BackgroundEndocrine disrupting chemicals (e.g., estrogens, androgens and their mimics) are known to affect reproduction in fish. 17α-ethynylestradiol is a synthetic estrogen used in birth control pills. 17β-trenbolone is a relatively stable metabolite of trenbolone acetate, a synthetic androgen used as a growth promoter in livestock. Both 17α-ethynylestradiol and 17β-trenbolone have been found in the aquatic environment and affect fish reproduction. In this study, we developed a physiologically-based computational model for female fathead minnows (FHM, Pimephales promelas), a small fish species used in ecotoxicology, to simulate how estrogens (i.e., 17α-ethynylestradiol) or androgens (i.e., 17β-trenbolone) affect reproductive endpoints such as plasma concentrations of steroid hormones (e.g., 17β-estradiol and testosterone) and vitellogenin (a precursor to egg yolk proteins).ResultsUsing Markov Chain Monte Carlo simulations, the model was calibrated with data from unexposed, 17α-ethynylestradiol-exposed, and 17β-trenbolone-exposed FHMs. Four Markov chains were simulated, and the chains for each calibrated model parameter (26 in total) converged within 20,000 iterations. With the converged parameter values, we evaluated the model's predictive ability by simulating a variety of independent experimental data. The model predictions agreed with the experimental data well.ConclusionsThe physiologically-based computational model represents the hypothalamic-pituitary-gonadal axis in adult female FHM robustly. The model is useful to estimate how estrogens (e.g., 17α-ethynylestradiol) or androgens (e.g., 17β-trenbolone) affect plasma concentrations of 17β-estradiol, testosterone and vitellogenin, which are important determinants of fecundity in fish.

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24Assessment of stress from varied sources are usually evaluated on individuals derived from a 25 single population, and are assumed to represent all populations of that species. However, recent 26 research has identified intraspecies variations in the stress response, which may be mediated by 27 life history. We examined how life history can influence the physiological responses to an acute 28 stress event by evaluating sea lamprey (Petromyzon marinus) parasitism response in two lake 29 trout (Salvelinus namaycush) morphotypes-the lean and siscowet. The morphotypes differ such 30 that the lean grows faster, is more fecund, and has a shorter life span. In contrast the siscowet 31 grows slower, is older at maturity, and lives longer. Our study compared long-term parasitism 32 responses between wild leans and siscowets in Lake Superior and immediate responses in 33 laboratory parasitism trials using lake trout reared under common environmental conditions. 34Leans, but not siscowets, showed changes in steroid binding protein function, and weak evidence 35 of parasitism gigantism in response to parasitism. Both morphotypes showed indications of 36 reproductive endocrine alterations in response to parasitism. Our results demonstrate intraspecies 37 variation in physiological stressor response, which is mediated by life history differences that 38 could potentially have differential population implications. 39 40 41 42 43 44 45 46

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As part of the Environmental Monitoring and Assessment Program for Great River Ecosystems (EMAP-GRE), sediment samples were collected from 447 randomly selected littoral sites along the main channels of the Ohio, Missouri, and Upper Mississippi Rivers between 2004 and 2006. Toxicity of these sediment samples was measured using a 7-day Hyalella azteca survival and growth test. Sixty-five sites (14.5%) exhibited lethal toxicity, and 130 sites (29.1%) exhibited decreased growth. In the EMAP-GRE probabilistic sampling design, each sampled site had a weight associated with it that determined the length (and proportion) of the river represented by that sample point in the population. Weighted whole-river estimates indicated that of the 4721 river km sampled, sediment from 15.9 ± 3.0% of the river (752 ± 50 km) were lethally toxic, 27.4 ± 3.5% (1289 ± 57 km) were toxic by way of growth inhibition, and 40.0 ± 3.7% (1887 ± 68 km) exhibited either lethal or growth toxicity. Selected toxic samples were analyzed for 21 pesticides, 20 polychlorinated biphenyl congeners, and 6 polybrominated diphenyl ether congeners. For all of the samples tested, the concentration levels of these analytes were mostly lower than known toxicity thresholds, and neither unionized ammonia concentration nor osmotic stress (as measured by conductivity) could account for the toxicity found in sediments. The spatial pattern of sediment toxicity cannot be readily explained by urbanization or agricultural land use at the subcatchment scale. We speculate that the distribution of toxic sediment is more likely due to a combination of localized sources, including polluted tributaries, and the redistribution of contaminated sediments from upriver. The sediment toxicity results from this study will be used, in combination with other sediment, biologic, and habitat metrics and indicators collected in the EMAP-GRE study, to help interpret and assess the condition of the Ohio, Upper Mississippi, and Missouri Rivers.

The inclusion of sublethal behavioral effects in population models has predicted lower estimates of cohort abundance and survival. Methylmercury, a persistent contaminant in the Great Lakes, has been shown to alter foraging and predator avoidance behaviors of larval Yellow Perch Perca flavescens, which may have indirect effects on recruitment. Poor recruitment of Yellow Perch in Lake Michigan has been associated with changes in trophic structure and adverse habitat conditions, but the potential effects of contaminants have not been fully explored. To test this, we adapted existing larval fish individual-based models to incorporate laboratory-derived methylmercury behavioral impairments on a larval Yellow Perch cohort in Lake Michigan. Overall, swimming speed reductions following methylmercury exposure did not drastically affect cohort survival. In contrast, the impairment to prey capture success resulted in an additional 8, 45, and 28% starvation of the cohort in simulations with tissue concentrations of 0.21, 0.95, and 3.14 μg/g total mercury whole-embryo wet weight, respectively. While our experimental methylmercury concentrations were higher than those typically found in Lake Michigan, our findings suggest that contaminants could be an additional factor impacting recruitment of Yellow Perch in systems highly contaminated with mercury.

The purpose of this study was to evaluate the effects of environmentally relevant dietary MeHg exposures on adult female yellow perch (Perca flavescens) and female zebrafish (Danio rerio) ovarian development and reproduction. Yellow perch were used in the study for their socioeconomic and ecological importance within the Great Lakes basin, and the use of zebrafish allowed for a detailed analysis of the molecular effects of MeHg following a whole life-cycle exposure. Chronic whole life dietary exposure of F zebrafish to MeHg mimics realistic wildlife exposure scenarios, and the twenty-week adult yellow perch exposure (where whole life-cycle exposures are difficult) captures early seasonal ovarian development. For both species, target dietary accumulation values were achieved prior to analyses. In zebrafish, several genes involved in reproductive processes were shown to be dysregulated by RNA-sequencing and quantitative real-time polymerase chain reaction (QPCR), but no significant phenotypic changes were observed regarding ovarian staging, fecundity, or embryo mortality. Yellow perch were exposed to dietary MeHg for 12, 16, or 20 weeks. In this species, a set of eight genes were assessed by QPCR in the pituitary, liver, and ovary, and no exposure-related changes were observed. The lack of genomic resources in yellow perch hinders the characterization of subtle molecular impacts. The ovarian somatic index, circulating estradiol and testosterone, and ovarian staging were not significantly altered by MeHg exposure in yellow perch. These results suggest that environmentally relevant MeHg exposures do not drastically reduce the reproductively important endpoints in these fish, but to capture realistic exposure scenarios, whole life-cycle yellow perch exposures are needed.