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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3 Pt 1
|
| pubmed:dateCreated |
1996-7-5
|
| pubmed:abstractText |
The present study determined the effects of vitamin A (vA) deficiency on the responses to ozone (O3) challenges in two inbred strains of mice that are differentially susceptible to O3-induced lung inflammation. Susceptible C57BL/6J (B6) and resistant C3H/HeJ (C3) dams at 2 wk gestation were fed test diets containing either 0 or 10 micrograms retinol/g diet. In mice that were maintained on vA-sufficient (vA+) diet, lung and liver tissue concentrations of vA and retinyl palmitate (RP) were significantly (P<0.05) lower in the B6 strain compared with C3, as measured by high-performance liquid chromatography techniques. vA and RP levels were significantly (P<0.05) reduced in lung and liver tissues of 8-wk old B6 and C3 mice that were maintained on a vA deficient (vA-) diet. vA+ and vA- mice of both strains were exposed to air or 0.3 ppm O3/72 h, and lung injury was assessed by differential cell count and total protein concentration in bronchoalveolar lavage (BAL) returns. O3 exposure caused significantly (P<0.05) greater increases in inflammatory cells and a total protein in BAL returns of vA+ B6 mice than vA+ C3 mice. vA deficiency significantly (P<0.05) enhanced O3-induced increases in polymorphonuclear leukocytes in C3 mice and epithelial cells loss in both strains. Compared with vA+ mice, lung permeability was also significantly (P<0.05) enhanced in vA- mice of both strains exposed to O3. vA replacement partially reversed the O3-induced lung injury that was enhanced by vA- diet. Results indicate that vA may have an important role in the pathogenesis of O3-induced lung injury in differentially susceptible inbred strains of mice.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0002-9513
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
270
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
L475-82
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:8638741-Analysis of Variance,
pubmed-meshheading:8638741-Animals,
pubmed-meshheading:8638741-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:8638741-Chromatography, High Pressure Liquid,
pubmed-meshheading:8638741-Epithelial Cells,
pubmed-meshheading:8638741-Epithelium,
pubmed-meshheading:8638741-Female,
pubmed-meshheading:8638741-Inflammation,
pubmed-meshheading:8638741-Liver,
pubmed-meshheading:8638741-Lung,
pubmed-meshheading:8638741-Lung Injury,
pubmed-meshheading:8638741-Lymphocytes,
pubmed-meshheading:8638741-Macrophages, Alveolar,
pubmed-meshheading:8638741-Male,
pubmed-meshheading:8638741-Mice,
pubmed-meshheading:8638741-Mice, Inbred C3H,
pubmed-meshheading:8638741-Mice, Inbred C57BL,
pubmed-meshheading:8638741-Ozone,
pubmed-meshheading:8638741-Species Specificity,
pubmed-meshheading:8638741-Vitamin A,
pubmed-meshheading:8638741-Vitamin A Deficiency
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
Vitamin A deficiency enhances ozone-induced lung injury.
|
| pubmed:affiliation |
Department of Environmental Health Sciences, The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205, USA.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|