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The aryl hydrocarbon receptor (AhR) pathway mediates many, if not all, responses of fish to dioxin-like compounds. The Southern Ocean is progressively exposed to increasing concentrations of anthropogenic pollutants. Antarctic fish are known to accumulate those pollutants, yet nothing is known about their capability to induce chemical biotransformation via the AhR pathway. The objective of the present study was to investigate whether Antarctic eelpout, Pachycara brachycephalum, respond to anthropogenic pollutants by activation of the AhR and its target gene cytochrome P4501A (CYP1A), and of superoxide dismutase (SOD), which served as a representative for oxidative stress. We exposed P. brachycephalum to 10 and 100 mg benzo[a]pyrene (BaP)/kg body weight for 10 d and measured the expression of AhR, CYP1A, and SOD in liver tissue via quantitative polymerase chain reaction. We identified two distinct AhR isoforms in the liver of P. brachycephalum. Antarctic eelpout responded to both BaP exposures by an up-regulation of AhR and SOD, and by a particularly strong induction of CYP1A expression, which remained high until day 10 of the exposure time. Our data suggest that P. brachycephalum possesses the potential to up-regulate xenobiotic biotransformation pathways, at least at the gene expression level. The time course of the AhR and CYP1A response points to an efficient but slow xenobiotics metabolism. Moreover, BaP exposure could include adverse effects such as oxidative stress. Environ Toxicol Chem 2018;37:1487-1495. © 2018 SETAC., (© 2018 SETAC.)

To examine the behavior of the estrogenic biomarker vitellogenin (VTG) under the combined impact of estrogens and pathogens, parasite-infected or noninfected rainbow trout were exposed to two doses of 17β-estradiol (E2). Infected and E2-exposed fish showed significantly lower hepatic VTG mRNA levels than healthy fish. Transcriptome data suggest that this was due to energetic constraints. Reduced responsiveness of the VTG biomarker in parasitized fish might obscure detection of low-level field exposure., (Copyright © 2012 SETAC.)

Sewage treatment works (STW) discharge estrogenic effluent into rivers, which leads to variable estrogenicity of river water. Here, we characterize how the factors effluent and hydrology influence the estrogenicity of river water. We selected a river for which good hydrological data are available and collected water samples upstream and downstream from a STW discharge; effluent was sampled as well. Sampling took place during four 12-d periods, associated with the seasons, and always occurred in the morning. We also investigated the estrogenicity along the river, both by grab sampling and by passive sampling. Estrogens were analyzed by a recombinant yeast assay (YES); the estrogenicity of a sample was equated to the 17beta-estradiol standard of the YES (ng/L). Estrogenicity upstream from the STW was mostly close to the detection limit of the YES (maximum, 0.4 ng/L). Estrogenicity of effluent ranged between 0.2 and 7.7 ng/L; lower estrogenicity was associated with higher hydraulic retention times. Downstream from the STW, estrogenicity exceeded 1 ng/L on 25% of the days (maximum, 2.1 ng/L). Measured river water estrogenicity correlated positively and significantly with predicted estrogenicity based on effluent estrogenicity and effluent dilution factor. Grab samples taken along the river indicate that no significant sources of estrogens were upstream from the STW; downstream from the STW, the pattern of estrogenicity was highly variable. However, passive sampling showed that the estrogenicity of river water downstream from the STW decreased continuously with increasing distance from the STW, which is largely explained by dilution.

This field study examined the vitellogenin (VTG) biomarker response under conditions of low and fluctuating activities of environmental estrogenicity. The present study was performed on immature brown trout (Salmo trutta) exposed to the small river Luetzelmurg, which is located in the prealpine Swiss midland region and receives effluents from a single sewage treatment plant (STP). To understand better factors influencing the relationship between estrogenic exposure and VTG induction, we compared VTG levels in caged (stationary) and feral (free-ranging) fish, VTG levels in fish from up- and downstream of the STP, and two different methods for quantifying VTG (enzyme-linked immunosorbent assay vs real-time reverse transcription-polymerase chain reaction), and we used passive samplers (polar organic chemical integrative sampler [POCIS]) to integrate the variable, bioaccumulative estrogenic load in the river water over time. The POCIS from the downstream site contained approximately 20-fold higher levels of bioassay-derived estrogen equivalents than the POCIS from the upstream site. In feral fish, this site difference in estrogenic exposure was reflected in VTG protein levels but not in VTG mRNA. In contrast, in caged fish, the site difference was evident only for VTG mRNA but not for VTG protein. Thus, the outcome of VTG biomarker measurements varied with the analytical detection method (protein vs mRNA) and with the exposure modus (caged vs feral). Our findings suggest that for environmental situations with low and variable estrogenic contamination, a multiple-assessment approach may be necessary for the assessment of estrogenic exposure in fish.

In our study, we aim to characterize the estrogenicity of 18 independent rivers that receive effluent from sewage treatment works. During the winter and summer of 2003, we collected multiple water samples and measured environmental estrogens with an in vitro yeast-based reporter gene assay; estrogenicity was expressed as ng 17beta-estradiol equivalents (EEQ) per L of water. Estradiol equivalents values in winter ranged from 0.3 to 2.0 ng/L and, in summer, from 0.4 to 7.0 ng/L. Winter and summer EEQ values were not correlated with each other or with the dilution factor of the effluent in the river. Variation in EEQ values was large and correlated from winter to summer. Part of this variation in estrogenicity is explained by water flow rates; variation is larger at reduced flow rates. We measured plasma vitellogenin concentrations in immature male brown trout. At five sites, vitellogenin concentrations exceeded 1 microg/ml; however, at the majority of the sites, plasma vitellogenin concentrations were below 0.5 microg/ml. Our data indicate that the exposure of brown trout to environmental estrogens in Swiss midland rivers is low. However, some sites show reoccurring higher EEQ values and, at some sites, plasma vitellogenin concentrations in male fish clearly are elevated.

To assess the importance of sewage treatment plant effluents on fish health, we studied gudgeon in two rivers in the Swiss midlands (Canton Lucerne). Both rivers receive pollution from diffuse sources, while one also receives the effluent of a sewage treatment plant. Male and female gudgeon during and outside of the spawning season were compared with respect to reproductive parameters and health status across both rivers as well as upstream and downstream of the STP. Several biomarkers were studied, including cytochrome P4501A, 7-ethoxyresorufin-O-deethylase, plasma vitellogenin, ovotestis, lipid, liver histology, condition factor, gonadosomatic index, splenosomatic index, parasites of spleen and liver, population structure, and species diversity. Gudgeons of both rivers exhibited signs of a moderately impaired health status. By a stepwise backward analysis, the cytochrome P4501A content, the splenosomatic index, and the incidence of parasites in the liver were found to provide the best discrimination of the three sampling sites. Evidence of a significant elevation in response to the sewage treatment plant effluent was found neither in vitellogenin concentration nor in the ovotestis rate. While population structure was analyzed upstream and downstream of the sewage treatment plant, only gudgeons of the latter site revealed a disturbed population structure, most probably caused by a former nitrite discharge.