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ToxSci Advance Access originally published online on May 16, 2006
Toxicological Sciences 2006 92(2):537-544; doi:10.1093/toxsci/kfl015
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Effects of 4-n-Nonylphenol and Tamoxifen on Salmon Gonadotropin-Releasing Hormone, Estrogen Receptor, and Vitellogenin Gene Expression in Juvenile Rainbow Trout

Angelique Vetillard*,1 and Thierry Bailhache{dagger}

* MRC Toxicology Unit, University of Leicester, Leicester LE1 9HN, United Kingdom; and {dagger} Endocrinologie Moléculaire de la Reproduction, UMR-CNRS 6026, Université de Rennes 1, Campus de Beaulieu, 35042 Rennes Cedex, France

Received March 12, 2006; accepted May 8, 2006

Alkylphenols such as nonylphenol (NP) are one of a wide variety of environmental chemicals reported to have estrogenic effects in both in vitro and in vivo studies. Induction of hepatic vitellogenin (Vg) gene expression is widely used as a biomarker for xenoestrogen exposure in fish. However, little work has been done to characterize the molecular effects of xenoestrogens on other potential target organs such as the brain. To evaluate brain and liver effects of 4-n-nonylphenol (4-NP), juvenile rainbow trout (Oncorhynchus mykiss) were exposed to waterborne 4-NP or 17ß-estradiol (E2). Changes in mRNA levels of salmon gonadotropin-releasing hormone (sGnRH) and estrogen receptor {alpha} (ER{alpha}) isoforms in the brain and ER{alpha} isoforms and Vg in the liver were measured after 3 and 6 days of exposure, with the help of a relative RT-PCR–based quantification method. Fish were treated with increasing doses of 4-NP ranging from 0.01 to 10µM (2.2 µg/l to 2.2 mg/l), and results were compared to the effect of E2 or tamoxifen, a specific ER modulator. In liver, E2 and the highest doses of 4-NP increased Vg and ER{alpha} long-isoform mRNA levels within 3 or 6 days of exposure, but 4-NP did not have any effect on ER{alpha} short-isoform transcription level. In the brain, 4-NP reduced sGnRH2 gene expression in a dose-dependent manner, but did not modify sGnRH1 or ER{alpha} mRNA levels.

Key Words: alkylphenol; endocrine disrupter; estrogen receptor; gonadotropin-releasing hormone; Oncorhynchus mykiss.


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A. D. Benninghoff and D. E. Williams
Identification of a Transcriptional Fingerprint of Estrogen Exposure in Rainbow Trout Liver
Toxicol. Sci., January 1, 2008; 101(1): 65 - 80.
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