Exposure and Recovery from Environmentally Relevant Levels of Waterborne Polycyclic Aromatic Hydrocarbons from Deepwater Horizon Oil: Effects on the Gulf Toadfish Stress Axis.

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 11ß-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.

Exposure and Recovery of the Gulf Toadfish (Opsanus beta) to Weathered Deepwater Horizon Slick Oil: Impacts on Liver and Blood Endpoints.

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.