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