ToxSci Advance Access published online on May 21, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfm124
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Published by Oxford University Press 2007.
Transcription of key genes regulating gonadal steroiodogenesis in control and ketoconazole- or vinclozolin-exposed fathead minnows.
U.S. Environmental Protection Agency, ORD, NHEERL, Mid-Continent Ecology Division, 6201 Congdon Blvd, Duluth, MN, USA, 55804
U.S. Environmental Protection Agency, ORD, NERL, Ecological Exposure Research Division, 25 W Martin Luther King Dr., Cincinnati, OH, USA, 45268
Pacific Northwest National Laboratory, P.O. Box 999, MSID K3-61, Richland, WA, USA, 99352
* Corresponding author Corresponding author address: same as listed above, e-mail: villeneuve.dan{at}epa.gov, telephone: 218-529-5217, fax: 218-529-5003
Received April 12, 2007; revision received May 3, 2007; accepted May 4, 2007
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Abstract |
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This study evaluated changes in the expression of steroidogenesis-related genes in male fathead minnows exposed to ketoconazole (KTC) or vinclozolin (VZ) for 21 d. The aim was to evaluate links between molecular changes and higher level outcomes after exposure to endocrine-active chemicals (EACs) with different modes of action. To aid our analysis and interpretation of EAC-related effects, we first examined variation in the relative abundance of steroidogenesis-related gene transcripts in the gonads of male and female fathead minnows as a function of age, gonad development, and spawning status, independent of EAC exposure. Gonadal expression of several genes varied with age and/or gonadal somatic index in either male or females. However, with the exception of aromatase, steroidogenesis-related gene expression did not vary with spawning status. Following the baseline experiments, expression of the selected genes in male fathead minnows exposed to KTC or VZ was evaluated in the context of effects observed at higher levels of organization. Exposure to KTC elicited changes in gene transcription that were consistent with an apparent compensatory response to the chemical's anticipated direct inhibition of steroidogenic enzyme activity. Exposure to VZ, an anti-androgen expected to indirectly impact steroidogenesis, increased pituitary expression of follicle-stimulating hormone ß-subunit and testis 20ßHSD transcript levels, but decreased luteinizing hormone receptor expression. Results of this study contribute to ongoing research aimed at understanding responses of the teleost hypothalamic-pituitary-gonadal axis to different types of EACs and how changes in molecular endpoints translate into apical outcomes reflective of either adverse effect or compensation.
Key Words: steroidogenesis inhibitor; anti-androgen; reproduction; gonad development; real-time PCR; testis.
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