IMIS | Flanders Marine Institute

Flanders Marine Institute

Platform for marine research


Publications | Institutes | Persons | Datasets | Projects | Maps
[ report an error in this record ]basket (0): add | show Printer-friendly version

Cytochrome P4501A is induced in endothelial cell lines from the kidney and lung of the bottlenose dolphin,Tursiops truncatus
Garrick, R.A.; Woodin, B.R.; Wilson, J.Y.; Middlebrooks, B.L.; Stegeman, J.J. (2006). Cytochrome P4501A is induced in endothelial cell lines from the kidney and lung of the bottlenose dolphin,Tursiops truncatus. Aquat. Toxicol. 76(3-4): 295-305.
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X, more
Peer reviewed article  

Available in  Authors 

    Circulatory system; Epithelia; Marine mammals; Cetacea [WoRMS]; Marine
Author keywords
    endothelium; CYP1A; EROD; dioxin; Cetacean; microvascular

Authors  Top 
  • Garrick, R.A.
  • Woodin, B.R.
  • Wilson, J.Y.
  • Middlebrooks, B.L.
  • Stegeman, J.J.

    Marine 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 truncates, and exposed to the AHR agonists ß-naphthoflavone (ßNF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). ßNF (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 ßNF, and more efficacious, with maximum induction of CYP1A1 activity 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.

All data in IMIS is subject to the VLIZ privacy policy Top | Authors