The impact of maternally derived dioxins on embryonic development and hepatic AHR signaling in a long-lived apex predator.

Dioxins and related contaminants are highly pervasive in aquatic systems and elicit deleterious effects in exposed organisms. Because dioxins exhibit a proclivity to bioaccumulate, long-lived predatory species are particularly vulnerable to their persistence in the environment. We have previously reported elevated expression of CYP1A2, a biomarker of dioxin exposure, in American alligator embryos collected from the Tom Yawkey Wildlife Center (YWC). This coastal population inhabits a system with historical dioxin contamination associated with industrial activities. Herein, we utilize ecological attributes of the alligator to address the persistence of dioxins and furans in yolk and their potential to drive changes in hepatic function. Specifically, we assess variation in expression of AHR signaling components in embryos and its connection to contaminant levels in matched yolk samples. Compared to a reference population, TEQ levels and total penta-, hexa-, octa-substituted CDDs were elevated at YWC. Contrary to predictions, TEQ levels were not significantly related to hepatic AHR1B or CYP1A2 expression. However, a significant association was detected between expression of both factors and embryo:yolk mass ratios, wherein decreasing embryo mass was negatively associated with CYP1A2 but positively associated with AHR1B. These findings suggest that variation in embryonic metabolism and developmental progression likely influence AHR signaling and dioxin toxicity in alligators and potentially other oviparous species. While dioxin concentrations observed in alligators in this study are lower than historical values reported for other wildlife species inhabiting this system, they indicate the continued presence and possible long-term influence of these contaminants in a high trophic status species.