Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants that can be responsible for a variety of deleterious effects on organisms. These adverse outcomes are relatively well studied, but at concentrations rarely found in the environment. Among the documented effects of sublethal acute PAH exposure are reductions in osmoregulatory capacity and immune function, and changes in the function of critical metabolic organs such as the liver. Gulf toadfish (Opsanus beta) were exposed to control seawater (0.006 µg tPAH₅₀/L) or water accommodated fractions of Deepwater Horizon spill oil diluted to 3 flow‐through exposure regimes (0.009, 0.059, and 2.82 µg tPAH₅₀/L) for 7 d, with a recovery period of equal duration. We hypothesized that these chronic exposures would induce the aryl hydrocarbon receptor (AhR)‐mediated pathways and result in significant impacts on markers of osmoregulatory, immune, and metabolic function. We further hypothesized that measurable reversal of these impacts would be observed during the recovery period. Our results indicate that activation of cytochrome P 450 (CYP)1A1 was achieved during exposure and reversed during the recovery phase. The only significant deviations from controls measured were a reduction in plasma glucose in fish exposed to medium and high levels of PAH after 7 d of exposure and a reduction in plasma osmolality fish exposed to high levels of PAHs after 7 d of recovery, when CYP1A1 messenger (m)RNA levels had returned to control levels. Our study illustrates a disconnect between the activation of CYP1A1 in response to environmentally realistic PAHs concentrations and several physiological endpoints and supports the idea that the AhR might not be associated with mediating osmoregulatory, immune, and metabolic changes in Gulf toadfish. Environ Toxicol Chem 2021;40:1075–1086. © 2020 SETAC

中文翻译：

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海湾蟾鱼（Opsanus beta）在风化的深水地平线浮油中的暴露和恢复：对肝脏和血液终点的影响

多环芳烃 (PAH) 是无处不在的污染物，可对生物产生多种有害影响。这些不利结果得到了相对深入的研究，但在环境中很少发现浓度。亚致死性急性多环芳烃暴露的记录影响包括渗透压调节能力和免疫功能的降低，以及肝脏等关键代谢器官的功能变化。海湾蟾鱼（Opsanus测试）暴露于控制海水（0.006微克TPAH ₅₀ / L）或的容水组分深水地平线溢油稀释至3流通接触途径（0.009，0.059，和2.82微克TPAH ₅₀/L) 7 d，恢复期相同。我们假设这些慢性暴露会诱导芳烃受体 (AhR) 介导的通路，并对渗透调节、免疫和代谢功能的标志物产生重大影响。我们进一步假设在恢复期间会观察到这些影响的可衡量逆转。我们的结果表明，细胞色素 P 450 (CYP)1A1 的激活在暴露期间实现，并在恢复阶段逆转。与对照测量的唯一显着偏差是暴露于中等和高水平 PAH 后 7 天的鱼的血浆葡萄糖降低，以及恢复 7 天后暴露于高水平 PAH 的鱼的血浆渗透压降低，当 CYP1A1 信使(m)RNA 水平已恢复到对照水平。环境毒理学化学2021；40：1075-1086。© 2020 SETAC