You are here:
Evidence for Compensatory Responses at the Molecular, Biochemical, and Tissue Level in Fathead Minnows Exposed to Steroidogenesis Inhibitors
Citation:
VILLENEUVE, D. L., L. B. BLAKE, J. CAVALLIN, K. GREENE, K. M. JENSEN, M. D. KAHL, D. MARTINOVIC, N. MUELLER, R. D. JOHNSON, AND G. T. ANKLEY. Evidence for Compensatory Responses at the Molecular, Biochemical, and Tissue Level in Fathead Minnows Exposed to Steroidogenesis Inhibitors. Presented at 5th Annual Aquatic Toxicity Workshop, Saskatoon, SK, CANADA, October 05 - 08, 2008.
Impact/Purpose:
These studies provide insights into compensatory responses at multiple levels of biological organization that have relevance to both exposure assessment and predictive effects assessment.
Description:
In order to survive, organisms require a capacity to adapt to a wide variety of biotic and abiotic stressors, including chemicals of both natural and synthetic origin. Recent studies in our laboratory have provided evidence of compensatory responses to endocrine active chemicals that act by inhibiting one or more enzymes involved in steroid biosynthesis. Specifically, we conducted a series of experiments in which fathead minnows were exposed to either the aromatase inhibitor, fadrozole, or the fungicide, ketoconazole, for varying durations (24 h to 21 d). Endpoints including gonadal mRNA transcript abundance, ex vivo steroid production, plasma steroid and vitellogenin concentrations, gonad histology, and reproductive success (fecundity) were examined. After just 24 h of exposure, fadrozole caused concentration-dependent decreases in both ex vivo estradiol (E2) production and plasma E2 concentrations in exposed females. However, by 8 d E2 concentrations had recovered to control levels. This recovery coincided with increased transcription of mRNAs coding for aromatase, P450 cholesterol side chain cleavage, and steroidogenic acute regulatory protein. Similarly, while exposure to ketoconazole reduced the rate of steroid production by fathead minnow testis tissue, it also elicited an overall increase in testis size relative to body mass and proliferation of the steroid producing interstitial cells, which appeared to offset the direct effect of the chemical. These studies provide insights into compensatory responses at multiple levels of biological organization that have relevance to both exposure assessment and predictive effects assessment.