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Your Environment. Your Health.

Progress Reports: Boston University: Mechanisms and Impacts of PCB Resistant Fish

Superfund Research Program

Mechanisms and Impacts of PCB Resistant Fish

Project Leader: Mark E. Hahn (Woods Hole Oceanographic Institution)
Co-Investigators: Sibel I. Karchner (Woods Hole Oceanographic Institution), Neelakanteswar Aluru (Woods Hole Oceanographic Institution)
Grant Number: P42ES007381
Funding Period: 1995-2020
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

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Progress Reports

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The overall objective of this project is to understand how natural populations of animals respond to prolonged exposures over multiple generations to high levels of dioxin-like chemicals, including certain polychlorinated biphenyls (PCBs).  Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) causes toxicity by activating a protein known as the aryl hydrocarbon receptor (AHR). In New Bedford Harbor, Massachusetts, a Superfund site that is highly contaminated with PCBs and other chemicals, a population of estuarine fish, Atlantic killifish (Fundulus heteroclitus), has developed resistance to dioxin and dioxin-like chemicals. The existence of this population provides a unique research opportunity to investigate the molecular mechanisms underlying differential sensitivity to the developmental toxicity of dioxin-like chemicals.

Previously, Dr. Mark Hahn’s group showed that killifish in New Bedford Harbor are approximately 14-fold less sensitive to dioxin-like compounds than killifish from a reference site, Scorton Creek, in Sandwich, Massachusetts. They also found that this “dioxin resistance” is heritable. The researchers identified two killifish aryl hydrocarbon receptors (AHR1 and AHR2) and an AHR repressor (AHRR), a protein that inhibits effects occurring through the AHRs. The specific objectives of this project are: 1) to understand the mechanisms by which killifish in New Bedford Harbor are less sensitive to the developmental toxicity of dioxin-like compounds that act through AHR-dependent signaling, and 2) to determine the impact of evolved dioxin resistance on the sensitivity to other environmental stressors, such as low oxygen (hypoxia).

In 2005, Hahn’s group made progress in several areas. They continued studies of AHR gene polymorphisms—that is, multiple forms of the gene that lead to variant AHR proteins—and their possible role in the mechanism of resistance. Using the single nucleotide polymorphisms (SNPs) in AHR1 and AHR2 genes that the researchers identified in individual fish from New Bedford Harbor and Scorton Creek (26 fish per site), they inferred the sets of associated SNPs—haplotypes—present in fish from each site. For AHR1, they found haplotypes that were shared between sites as well as unique haplotypes found only at one site. For AHR2, most of the haplotypes at each site were found only at that site. In preparation for future studies that will examine the relationship between specific haplotypes and sensitivity to dioxins in individual fish, they obtained offspring of fish from New Bedford Harbor and Scorton Creek (the F1 fish generation) from collaborators at the EPA Atlantic Ecology Division Laboratory in Narragansett, Rhode Island.

In 2005, Hahn’s group also began to develop genomic resources that will allow them to perform gene expression profiling, using microarrays, in killifish embryos exposed to PCBs and hypoxia. A workshop was held to discuss how to coordinate the development and distribution of killifish microarrays for use by several research groups studying this species. Plans for preliminary microarray experiments were made, and a follow-up workshop has been set for spring 2006. Hahn’s group also collaborated with Gloria Callard (BU SBRP Project “Estrogen Receptor-Arylhydrocarbon Receptor Interactions in the CNS”) to begin to explore estrogenic signaling pathways in fish from Scorton Creek and New Bedford Harbor.

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