OBJECTIVE: This study was aimed to determine the effects of Gclm expression on lung inflammation following DEP exposure in mice. MATERIALS AND METHODS: We exposed Gclm wild type, heterozygous, and null mice to DEP via intranasal instillation and assessed lung inflammation as determined by neutrophils and inflammatory cytokines in lung lavage, inflammatory cytokine mRNA levels in lung tissue, as well as total lung GSH, Gclc, and Gclm protein levels. RESULTS: The Gclm heterozygosity was associated with a significant increase in DEP-induced lung inflammation when compared to that of wild type mice. DISCUSSION AND CONCLUSION: This finding indicates that GSH synthesis can mediate DEP-induced lung inflammation and suggests that polymorphisms in Gclm may be an important factor in determining adverse health outcomes in humans following inhalation of PM₂.₅.
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Authors | Chad S Weldy, Collin C White, Hui-Wen Wilkerson, Timothy V Larson, James A Stewart, Sean E Gill, William C Parks, Terrance J Kavanagh |
Journal | Inhalation toxicology
(Inhal Toxicol)
Vol. 23
Issue 12
Pg. 724-35
(Oct 2011)
ISSN: 1091-7691 [Electronic] England |
PMID | 21967497
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- Air Pollutants
- Particulate Matter
- Protein Subunits
- Vehicle Emissions
- GCLM protein, mouse
- Glutamate-Cysteine Ligase
- Glutathione
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Topics |
- Air Pollutants
(chemistry, toxicity)
- Animals
- Bronchoalveolar Lavage Fluid
(chemistry)
- Gene Expression Regulation
(drug effects, physiology)
- Glutamate-Cysteine Ligase
(genetics, metabolism)
- Glutathione
(chemistry, metabolism)
- Heterozygote
- Inflammation
(chemically induced, genetics)
- Lung Diseases
(chemically induced, genetics)
- Male
- Mice
- Particulate Matter
(chemistry, toxicity)
- Protein Subunits
- Vehicle Emissions
(analysis)
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