The Deepwater Horizon disaster released more than 636 million L of crude oil into the northern Gulf of Mexico. The spill oiled upper surface water spawning habitats for many commercially and ecologically important pelagic fish species. Consequently, the developing spawn (embryos and larvae) of tunas, swordfish, and other large predators were potentially exposed to crude oil-derived polycyclic aromatic hydrocarbons (PAHs). Fish embryos are generally very sensitive to PAH-induced cardiotoxicity, and adverse changes in heart physiology and morphology can cause both acute and delayed mortality. Cardiac function is particularly important for fast-swimming pelagic predators with high aerobic demand. Offspring for these species develop rapidly at relatively high temperatures, and their vulnerability to crude oil toxicity is unknown. We assessed the impacts of field-collected Deepwater Horizon (MC252) oil samples on embryos of three pelagic fish: bluefin tuna, yellowfin tuna, and an amberjack. We show that environmentally realistic exposures (1-15 μg/L total PAH) cause specific dosedependent defects in cardiac function in all three species, with circulatory disruption culminating in pericardial edema and other secondary malformations. Each species displayed an irregular atrial arrhythmia following oil exposure, indicating a highly conserved response to oil toxicity. A considerable portion of Gulf water samples collected during the spill had PAH concentrations exceeding toxicity thresholds observed here, indicating the potential for losses of pelagic fish larvae. Vulnerability assessments in other ocean habitats, including the Arctic, should focus on the developing heart of resident fish species as an exceptionally sensitive and consistent indicator of crude oil impacts.oil spill | damage assessment | heart development | embryology

The Deepwater Horizon incident likely resulted in exposure of commercially and ecologically important fish species to crude oil during the sensitive early life stages. We show that brief exposure of a water-accommodated fraction of oil from the spill to mahi-mahi as juveniles, or as embryos/larvae that were then raised for ∼25 days to juveniles, reduces their swimming performance. These physiological deficits, likely attributable to polycyclic aromatic hydrocarbons (PAHs), occurred at environmentally realistic exposure concentrations. Specifically, a 48 h exposure of 1.2 ± 0.6 μg L(-1) ΣPAHs (geometric mean ± SEM) to embryos/larvae that were then raised to juvenile stage or a 24 h exposure of 30 ± 7 μg L(-1) ΣPAHs (geometric mean ± SEM) directly to juveniles resulted in 37% and 22% decreases in critical swimming velocities (Ucrit), respectively. Oil-exposed larvae from the 48 h exposure showed a 4.5-fold increase in the incidence of pericardial and yolk sac edema relative to controls. However, this larval cardiotoxicity did not manifest in a reduced aerobic scope in the surviving juveniles. Instead, respirometric analyses point to a reduction in swimming efficiency as a potential alternative or contributing mechanism for the observed decreases in Ucrit.

No abstract

The Deepwater Horizon (DWH) oil spill contaminated the spawning habitats for numerous commercially and ecologically important fishes. Exposure to the water accommodated fraction (WAF) of oil from the spill has been shown to cause cardiac toxicity during early developmental stages across fishes. To better understand the molecular events and explore new pathways responsible for toxicity, RNA sequencing was performed in conjunction with physiological and morphological assessments to analyze the time-course (24, 48, and 96 h post fertilization (hpf)) of transcriptional and developmental responses in embryos/larvae of mahi-mahi exposed to WAF of weathered (slick) and source DWH oils. Slick oil exposure induced more pronounced changes in gene expression over time than source oil exposure. Predominant transcriptomic responses included alteration of EIF2 signaling, steroid biosynthesis, ribosome biogenesis and activation of the cytochrome P450 pathway. At 96 hpf, slick oil exposure resulted in significant perturbations in eye development and peripheral nervous system, suggesting novel targets in addition to the heart may be involved in the developmental toxicity of DHW oil. Comparisons of changes of cardiac genes with phenotypic responses were consistent with reduced heart rate and increased pericardial edema in larvae exposed to slick oil but not source oil.

