Potentiation of the vitellogenic response to 17alpha-ethinylestradiol by cortisol in the fathead minnow Pimephales promelas.
The effects of elevated plasma cortisol levels on vitellogenin (VTG) induction were examined in the fathead minnow (Pimephales promelas) in an attempt to evaluate the potential influence of stress on this commonly used biomarker of estrogenicity. Two separate experiments were conducted in which fish plasma cortisol was elevated to various levels for 14 d by noninvasive additions of cortisol to the aquaria water. Fathead minnows were exposed to either cortisol alone, 17alpha-ethinylestradiol (EE2) alone, or a combination of the two hormones, and plasma levels of VTG as well as liver expression of VTG mRNA were measured. Both experiments gave similar results, with an exposure to 4 ng/L of EE2 resulting in significantly greater levels of plasma VTG in the presence of, compared to that in absence of, cortisol, whereas exposure to cortisol alone at concentrations between 144 and 800 microg/L had no effect on plasma VTG levels. This potentiation of the EE2-induced vitellogenesis by cortisol was dose-dependent, with plasma VTG reaching 125, 167, and 295% of the values obtained with EE2 alone when 144, 360, and 800 microg/L of cortisol, respectively, were added to the water. Liver mRNA results were consistent with plasma VTG, although they generally were more variable. The present study demonstrates that cortisol does not independently induce vitellogenesis but can potentiate estrogen-induced VTG synthesis in fathead minnow. The implications of these findings for the use of VTG as a biomarker of estrogenicity are discussed.
Brodeur
Julie C
JC
Toxicology and Environmental Research and Consulting, Dow Chemical Company, 1803 Building, Midland, Michigan 48674, USA. julbrodeur@yahoo.ca
Woodburn
Kent B
KB
Klecka
Gary M
GM
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D003530:Cyprinidae; D004347:Drug Interactions; D004703:Endocrine System / Q000187:drug effects* / Q000378:metabolism; D006854:Hydrocortisone / Q000633:toxicity*; D008099:Liver / Q000378:metabolism; D019055:No-Observed-Adverse-Effect Level; D009641:Norethynodrel / Q000031:analogs & derivatives* / Q000633:toxicity; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013997:Time Factors; D014819:Vitellogenins / Q000378:metabolism
D015415:Biomarkers; D012333:RNA, Messenger; D014819:Vitellogenins; C002029:17alpha-ethynylestr-5(10)-ene-3alpha,17beta-diol; D009641:Norethynodrel; D006854:Hydrocortisone