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Matthew Alloy

Effects of Polycyclic Aromatic Hydrocarbon Exposure on Gulf Toadfish (Opsanus beta) and Resiliency to Co-Stressors
Poster Presenter #1
Postdoctoral Fellow in Ecotoxicology
Polycyclic aromatic hydrocarbons (PAHs) are a ubiquitous class of contaminants associated with natural geologic petroleum deposits, and pyrogenic origins Because of widespread atmospheric deposition, urban runoff, and very intensive release, such as during the Deepwater Horizon (DWH) oil spill, PAHs are an important class of contaminants.

Exposure to PAHs can be a stressor to fish; however, the response at the level of the hypothalamic-pituitary-interrenal (HPI) axis is complex. If a stress response is induced by PAH exposure, which initiates a greater production of glucocorticoids, a suite of responses follows. Two such responses examined in this work are carbohydrate metabolism and immune cell mobilization. Glucocorticoids often increase gluconeogenesis. Greater glycogen breakdown in fish has been associated with poorer body condition factors. We hypothesize that stress associated with PAH exposure will favor carbohydrate metabolism, resulting in increased gluconeogenesis, increased plasma glucose, and decreased condition factors relative to controls. There is a growing weight of data in the literature that chronic exposure to PAHs may interfere with the vertebrate immune response. This would reduce an organism’s ability to cope with parasites, wounds, and opportunistic infections, all of which may reduce survival and fitness. We hypothesize that metabolic and immune changes induced by PAH exposure will be exacerbated by additional stressors such as a simulated predator pursuit.

This investigation exposed Gulf toadfish (Opsanus beta) to relatively low concentrations of PAHs (>10 µg total PAHs/L) for 7 d, followed by a depuration period of equal length. O. beta tissues were sampled at several timepoints during exposure, and parallel timepoints during depuration. Metabolic change was measured as body condition factor, and hepatosomatic index. Immune response was assessed as immune cell counts. Exposure was assessed by mRNA expression of CYP1A, a gene associated with metabolic response to PAHs. Over the timecourse of the present study there were no statistically significant differences between control and exposures in body condition factor, hepatosomatic index, blood glucose, or blood cell counts (p>0.05). However, CYP1A expression was significantly upregulated in the highest treatment (p<0.01), and expression faded during the depuration period (p=0.10).