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Exposure to oiled sediments can negatively impact the health of fish species. Here, we examine the effects of chronic exposure of juvenile southern flounder, Paralichthys lethostigma, to a sediment-oil mixture. Oil:sediment mixtures are persistent over time and can become bioavailable following sediment perturbation or resuspension. Juvenile flounder were exposed for 32 days under controlled laboratory conditions to five concentrations of naturally weathered Macondo MC252 oil mixed into uncontaminated, field-collected sediments. The percent composition of individual polycyclic aromatic hydrocarbons (PAHs) of the weathered oil did not change after mixing with the sediment. Spiked exposure sediments contained 0.04-395mg/kg tPAH50 (sum of 50 individual PAH concentration measurements). Mortality increased with both exposure duration and concentration of sediment-associated PAHs, and flounder exposed to concentrations above 8mg/kg tPAH50 showed significantly reduced growth over the course of the experiment. Evident histopathologic changes were observed in liver and gill tissues of fish exposed to more than 8mg/kg tPAH50. All fish at these concentrations showed hepatic intravascular congestion, macrovesicular hepatic vacoulation, telangiectasia of secondary lamellae, and lamellar epithelial proliferation in gill tissues. Dose-dependent upregulation of Cyp1a expression in liver tissues was observed. Taxonomic analysis of gill and intestinal commensal bacterial assemblages showed that exposure to oiled sediments led to distinct shifts in commensal bacterial population structures. These data show that chronic exposure to environmentally-relevant concentrations of oiled sediments produces adverse effects in flounder at multiple biological levels., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Estrogens and estrogen mimics are aquatic contaminants that can elicit a variety of deleterious effects in exposed fauna. One of the most potent xenoestrogens found in the aquatic environment is 17α-ethinylestradiol (EE(2)), the pharmaceutically derived semi-synthetic hormone found in oral contraceptives and hormone replacement therapies. Exposure to 100 ng/L EE(2) has previously been shown to profoundly decrease functional hepatic nucleotide excision repair (NER) processes in adult zebrafish in correlation with dramatic decreases in the abundance of hepatic XPC and XPA transcripts; however, its effects on these processes in embryos are currently unknown. Because developing organisms are known to have increased sensitivities to endocrine disrupting compounds such as EE(2), the goal of this study was to examine the impacts of estrogen exposure on mRNA expression of these two key NER genes in zebrafish embryos during the first 4 days of development. Embryos were exposed from 0 h post fertilization (hpf) to waterborne EE(2), its major metabolite, estrone (E(1)), or combinations of the two compounds and sampled at 12, 24, 48, 72 and 96 hpf. Increased abundance of vitellogenin-1 (VTG1) mRNA, a bioindicator of estrogen exposure, was evident as early as 24 hpf in embryos that were co-exposed to EE(2) and E(1) and this effect was sustained throughout 96 hpf. Embryos exposed to EE(2) alone exhibited elevated VTG1 beginning at 72 hpf. In contrast to observations from adult zebrafish exposed to EE(2), embryos did not show any change in mRNA abundance of the excision repair gene, XPC, during the first 4 days of development. However, co-exposure to EE(2) and E(1) elicited an increase in XPA mRNA abundance at 48 and 72 hpf, which was the opposite response as that observed in exposed adults where hepatic XPA mRNA abundance decreased after EE(2) exposure. These differences between embryos and adults suggest that alteration of NER gene transcription by EE(2) is operating under different stimuli during development., (Copyright © 2013 Elsevier Inc. All rights reserved.)