Cytochrome P4501A induced differentially in endothelial cells cultured from different organs of Anguilia rostrata |
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Authors: | Rita Anne Garrick Bruce R Woodin John J Stegeman |
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Institution: | (1) Department of Natural Sciences, Fordham University, 113 W. 60th Street, 10023 New York, New York;(2) Department of Biology, Woods Hole Oceanographic Institution, 02543 Woods Hole, Massachusetts |
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Abstract: | Summary Endothelial cells are a structural barrier and an active regulator of many bodily processes. Cytochrome P4501A (CYPIA) 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 aryl hydrocarbon receptor (AhR) agonists. In heart endothelial cells, the maximum response (based on O-deethylation of
7-ethoxyresorufin to resorufin EROD] activity) to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 113 pmol/mg/min, was at 1 nM TCDD and the peak response to β-napthoflavone (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 dimethylsulfoxide-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. |
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Keywords: | teleost eel fish microvasculature endothelium pHAH cytochrome P450 EROD dioxin CYPIA |
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