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ToxSci Advance Access originally published online on September 6, 2007
Toxicological Sciences 2008 101(1):65-80; doi:10.1093/toxsci/kfm238
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© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Identification of a Transcriptional Fingerprint of Estrogen Exposure in Rainbow Trout Liver

Abby D. Benninghoff*,1 and David E. Williams*,{dagger}

* Department of Environmental and Molecular Toxicology, the Marine and Freshwater Biomedical Sciences Center and the Environmental Health Sciences Center, 1007 Agricultural and Life Sciences Building, Corvallis, Oregon 97331 {dagger} Linus Pauling Institute, Oregon State University, 571 Weniger Hall, Corvallis, Oregon 97331

1 To whom correspondence should be addressed at Department of Environmental and Molecular Toxicology, the Marine and Freshwater Biomedical Sciences Center and the Environmental Health Sciences Center, 1007 Agricultural and Life Sciences Building, Corvallis, Oregon 97331. Fax: (541) 737-7966. E-mail: benninga{at}science.oregonstate.edu.

Received July 12, 2007; accepted August 31, 2007


  Abstract

The goal of this study was to identify a set of hepatic genes regulated by ligand-dependent activation of the estrogen receptor in juvenile rainbow trout (Oncorhynchus mykiss). A custom rainbow trout oligo DNA microarray, which contains probes targeting approximately 1450 genes relevant to carcinogenesis, toxicology, endocrinology, and stress physiology was utilized to identify transcriptional fingerprints of in vivo dietary exposure to 17β-estradiol (E2), tamoxifen (TAM), estradiol + tamoxifen (E2 + TAM), diethylstilbestrol (DES), dehydroepiandrosterone (DHEA), dihydrotestosterone (DHT), and cortisol (CORT). Estrogen exposure altered the expression of up to 49 genes involved in reproduction, immune response, cell growth, transcriptional regulation, protein synthesis and modification, drug metabolism, redox regulation, and signal transduction. E2, DES, and DHEA regulated 18 genes in common, mostly those associated with vitellogenesis, cell proliferation, and signal transduction. Interestingly, DHEA uniquely regulated several complement component genes of importance to immune response. While the effect of TAM on E2-induced changes in gene expression was mostly antagonistic, TAM alone increased expression of VTG1 and other genes associated with egg development and immune response. Few genes responded to CORT treatment, and DHT significantly altered expression of only one gene targeted by the OSUrbt array. Hierarchical cluster and principal components analyses revealed distinct patterns of gene expression corresponding to estrogens and non-estrogens, though unique patterns could also be detected for individual chemicals. A set of estrogen-responsive genes has been identified that can serve as a biomarker of environmental exposure to xenoestrogens.

Key Words: estrogen; toxicogenomics; transcription profile; dehydroepiandrosterone; tamoxifen; genomics.


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