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Investigating TCDD toxicity using a model of zebrafish liver regernation.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TODD), an environmental pollutant, mediates toxicity through the aryl hydrocarbon receptor (AhR), a soluble, ligandactivated transcription factor. Toxicity of TODD includes aberrant cell cycle progression, and exposure to TCDD suppresses hepatocyte proliferation in a mouse model of liver regeneration elicited by partial hepatectomy (PH). This study aimed to establish the PH model system in zebrafish, with the long-term goal of using unique, zebrafish-specific genetic tools to identify mechanisms by which TODD disrupts cell cycle progression. Adult zebrafish were injected with TODD (20 mg/kg) or DMSO control 24 hours prior to PH. Zebrafish were euthanized 36 hours post-surgery, and livers were either homogenized or fixed in formalin. Western blot analysis indicates that exposure to TCDD induced AhR activation, as evidenced by expression of cytochrome P4501A1, encoded by the AhR-regulated gene Cyp1a1. Liver tissue was stained to detect proliferating cell nuclear antigen, a marker of cell proliferation, but further optimization is needed to determine if hepatocyte proliferation is diminished in TCDD-treated zebrafish. This study may demonstrate the feasibility of using zebrafish to investigate mechanisms by which TCDD deregulates cell cycle progression.

Christopher J. Horras *, Jason C. Hanley, Kristen A. Mitchell, Boise State University, Boise, ID 83725

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Author:Horras, Christopher J.; Hanley, Jason C.; Mitchell, Kristen A.
Publication:Journal of the Idaho Academy of Science
Article Type:Report
Geographic Code:1USA
Date:Jun 1, 2010
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