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Histopathologic Alterations Associated with Global Gene Expression Due to Chronic Dietary TCDD Exposure in Juvenile Zebrafish Public Deposited

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https://ir.library.oregonstate.edu/concern/articles/707959415

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  • The goal of this project was to investigate the effects and possible developmental disease implication of chronic dietary TCDD exposure on global gene expression anchored to histopathologic analysis in juvenile zebrafish by functional genomic, histopathologic and analytic chemistry methods. Specifically, juvenile zebrafish were fed Biodiet starter with TCDD added at 0, 0.1, 1, 10 and 100 ppb, and fish were sampled following 0, 7, 14, 28 and 42 d after initiation of the exposure. TCDD accumulated in a dose- and time-dependent manner and 100 ppb TCDD caused TCDD accumulation in female (15.49 ppb) and male (18.04 ppb) fish at 28 d post exposure. Dietary TCDD caused multiple lesions in liver, kidney, intestine and ovary of zebrafish and functional dysregulation such as depletion of glycogen in liver, retrobulbar edema, degeneration of nasal neurosensory epithelium, underdevelopment of intestine, and diminution in the fraction of ovarian follicles containing vitellogenic oocytes. Importantly, lesions in nasal epithelium and evidence of endocrine disruption based on alternatively spliced vasa transcripts are two novel and significant results of this study. Microarray gene expression analysis comparing vehicle control to dietary TCDD revealed dysregulated genes involved in pathways associated with cardiac necrosis/cell death, cardiac fibrosis, renal necrosis/cell death and liver necrosis/cell death. These baseline toxicological effects provide evidence for the potential mechanisms of developmental dysfunctions induced by TCDD and vasa as a biomarker for ovarian developmental disruption.
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  • Liu Q, Spitsbergen JM, Cariou R, Huang C-Y, Jiang N, et al. (2014) Histopathologic Alterations Associated with Global Gene Expression Due to Chronic Dietary TCDD Exposure in Juvenile Zebrafish. PLoS ONE 9(7): e100910. doi:10.1371/journal.pone.0100910
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  • 9
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  • 7
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  • This work was funded by the University of Wisconsin Sea Grant Institute under grants from the National Sea Grant College Program, National Oceanicand Atmospheric Administration, U.S. Department of Commerce, and from the State of Wisconsin. Federal grant number NA060AR4170011, project number R/BT-21. This work was also supported by the UWM Children’s Environmental Health Sciences Core Center (NIEHS 2P30ES004184), and the Shaw Fund of the GreaterMilwaukee Foundation.
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  • description.provenance : Made available in DSpace on 2014-10-09T19:46:17Z (GMT). No. of bitstreams: 3 license_rdf: 1370 bytes, checksum: cd1af5ab51bcc7a5280cf305303530e9 (MD5) SpitsbergenJanMicrobiologyHistopathologicAlterationsAssociated.pdf: 2911886 bytes, checksum: 9586f1eee117cfb41ace544b8c8e441a (MD5) SpitsbergenJanMicrobiologyHistopathologicAlterationsAssociated_SupportingInformation.zip: 2905394 bytes, checksum: f5112da5652f536ba65cad7419bbe149 (MD5) Previous issue date: 2014-07-02
  • description.provenance : Submitted by Erin Clark (erin.clark@oregonstate.edu) on 2014-10-09T19:45:55Z No. of bitstreams: 3 license_rdf: 1370 bytes, checksum: cd1af5ab51bcc7a5280cf305303530e9 (MD5) SpitsbergenJanMicrobiologyHistopathologicAlterationsAssociated.pdf: 2911886 bytes, checksum: 9586f1eee117cfb41ace544b8c8e441a (MD5) SpitsbergenJanMicrobiologyHistopathologicAlterationsAssociated_SupportingInformation.zip: 2905394 bytes, checksum: f5112da5652f536ba65cad7419bbe149 (MD5)
  • description.provenance : Approved for entry into archive by Erin Clark(erin.clark@oregonstate.edu) on 2014-10-09T19:46:17Z (GMT) No. of bitstreams: 3 license_rdf: 1370 bytes, checksum: cd1af5ab51bcc7a5280cf305303530e9 (MD5) SpitsbergenJanMicrobiologyHistopathologicAlterationsAssociated.pdf: 2911886 bytes, checksum: 9586f1eee117cfb41ace544b8c8e441a (MD5) SpitsbergenJanMicrobiologyHistopathologicAlterationsAssociated_SupportingInformation.zip: 2905394 bytes, checksum: f5112da5652f536ba65cad7419bbe149 (MD5)

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