Effects of 17alpha-ethynylestradiol on early-life development, sex differentiation and vitellogenin induction in mummichog (Fundulus heteroclitus).

Department of Biology and Canadian Rivers Institute, University of New Brunswick, Saint John, NB, Canada.
Marine environmental research (Impact Factor: 2.34). 10/2009; 69(3):178-86. DOI: 10.1016/j.marenvres.2009.10.002
Source: PubMed

ABSTRACT Fertilized mummichog eggs retrieved from 17alpha-ethynylestradiol (EE(2)) exposed adult fish were raised in concentrations of EE(2) ranging from 0 to 100 ng/L (100 ng/L EE(2) estimated to have actual average exposure concentrations of 30% of nominal; 0.1-10 ng/L were below detect throughout 24-h exposure period) for 61 weeks post-hatch. Eggs exposed at 100 ng/L hatched sooner, the larvae were longer, and survival of juvenile fish from hatch to study termination was greater than all other treatments, though fewer hatched at this treatment. Sex ratios were skewed (>80% female phenotype) at 100 ng/L EE(2), and some gonadal male fish displayed female secondary sex characteristics. Condition factor, gonadosomatic index (GSI), and liver somatic index (LSI) were found to decrease in both sexes between 52 and 61 weeks post-hatch. Female fish had increased hepatic vitellogenin (VTG) at 52 weeks post-hatch. When exposed to 1, 10 and 100 ng/L EE(2), female fish had a higher proportion of vitellogenic follicles in the ovarian tissue. Males exposed at 100 ng/L may have had disruption at some endpoints (GSI, VTG) that is masked due to reduced sample size compared to other treatments. Fish exposed to concentrations of EE(2) at or below 10 ng/L showed inconsistent effects on development and reproductive potential. This study indicates the potential for population-level effects at the high range of environmental EE(2) at concentrations equivalent to those at which consistent effects in fecundity in the adult mummichog reproductive test have been measured. This work demonstrates that chronic EE(2) exposure causes developmental effects at concentrations similar to those which cause effects in the shorter-term adult mummichog reproductive test. Effects are at higher concentrations than have been noted for freshwater model species. Whether this is because of species sensitivity or due to differences between freshwater and saltwater availability of EE(2) or its uptake requires further study.

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    ABSTRACT: Exposure to 17α-ethinylestradiol (EE2), a synthetic estrogen, has previously been shown to decrease reproductive endocrine status and egg production in northern mummichog (Fundulus heteroclitus macrolepidotus). The objective of this study was to evaluate if variations in salinity or temperature conditions of EE2-exposed mummichog modify the effect on whole organism reproductive endocrine status and gonadal steroidogenesis. Mummichog were exposed in vivo for 14 days to 0, 50 and 250ng/L EE2 in 0, 16 and 32ppt salinity at 18°C and to 0 and 250ng/L EE2 at 10, 18 and 26°C at 16ppt. There was a little overall effect of salinity on measured endpoints. In the salinity exposure, 250ng/L EE2-exposed females had significantly reduced 17β-estradiol (E2) levels. Increased temperature triggered gonadal growth in both sexes and increased plasma E2 and E2 production and decreased 11-KT (11-ketotestosterone) production. EE2 counteracted the effect of temperature by depressing gonadal growth in males. In both exposures, EE2 effects on testosterone (T) production were variable. The use of steroidogenic precursors (25-OH-cholesterol, and/or pregnenolone and/or testosterone) in the in vitro gonadal incubations indicated decreased E2 production in females and 11-KT production in males were predominately due to suppression of the terminal conversion step between T and E2 or 11-KT. Ovarian aromatase A (cyp19a) gene expression at 16ppt and 18°C was not affected by 250ng/L EE2 (the only treatment combinations tested). Overall, temperature is a factor regulating northern mummichog reproduction; EE2 overrides its effects and disrupts the terminal step of steroidogenesis. Our results should be considered in designing future estuarine fish bioassays and in understanding effects of estrogenic endocrine disruptors in estuaries.
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    ABSTRACT: The synthetic estrogen 17α-ethynylestradiol (EE2), an endocrine disruptor originating from birth control and hormone replacement therapy, is discharged in wastewater treatment plant (WWTP) effluents. The present study employed radio-labeled EE2 to examine the impact of temperature and salinity on the uptake of EE2 in male killifish (Fundulus heteroclitus), a model euryhaline teleost. Fish were exposed to a nominal concentration of 100 ng/L EE2 for 2 h. Actual concentrations were lower due to EE2 adsorption to the exposure system, but uptake rates were normalized to 100 ng/L. Oxygen consumption rates (MO2), whole body EE2 uptake rates, and tissue-specific EE2 distribution were monitored. EE2 uptake by freshly killed fish was negligible. In killifish acclimated to 18OC at 16 ppt (50 % seawater), MO2 and EE2 uptake were both much lower after 24-h exposure to 10OC and 4OC, and increased after 24-h exposure to 26OC. Transfer of killifish to fresh water for 24 h tended to lower EE2 uptake rate, and long-term acclimation to fresh water reduced it by about 70 %. Long-term acclimation to 100 % sea water (32 ppt) also reduced EE2 uptake rate by about 50 % relative to 16 ppt. However this was not seen in juvenile rainbow trout (Oncorhynchus mykiss) where uptake rates were the same in FW- and 16 ppt-acclimated trout. The tissue-specific accumulation of EE2 was found to be the highest (40-60 % of the total) in the liver plus gall bladder across all exposures, and the great majority of this was in the bile in killifish, regardless of temperature or salinity, whereas in trout accumulation was the highest in the carcass at 70 % of the total. The carcass was the next highest accumulator (30-40 %) in killifish, followed by the gut (10-20 %) with only small amounts in gills and spleen. Drinking rate, measured with radio-labeled polyethylene glycol-4000, was about 25-times greater in 16 ppt-acclimated killifish relative to freshwater-acclimated animals. However, drinking accounted for less than 30 % of gut accumulation, and therefore a negligible percentage of whole body EE2 uptake rates. In general, there were strong positive relationships between EE2 uptake rates and MO2, suggesting similar pathways for uptake across the gills of these lipophilic molecules. These data will be useful in developing a predictive model of how variations in key environmental parameters (salinity, temperature, dissolved oxygen) affect EE2 uptake in estuarine fish, so as to determine optimal timing and location of WWTP discharges.
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    ABSTRACT: 17α-ethynylestradiol (EE2) is a synthetic hormone, which is a derivative of the natural hormone, estradiol (E2). EE2 is an orally bio-active estrogen, and is one of the most commonly used medications for humans as well as livestock and aquaculture activity. EE2 has become a widespread problem in the environment due to its high resistance to the process of degradation and its tendency to (i) absorb organic matter, (ii) accumulate in sediment and (iii) concentrate in biota. Numerous studies have reported the ability of EE2 to alter sex determination, delay sexual maturity, and decrease the secondary sexual characteristics of exposed organisms even at a low concentration (ng/L) by mimicking its natural analogue, 17β-estradiol (E2). Thus, the aim of this review is to provide an overview of the science regarding EE2, the concentration levels in the environment (water, sediment and biota) and summarize the effects of this compound on exposed biota at various concentrations, stage life, sex, and species. The challenges in respect of EE2 include the extension of the limited database on the EE2 pollution profile in the environment, its fate and transport mechanism, as well as the exposure level of EE2 for better prediction and definition revision of EE2 toxicity end points, notably for the purpose of environmental risk assessment.
    Environment international 05/2014; 69C:104-119. · 6.25 Impact Factor

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