Crude oils from distinct geological sources worldwide are toxic to developing fish hearts. When oil spills occur in fish spawning habitats, natural resource injury assessments often rely on conventional morphometric analyses of heart form and function. The extent to which visible indicators correspond to molecular markers for cardiovascular stress is unknown for pelagic predators from the Gulf of Mexico. Here we exposed mahi (Coryphaena hippurus) embryos to field-collected crude oil samples from the 2010 Deepwater Horizon disaster. We compared visible heart defects (edema, abnormal looping, reduced contractility) to changes in expression of cardiac-specific genes that are diagnostic of heart failure in humans or associated with loss-of-function zebrafish cardiac mutants. Mahi exposed to crude oil during embryogenesis displayed typical symptoms of cardiogenic syndrome as larvae. Contractility, looping, and circulatory defects were evident, but larval mahi did not exhibit downstream craniofacial and body axis abnormalities. A gradation of oil exposures yielded concentration-responsive changes in morphometric and molecular responses, with relative sensitivity being influenced by age. Our findings suggest that 1) morphometric analyses of cardiac function are more sensitive to proximal effects of crude oil-derived chemicals on the developing heart, and 2) molecular indicators reveal a longer-term adverse shift in cardiogenesis trajectory.

This paper describes advances in hatchery and growout technology of cobia (Rachycentron canadum, Linnaeus). In 2007, methods for capture, transport, acclimation, sampling, conditioned spawning, larval rearing, ¢ngerling production, nursery, shipping and grow-out have been perfected. Survival rates ranging from 17.5% to 35% were achieved from egg to shipping size ¢ngerlings (1.0 g) in 2007 at the University of Miami Experimental Fish Hatchery, with production of approximately 20 000 ¢ngerlings per 12000 L tank. Wild and F1 broodstock cobia have been conditioned to spawn through temperature manipulation producing viable eggs for experimental and production level larval rearing trials in several hatcheries. Brood ¢sh have also been induced to spawn using hormones. Cobia appear to be susceptible to infestations by parasitic protozoa such as Amyloodinium ocellatum and to infections caused by deleterious bacteria such as Photobacterium spp. and Vibrio spp. Prophylactic methods used to prevent and control epizootic diseases at the hatchery are summarized. Improved techniques for cage management were implemented, and both novel designs of submerged cages deployed in exposed areas and traditional gravity cages in protected areas have been used for commercial ongrowing of cobia in the Americas and the Caribbean region.

The 2010 Deepwater Horizon oil spill resulted in the accidental release of millions barrels of crude oil into the Gulf of Mexico. Photoinduced toxicity following coexposure to ultraviolet (UV) radiation is one mechanism by which polycyclic aromatic hydrocarbons (PAHs) from oil spills may exert toxicity. Mahi-mahi (Coryphaena hippurus), an important fishery resource, have positively buoyant, transparent eggs. These characteristics may result in mahi-mahi embryos being at particular risk from photoinduced toxicity. The goal of this study was to determine whether exposure to ultraviolet radiation as natural sunlight enhances the toxicity of crude oil to embryonic mahi-mahi. Mahi-mahi embryos were exposed to several dilutions of water accommodated fractions (WAF) from slick oil collected during the 2010 spill and gradations of natural sunlight in a fully factorial design. Here, we report that coexposure to natural sunlight and WAF significantly reduced percent hatch in mahi-mahi embryos. Effect concentrations of PAH in WAF were within the range of surface PAH concentrations reported in the Gulf of Mexico during the Deepwater Horizon spill. These data suggest that laboratory toxicity tests that do not include UV may underestimate the toxicity of oil spills to early lifestage fish species.

The temporal and geographic attributes of the Deepwater Horizon incident in 2010 likely exposed pelagic game fish species, such as mahi-mahi, to crude oil. Although much of the research assessing the effects of the spill has focused on early life stages of fish, studies examining whole-animal physiological responses of adult marine fish species are lacking. Using swim chamber respirometry, the present study demonstrates that acute exposure to a sublethal concentration of the water accommodated fraction of Deepwater Horizon crude oil results in significant swim performance impacts on young adult mahi-mahi, representing the first report of acute sublethal toxicity on adult pelagic fish in the Gulf of Mexico following the spill. At an exposure concentration of 8.4 ± 0.6 µg L sum of 50 selected polycyclic aromatic hydrocarbons (PAHs; mean of geometric means ± standard error of the mean), significant decreases in the critical and optimal swimming speeds of 14% and 10%, respectively (p < 0.05), were observed. In addition, a 20% reduction in the maximum metabolic rate and a 29% reduction in aerobic scope resulted from exposure to this level of ΣPAHs. Using environmentally relevant crude oil exposure concentrations and a commercially and ecologically valuable Gulf of Mexico fish species, the present results provide insight into the effects of the Deepwater Horizon oil spill on adult pelagic fish. Environ Toxicol Chem 2016;35:2613-2622. © 2016 SETAC.