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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 the impact of long-term, multi-generational exposure to polychlorinated biphenyls (PCBs), a persistent organic pollutant. Dr. Mark Hahn and his team of researchers are studying a population of Atlantic killifish inhabiting New Bedford Harbor, MA (NBH), a Superfund site that is highly contaminated with PCBs. NBH killifish are much less sensitive to PCBs than killifish from a reference site, Scorton Creek (SC). PCBs cause toxicity in part by activating aryl hydrocarbon receptor (AHR) proteins.  Killifish have two AHRs (AHR1 and AHR2) and an AHR repressor (AHRR), a protein that inhibits AHRs. The specific objectives of their research are: 1) to understand the mechanisms by which NBH killifish are less sensitive to the developmental toxicity of DLCs that act through AHRs, and 2) to determine the impact of evolved dioxin resistance on the sensitivity to low oxygen (hypoxia).

Previously, the research team has identified two AHR2 variants that were more prevalent at NBH and two that were more prevalent at SC. Several experiments were formed to test the ability of each variant to activate transcription.  All four variants were able to activate transcription, and there were no dramatic differences in the sensitivity to the pollutants TCDD or PCB-126.

They also performed two experiments to compare the response of SC and NBH fish to PCB-126, either alone or in combination with hypoxia.  In the first experiment, embryos were exposed to PCB and sampled at 5, 10, and 15 days post fertilization. The result demonstrates that fish from NBH are still resistant to PCBs, despite the partial clean-up of the site, and shows that their previous results showing non-responsiveness of AHRR in NBH adults can be extended also to embryos.

In the second experiment, killifish larvae spawned from SC or NBH adults were exposed to PCB-126 (0, 10, 50, or 100 nM) in combination with one of four oxygen concentrations: ambient, 20%, 10%, or 5%.  NBH larvae were more sensitive to hypoxia (5%) as compared to SC fish.  Analysis of gene expression is in progress.

The team has continued to work with Margie Oleksiak (BU and Duke SBRPs) and Rich DiGiulio (Duke SBRP) to develop microarrays for measuring transcriptional changes in killifish embryos co-exposed to chemicals and hypoxia.  Arrays have been printed and are being used to analyze samples in hand.

This research explores how natural populations of animals respond to prolonged, high-level exposure to contaminants.  Dr. Hahn uses fish as models to investigate the mechanisms underlying differential sensitivity to the developmental toxicity of dioxin-like chemicals. The existence of dioxin-sensitive and dioxin-resistant populations of killifish provides a unique opportunity to understand the molecular mechanisms of differential dioxin sensitivity and the impact of evolved resistance on the sensitivity of fish to other environmental stressors.

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