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¹ Department of Pharmacology and Therapeutics,² Department of Physiological Sciences,³ Center of Environmental and Human Toxicology,⁴ Analytical Toxicology Core Laboratory,⁵ Department of Biochemistry and Molecular Biology and ⁶ Department of Pathology,, Immunology and Laboratory Medicine, University of Florida, PO Box 110885, Gainesville, Florida 32611, USA ⁷ Department of Environmental Health Sciences,, University of South Carolina, Columbia, South Carolina, USA ⁸ Enviro-Test Laboratories,, Edmonton, Alberta, Canada

(Correspondence should be addressed to N D Denslow; Email: ndenslow{at}ufl.edu)

These studies were supported by the Superfund Basic Research Program from the National Institute of Environmental Health Sciences, P42 ES 07375 and NIEHS RO1 ES015449 to ND and NIH grant GM25154 to RM for salary support of ZF. The authors declare no conflict of interest.

T Sabo-Attwood and J L Blum contributed equally to this work

The estrogen receptor (ER) signaling cascade is a vulnerable target of exposure to environmental xenoestrogens, like nonylphenol (NP), which are causally associated with impaired health status. However, the impact of xenoestrogens on the individual receptor isotypes (, ßa, and ßb) is not well understood. The goal of these studies was to determine the impact of NP on largemouth bass (Micropterus salmoides) ER isotype expression and activity. Here, we show that hepatic expression levels of three receptors are not equivalent in male largemouth bass exposed to NP by injection. Transcript levels of the ER subtype were predominantly induced in concert with vitellogenin similarly to fish exposed to 17ß-estradiol (E₂) as measured by quantitative real-time PCR. NP also induced circulating plasma levels of estrogen, which may contribute to overall activation of the ERs. To measure the activation of each receptor isotype by E₂ and NP, we employed reporter assays using an estrogen response element (ERE)–luciferase construct. Results from these studies show that ER had the greatest activity following exposure to E₂ and NP. This activity was inhibited by the antagonists ICI 182 780 and ZM 189 154. Furthermore, both ßb and ßa subtypes depressed ER activation, suggesting that the cellular composition of receptor isotypes may contribute to the overall actions of estrogen and estrogenic contaminants via the receptors. Results from these studies collectively reveal the differential response of fish ER isotypes in response to xenoestrogens.