There is evidence that the combination of polycyclic aromatic hydrocarbons (PAHs) released in the Deepwater Horizon oil spill impairs the glucocorticoid stress response of vertebrates in the Gulf of Mexico, but the mechanisms are unclear. We hypothesized that inhibition of cortisol release may be due to 1) overstimulation of the hypothalamic–pituitary–inter‐renal (HPI) axis, or 2) an inhibition of cortisol biosynthesis through PAH activation of the aryl hydrocarbon receptor (AhR). Using a flow‐through system, Gulf toadfish (Opsanus beta) were continuously exposed to control conditions or one of 3 environmentally relevant concentrations of PAHs from Deepwater Horizon oil (∑PAH₅₀ = 0–3 μg L^–1) for up to 7 d. One group of toadfish was then exposed to a recovery period for up to 7 d. No changes in corticotrophin‐releasing factor mRNA expression, adrenocorticotropic hormone (ACTH), or pituitary mass suggested that overstimulation of the HPI axis was not a factor. The AhR activation was measured by an elevation of cytochrome P4501A1 (CYP1A) mRNA expression within the HPI axis in fish exposed to high PAH concentrations; however, CYP1A was no longer induced after 3 d of recovery in any of the tissues. At 7 d of recovery, there was an impairment of cortisol release in response to an additional simulated predator chase that does not appear to be due to changes in the mRNA expression of the kidney steroidogenic pathway proteins steroidogenic acute regulatory protein, cytochrome P450 side chain cleavage, and 11β‐hydroxylase. Future analyses are needed to determine whether the stress response impairment is due to cholesterol availability and/or down‐regulation of the melanocortin 2 receptor. Environ Toxicol Chem 2021;40:1062–1074. © 2020 SETAC

中文翻译：

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从深水地平线油中环境相关水平的水性多环芳烃的暴露和回收：对海湾蟾鱼应力轴的影响

有证据表明，深水地平线漏油事件中释放的多环芳烃（PAHs）的组合损害了墨西哥湾脊椎动物的糖皮质激素应激反应，但机制尚不清楚。我们假设皮质醇释放的抑制可能是由于 1) 下丘脑-垂体-肾间 (HPI) 轴的过度刺激，或 2) 通过芳烃受体 (AhR) 的 PAH 激活抑制皮质醇生物合成。使用流通系统，墨西哥湾蟾蜍 ( Opsanus beta ) 持续暴露于控制条件或来自深水地平线油 (∑PAH ₅₀  = 0–3 μg L ^–1) 长达 7 天。然后将一组蟾鱼暴露于长达 7 天的恢复期。促肾上腺皮质激素释放因子 mRNA 表达、促肾上腺皮质激素 (ACTH) 或垂体质量没有变化表明 HPI 轴的过度刺激不是一个因素。AhR 激活是通过暴露于高浓度 PAH 的鱼中 HPI 轴内细胞色素 P4501A1 (CYP1A) mRNA 表达的升高来衡量的；然而，在任何组织中恢复 3 天后 CYP1A 不再被诱导。在恢复的第 7 天，皮质醇释放受到损害，以响应额外的模拟捕食者追逐，这似乎不是由于肾脏类固醇生成途径蛋白类固醇生成急性调节蛋白、细胞色素 P450 侧链裂解的 mRNA 表达的变化, 和 11 β-羟化酶。需要进一步分析来确定应激反应损害是否是由于胆固醇可用性和/或黑皮质素 2 受体的下调。环境毒理学化学2021；40：1062-1074。© 2020 SETAC