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dc.contributor.authorGarrick, Rita Anne  Concept link
dc.contributor.authorWoodin, Bruce R.  Concept link
dc.contributor.authorWilson, Joanna Y.  Concept link
dc.contributor.authorMiddlebrooks, Bobby L.  Concept link
dc.contributor.authorStegeman, John J.  Concept link
dc.date.accessioned2006-04-07T19:12:51Z
dc.date.available2006-04-07T19:12:51Z
dc.date.issued2005-10-15
dc.identifier.urihttps://hdl.handle.net/1912/844
dc.descriptionAuthor Posting. © The Authors, 2005. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Aquatic Toxicology 76 (2006): 295-305, doi:10.1016/j.aquatox.2005.10.005.en
dc.description.abstractMarine mammals respond to the presence of polycyclic and planar halogenated aromatic hydrocarbons (PAH or PHAH) with the induced expression in endothelium of cytochrome P4501A1, regulated through the aryl hydrocarbon receptor (AHR) transcription factor. Physiological responses in other animals, such as edema and inflammation indicate that the endothelium may be compromised by exposure to AHR agonists, which are ubiquitous in the marine environment. In other mammals and fish the cellular and molecular consequences of exposure to AHR agonists have been elucidated in cultured endothelial cells. We have cultured and characterized cetacean endothelial cells (EC) and used them in induction studies. Endothelial cells were cultured from the lung and kidney of the bottlenose dolphin Tursiops truncatus and exposed to the AHR agonists β-naphthoflavone (βNF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). βNF (1-3 μM) induced significant increases in CYP1A1(O-deethylation of 7-ethoxyresorufin to resorufin;EROD) activity to 3.6 and 0.92 pmol/mg/min in lung and kidney EC, respectively. TCDD was more potent than βNF, and more efficacious, with maximum induction of CYP1A1activity of 10.1 and 15.2 pmol/mg/min in lung and kidney EC at 3-10 nM TCDD. The differential response indicates that the lung and kidney endothelial cells in culture retain the ability to respond in a selective manner to specific stimuli. Both the molecular mechanisms of induction and the physiological consequences, especially in the vasculature, of toxicant exposure can be studied in this system.en
dc.description.sponsorshipPart of this work was completed during a faculty fellowship from Fordham University for RAG. The Faculty Research Council of Fordham University provided partial support for RAG. This research was supported by NIH grant 5- P42-ES07381 and by U.S.EPA grant R827102-01-0. This research is an outgrowth and continuing impact of Sea Grant Number Grant No. NA90- AA-D-SG480, project NA86RG0075-R/P61.en
dc.format.extent850302 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen_USen
dc.relation.urihttps://doi.org/10.1016/j.aquatox.2005.10.005
dc.subjectEndotheliumen
dc.subjectCYP1Aen
dc.subjectERODen
dc.subjectDioxinen
dc.subjectCetaceanen
dc.subjectMicrovascularen
dc.titleCytochrome P4501A is induced in endothelial cell lines from the kidney and lung of the bottlenose dolphin, Tursiops truncatusen
dc.typePreprinten


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