5 research outputs found
Cytochrome P4501A is Induced in Endothelial Cell Lines From the Kidney and Lung of the Bottlenose Dolphin, \u3ci\u3eTursiops truncatus\u3c/i\u3e
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 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 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
Cytochrome P4501A is induced in endothelial cell lines from the kidney and lung of the bottlenose dolphin, Tursiops truncatus
Author 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.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 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.Part 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
Cytochrome P450 induced differentially in endothelial cells cultured from different organs of Anguilla rostrata
Author Posting. © The Authors, 2004. This is the author's version of the work. It is posted here by permission of Society for In Vitro Biology for personal use, not for redistribution. The definitive version was published in In Vitro Cellular & Developmental Biology - Animal 41 (2005): 57-63, doi:10.1290/0409063.1.Endothelial cells are a structural barrier and an active regulator of many bodily
processes. CYP1A activity is induced in the endothelium of teleosts and mammals
exposed to lipophilic xenobiotics, such as polycyclic aromatic hydrocarbons, and can
have significant consequences for endothelial functions. We exposed cultures of
characterized endothelial cells from the heart, kidney and rete mirabile of the eel,
Anguilla rostrata, to AhR agonists. In heart endothelial cells the maximum response
(based on EROD activity) to TCDD, 113 pmol/mg-min, was at 1 nM TCDD and the peak
response to βNF, 135 pmol/mg-min, was at 3 μM βNF. The maximum response to
TCDD in the kidney endothelial cells is 12 pmol/mg-min at 0.3 nM TCDD. The rete
mirabile capillary endothelial cells responded minimally or not at all to exposure to
TCDD and βNF. Both the heart and kidney endothelial cells (but not the rete mirabile
capillary cells) have a low level of EROD activity (12.7 and 5.2 pmol/mg-min
respectively) in untreated or DMSO-treated cells. The robust response of the heart
endothelial cells to induction and the lack of response in the rete mirabile capillary
endothelial cells indicate that these cells are a good resource to use to investigate the
physiological consequences of AhR agonist exposure and CYP1A induction in different
areas of the vasculature.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