Bioenergetic and Fitness Costs of PAH Adapted Fundulus heteroclitus to Early Life PAH and Hypoxia Exposures

Growing evidence suggests that acute polycyclic aromatic hydrocarbon (PAH) exposures have toxic mitochondrial effects and may inhibit aerobic respiration. However, the effect of subteratogenic exposures during development is not well described in literature – especially in the presence of other deleterious environmental conditions. For example, Atlantic teleost fishes experience seasonal hypoxia that may exacerbate co-occurring PAH exposure due to molecular crosstalk with the aryl hydrocarbon receptor (AhR) pathway. This study investigated the potential link between sustained swimming performance and mitochondrial oxygen consumption in two populations of Fundulus heteroclitus months after a single initial exposure to a PAH mixture with and without hypoxia. This study used lab-reared embryos from killifish originating in the Elizabeth River (Portsmouth, VA) near a polluted wood treatment facility where the fish have become highly resistant to developmental cardiac teratogenicity (Republic Creosoting; ~113886 ng PAHs/g dry sediment). Another population of killifish were sourced from an undeveloped reference location (King’s Creek; ~526 ng PAHs/g dry sediment) outside the Elizabeth River. Subset individuals were treated with either a subteratogenic dilution of a complex PAH mixture (∑[PAHs] ≈ 25.2 μg/L) for 24 hours post-fertilization (hpf), diurnal hypoxia exposure for 14 days post-fertilization (dpf), or both. Upon reaching 6 months of age, their sustained swimming velocity (Ucrit) was measured in a recirculating swim chamber. A separate subset was processed for basal and mitochondrial oxygen consumption rate (OCR) analysis. The study found that killifish population that had historically little PAH exposure had a higher sustained swimming performance than killifish adapted to PAHs. Additionally, mitochondrial oxygen consumption, at baseline and at an induced maximal rate, increases with PAH exposure for the non-adapted fish and hypoxia exposure for PAH-adapted fish.