Are Ahr2 variant Atlantic tomcod from the Hudson River cross-resistant to toxicity from polycyclic aromatic hydrocarbons?

Abstract

All life-stages of Atlantic tomcod from the Hudson River (HR) estuary, New York, are highly resistant to toxicity from coplanar PCBs and TCDD, and this resistance results from a six-base-pair deletion in the Aryl hydrocarbon receptor 2 (ahr2) gene. Tomcod in the HR estuary are also exposed to high levels of PAHs; however, their sensitivity to toxicity from a suite of PAHs has yet to be evaluated. Based on preliminary studies, we hypothesized that HR tomcod are also resistant to PAH toxicity, but not as strongly as to PCBs and TCDD, and that the magnitude of resistance will vary among structurally diverse PAHs. In this study, tomcod adults were collected from the HR and tributaries of Cobscook Bay in Downeast Maine, bred, their embryos exposed for 48 h to graded doses of PCB126 and four structurally diverse PAHs (BaA, BaP, BkF, and DMBA), and the responses of young life-stages were compared at a variety of toxic endpoints that are likely mediated by ahr2 and are representative of adult fitness. HR tomcod embryos were highly resistant, by at least 100-fold to toxicity from PCB126 at all endpoints investigated. They also exhibited resistance to all four PAHs, although the strength of the resistance phenotype varied among the different toxic endpoints. We also found that the resistance phenotype varied among the four PAHs with it being strongest for BaA and BkF. We conclude that HR tomcod are resistant to PAHs, but the magnitude of the resistance phenotype is significantly less than for PCBs.

Keywords: Aryl hydrocarbon receptor (AHR) pathway; Cardiac morphology and function; Fitness; Gene expression; Morphometrics.