Atlantic sturgeon and shortnose sturgeon co-occur in many estuaries along the Atlantic Coast of North America. Both species are protected under the U.S. Endangered Species Act and internationally on the IUCN Red list and by CITES. Early life-stages of both sturgeons may be exposed to persistent aromatic hydrocarbon contaminants such as PCBs and PCDD/Fs which are at high levels in the sediments of impacted spawning rivers. Our objective was to compare the PCBs and TCDD sensitivities of both species with those of other fishes and to determine if environmental concentrations of these contaminants approach those that induce toxicity to their young life-stages under controlled laboratory conditions. Because our previous studies suggested that young life-stages of North American sturgeons are among the more sensitive of fishes to coplanar PCB and TCDD-induced toxicities, we were interested in identifying the molecular bases of this vulnerability. It is known that activation of the aryl hydrocarbon receptor 2 (AHR2) in fishes mediates most toxicities to these contaminants and transcriptional activation of xenobiotic metabolizing enzymes such as cytochrome P4501A (CYP1A). Previous studies demonstrated that structural and functional variations in AHRs are the bases for differing sensitivities of several vertebrate taxa to aromatic hydrocarbons. Therefore, in this study we characterized AHR2 and its expression in both sturgeons as an initial step in understanding the mechanistic bases of their sensitivities to these contaminants. We also used CYP1A expression as an endpoint to develop Toxicity Equivalency Factors (TEFs) for these sturgeons. We found that critical amino acid residues in the ligand binding domain of AHR2 in both sturgeons were identical to those of the aromatic hydrocarbon-sensitive white sturgeon, and differed from the less sensitive lake sturgeon. AHR2 expression was induced by TCDD (up to 6-fold) and by three of four tested coplanar PCB congeners (3–5-fold) in Atlantic sturgeon, but less so in shortnose sturgeon. We found that expression of AHR2 and CYP1A mRNA significantly covaried after exposure to TCDD and PCB77, PCB81, PCB126, but not PCB169 in both sturgeons. We also determined TEFs for the four coplanar PCBs in shortnose sturgeon based on comparison of CYP1A mRNA expression across all doses. Surprisingly, the TEFs for all four coplanar PCBs in shortnose sturgeon were much higher (6.4–162 times) than previously adopted for fishes by the WHO.

北美沿大西洋沿岸的许多河口同时出现大西洋st和短鼻co。两种物种均受到《美国濒危物种法》的保护，并在国际自然保护联盟红色名录和《濒危野生动植物种国际贸易公约》中得到保护。两种st鱼的早期生命阶段都可能暴露于持久性芳烃污染物中，例如多氯联苯和PCDD / Fs，这些污染物在受灾产卵河的沉积物中含量很高。我们的目标是比较两个物种与其他鱼类对PCBs和TCDD的敏感性，并确定这些污染物的环境浓度是否接近在受控实验室条件下对其幼年生命期产生毒性的那些污染物。因为我们先前的研究表明，北美st鱼的年轻生命期是鱼类对共面PCB和TCDD诱导的毒性更敏感的鱼类，所以我们有兴趣确定这种脆弱性的分子基础。众所周知，鱼类中芳烃受体2（AHR2）的激活介导了对这些污染物的大多数毒性，异种生物代谢酶（例如细胞色素P4501A（CYP1A））的转录激活。先前的研究表明，AHR中的结构和功能变异是几种脊椎动物类群对芳烃的敏感性不同的基础。因此，在这项研究中，我们表征了AHR2及其在两种st鱼中的表达，作为了解它们对这些污染物的敏感性的机械基础的第一步。我们还使用CYP1A表达作为终点来开发这些develop鱼的毒性当量因子（TEF）。我们发现在两个st鱼中，AHR2配体结合域中的关键氨基酸残基与芳香烃敏感的白色st鱼相同，并且与不太敏感的湖泊st鱼不同。AHR2的表达是由TCDD（最多6倍）和四个经过测试的共平面PCB同系物中的三个（3至5倍）诱导的，而在短鼻st中则较少。我们发现在两个urge鱼中，TCR和PCB77，PCB81，PCB126而不是PCB169暴露后，AHR2和CYP1A mRNA的表达显着协变。我们还通过比较所有剂量下CYP1A mRNA的表达，确定了短鼻st中四个共面PCB的TEF。出奇，