Source:http://linkedlifedata.com/resource/pubmed/id/11158718
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2001-2-22
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| pubmed:abstractText |
JP-8 jet fuel is handled extensively by personnel in the military and commercial airlines, despite the paucity of information regarding its potential human health effects. JP-8 is a complex mixture primarily consisting of kerosene plus aliphatic and aromatic hydrocarbons. Recent reports indicate that acute JP-8 exposure via inhalation or dermal routes can overtly and persistently impair immune function in mice. Data from preliminary studies in this laboratory assessing the immunotoxicity of JP-8 indicated that oral JP-8 exposure caused an increase in liver weight, a decrease in thymus weight, and a decrease in the PFC response. As these results were similar to classic effects elicited by TCDD, a strong AhR ligand, it was hypothesized that JP-8 may exert immunosuppression via a similar mechanism. To test this hypothesis, an Ah-responsive mouse strain (B6C3F1) and a classically non-responsive mouse strain (DBA/2) bearing a lower affinity AhR were gavaged with JP-8 for 7 days. The results suggest that both mouse strains were equally sensitive to JP-8's toxicity at several endpoints including thymus weight and cellularity, liver weight, and specific IgM antibody responses. Furthermore, JP-8 did not induce CYP1A1 or promote down regulation of the AhR when evaluated by Western blot in either B6C3F1 or DBA/2 mice. In vitro studies corroborated these findings as JP-8 did not induce CYP1A1, promote down regulation of the AhR, or activate an XRE-driven reporter gene in murine Hepa-1 cells. These results suggest that JP-8 may exert its toxicity via an AhR-independent mechanism.
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| pubmed:commentsCorrections | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytochrome P-450 CYP1A1,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrocarbons,
http://linkedlifedata.com/resource/pubmed/chemical/JP8 aviation fuel,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Aryl Hydrocarbon,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrachlorodibenzodioxin
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| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
1096-6080
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
59
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
251-9
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| pubmed:dateRevised |
2010-9-17
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| pubmed:meshHeading |
pubmed-meshheading:11158718-Administration, Oral,
pubmed-meshheading:11158718-Animals,
pubmed-meshheading:11158718-Antibody Formation,
pubmed-meshheading:11158718-Blotting, Western,
pubmed-meshheading:11158718-Cell Count,
pubmed-meshheading:11158718-Cells, Cultured,
pubmed-meshheading:11158718-Cytochrome P-450 CYP1A1,
pubmed-meshheading:11158718-Enzyme Induction,
pubmed-meshheading:11158718-Female,
pubmed-meshheading:11158718-Genes, Reporter,
pubmed-meshheading:11158718-Hemolytic Plaque Technique,
pubmed-meshheading:11158718-Hydrocarbons,
pubmed-meshheading:11158718-Immunity,
pubmed-meshheading:11158718-Liver,
pubmed-meshheading:11158718-Mice,
pubmed-meshheading:11158718-Mice, Inbred C57BL,
pubmed-meshheading:11158718-Mice, Inbred DBA,
pubmed-meshheading:11158718-Microsomes, Liver,
pubmed-meshheading:11158718-Organ Size,
pubmed-meshheading:11158718-Receptors, Aryl Hydrocarbon,
pubmed-meshheading:11158718-Tetrachlorodibenzodioxin,
pubmed-meshheading:11158718-Thymus Gland
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| pubmed:year |
2001
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| pubmed:articleTitle |
An aryl hydrocarbon receptor independent mechanism of JP-8 jet fuel immunotoxicity in Ah-responsive and Ah-nonresponsive mice.
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| pubmed:affiliation |
Department of Environmental Studies, The Medical University of South Carolina, Charleston, South Carolina, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.
|