| pubmed-article:11158718 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C0052441 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C0085862 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C1299583 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C0596763 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C1608386 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C1549571 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:11158718 | lifeskim:mentions | umls-concept:C0387841 | lld:lifeskim |
| pubmed-article:11158718 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11158718 | pubmed:dateCreated | 2001-2-22 | lld:pubmed |
| pubmed-article:11158718 | 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. | lld:pubmed |
| pubmed-article:11158718 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11158718 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11158718 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11158718 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11158718 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11158718 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11158718 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11158718 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11158718 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11158718 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:11158718 | pubmed:issn | 1096-6080 | lld:pubmed |
| pubmed-article:11158718 | pubmed:author | pubmed-author:PollenzR SRS | lld:pubmed |
| pubmed-article:11158718 | pubmed:author | pubmed-author:KeilD EDE | lld:pubmed |
| pubmed-article:11158718 | pubmed:author | pubmed-author:Peden-AdamsM... | lld:pubmed |
| pubmed-article:11158718 | pubmed:author | pubmed-author:DudleyA CAC | lld:pubmed |
| pubmed-article:11158718 | pubmed:author | pubmed-author:EuDalyJJ | lld:pubmed |
| pubmed-article:11158718 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11158718 | pubmed:volume | 59 | lld:pubmed |
| pubmed-article:11158718 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11158718 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11158718 | pubmed:pagination | 251-9 | lld:pubmed |
| pubmed-article:11158718 | pubmed:dateRevised | 2010-9-17 | lld:pubmed |
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| pubmed-article:11158718 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11158718 | pubmed:articleTitle | An aryl hydrocarbon receptor independent mechanism of JP-8 jet fuel immunotoxicity in Ah-responsive and Ah-nonresponsive mice. | lld:pubmed |
| pubmed-article:11158718 | pubmed:affiliation | Department of Environmental Studies, The Medical University of South Carolina, Charleston, South Carolina, USA. | lld:pubmed |
| pubmed-article:11158718 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11158718 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
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