Abstract
The Corpus Christi Inner Harbor in Texas is a major center of industrial activity and contains high levels of persistent pollutants, including dioxins, furans, polycyclic aromatic hydrocarbons (PAHs), and polychlorinated biphenyls (PCBs). The Gulf killifish, Fundulus grandis , is an estuarine species inhabiting the Gulf of Mexico. F. grandis populations from the Houston Ship Channel (Galveston Bay, Texas) have been previously shown to be resistant to PCB-induced cardiac teratogenesis via a recalcitrant aryl hydrocarbon receptor (AHR) pathway. In this study, embryos from two F. grandis populations collected from the Corpus Christi Inner Harbor were exposed to varying doses of PCB-126 and evaluated for heart deformities at 144 h post fertilization. Both populations displayed significant resistance to PCB-induced cardiac teratogenesis compared to a reference population, representing the second documented cluster of adapted populations of F. grandis . Additionally, these populations exhibited lower basal cytochrome P4501A (CYP1A) activity (as measured via EROD assay) and reduced inducibility, indicating that a recalcitrant AHR pathway is at least partially responsible for the observed PCB resistance. Finally, we found that PCB-induced cardiac teratogenesis and CYP1A induction were highly correlated at the population level; however, individual CYP1A activity did not predict cardiac deformity. We propose a theoretical model in which inter-individual variation in CYP1A response explains this discrepancy and offers a conceptual framework for understanding individual variation within adapted populations. Collectively, these findings provide new insight into the mechanisms underlying adaptive responses to persistent pollutants and further establish F. grandis as a valuable model for evolutionary toxicology.