Linked Life Data

9514655

Source:http://linkedlifedata.com/resource/pubmed/id/9514655

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-4-20
pubmed:abstractText
Prostaglandin endoperoxide H synthases (PGHS-1 and PGHS-2) catalyze an intermediate step in the biosynthesis of prostaglandins and thromboxanes. Recently, it was observed that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) modulates the expression of PGHS-2 mRNA in different cell lines. The main aim of this study was to examine whether PGHS-2 mRNA expression can be changed by acute TCDD in vivo and, second, we were also interested in whether modulation of PGHS-2 is mediated by the aryl hydrocarbon receptor (AhR) which is known to be involved in the transcriptional control of TCDD-induced phase 1 and phase 2 enzymes. Initially C57BL/6J mice were treated with a single dose of 10,000 ng TCDD/kg and the PGHS-1 and PGHS-2 mRNAs were analyzed in liver, lung, thymus, kidney, and spleen. In all tissues examined the expression of PGHS-1 mRNA was not affected by TCDD. However, TCDD treatment enhanced the PGHS-2 mRNA levels in lung and spleen. No effect of TCDD on PGHS-2 expression was found in liver and kidney. For dose-response studies C57BL/6J and DBA/2J mice were treated for 24 h with various doses of TCDD (1-50,000 ng/kg) and the PGHS-2 mRNA increases were analyzed in lungs and spleens. A significant increase of PGHS-2 mRNA in lungs of C57BL/6J mice was found at a dose of 100 ng TCDD/kg, whereas a nearly 100-fold higher TCDD dose was needed to increase PGHS-2 in DBA/2J mice. A similar dose-dependent induction of PGHS-2 was found in spleens of C57BL/6J mice; however, no significant increase of PGHS-2 was found in spleens of DBA/2 mice. These results indicate an involvement of AhR in TCDD-mediated changes of PGHS-2 expression. This suggestion is supported by studies in AhR-deficient animals which showed that TCDD had no effect on PGHS-2 mRNA. When changes of PGHS-2 mRNA expression are compared with those of CYP1A1 between 4 and 72 h after TCDD, it is noteworthy that TCDD led to a delayed and more transient increase of PGHS-2. These data suggest that the mechanism of modulation of both genes by TCDD may be different.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0003-9861
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Academic Press.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
351
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
265-71
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed-meshheading:9514655-Animals, pubmed-meshheading:9514655-Cyclooxygenase 1, pubmed-meshheading:9514655-Cyclooxygenase 2, pubmed-meshheading:9514655-Cytochrome P-450 CYP1A1, pubmed-meshheading:9514655-Dose-Response Relationship, Drug, pubmed-meshheading:9514655-Enzyme Induction, pubmed-meshheading:9514655-Female, pubmed-meshheading:9514655-Gene Expression Regulation, pubmed-meshheading:9514655-Isoenzymes, pubmed-meshheading:9514655-Membrane Proteins, pubmed-meshheading:9514655-Mice, pubmed-meshheading:9514655-Mice, Inbred Strains, pubmed-meshheading:9514655-Mice, Knockout, pubmed-meshheading:9514655-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:9514655-RNA, Messenger, pubmed-meshheading:9514655-Receptors, Aryl Hydrocarbon, pubmed-meshheading:9514655-Tetrachlorodibenzodioxin
pubmed:year
1998
pubmed:articleTitle
Modulation of prostaglandin H synthase-2 mRNA expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice.
pubmed:affiliation
Division of Toxicology, Heinrich-Heine-University of Düsseldorf, Auf'm Hennekamp 50, Düsseldorf, 40225, Germany.
pubmed:publicationType
Journal Article