Parental dietary seleno-L-methionine exposure and resultant offspring developmental toxicity.
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Selenium (Se) leaches into water from agricultural soils and from storage sites for coal fly ash. Se toxicity causes population and community level effects in fishes and birds. We used the laboratory aquarium model fish, Japanese medaka (Oryzias latipes), an asynchronous breeder, to determine aspects of uptake in adults and resultant developmental toxicity in their offspring. The superior imaging properties of the model enabled detailed descriptions of phenotypic alterations not commonly reported in the existing Se literature. Adult males and females in treatment groups were exposed, separately and together, to a dry diet spiked with 0, 12.5, 25, or 50 μg/g (dry weight) seleno-L-methionine (SeMet) for 6 days, and their embryo progeny collected for 5 days, maintained under controlled conditions and observed daily for hatchability, mortality and/or developmental toxicity. Sites of alteration included: craniofacial, pericardium and abdomen (Pc/Ab), notochord, gall bladder, spleen, blood, and swim bladder. Next, adult tissue Se concentrations (liver, skeletal muscle, ovary and testis) were determined and compared in treatment groups of bred and unbred individuals. No significant difference was found across treatment groups at the various SeMet concentrations; and, subsequent analysis compared exposed vs. control in each of the treatment groups at 10 dpf. Increased embryo mortality was observed in all treatment groups, compared to controls, and embryos had a decreased hatching rate when both parents were exposed. Exposure resulted in significantly more total altered phenotypes than controls. When altered phenotypes following exposure of both parents were higher than maternal only exposure, a male role was suggested. The comparisons between treatment groups revealed that particular types of phenotypic change may be driven by the sex of the exposed parent. Additionally, breeding reduced Se concentrations in some adult tissues, specifically the liver of exposed females and skeletal muscle of exposed males. Detailed phenotypic analysis of progeny from SeMet exposed parents should inform investigations of later life stages in an effort to determine consequences of early life exposure.
Published Version (Please cite this version)
Chernick, Melissa, Megan Ware, Elizabeth Albright, Kevin WH Kwok, Wu Dong, Na Zheng and David E Hinton (2016). Parental dietary seleno-L-methionine exposure and resultant offspring developmental toxicity. Aquatic toxicology (Amsterdam, Netherlands), 170. pp. 187–198. 10.1016/j.aquatox.2015.11.004 Retrieved from https://hdl.handle.net/10161/19203.
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Elizabeth's current research centers on how policies and decisions are made in response to extreme climatic events. Further, she is interested in collaborative decision making processes, particularly in the realm of water resource management. She has received a grant from the National Science Foundation and a Fulbright Scholarship to support her scholarship. The Midwest Political Science Associated recently awarded Elizabeth the 'Best Paper by an Emerging Scholar' award at their national conference. Her geographic regions of interest include the southeast US and Central and Eastern Europe. Prior to completing her Ph.D. Elizabeth worked for the State of North Carolina in water resource management.
The Hinton laboratory focuses on mechanistic toxicity in all life stages of small, aquarium model fish and in selected species with particular environmental relevance (freshwater and marine). With the latter, investigations focus on stressor responses and include follow up studies after oil spills. Studies with the laboratory model fish take advantage of the compressed life cycle to improve understanding of organellar, cellular and tissues responses that arise after exposure and follow either a temporal and/or a concentration gradient. At the end of these serial examinations, we have pioneered the use of high resolution light and fluorescent microscopy and electron microscopy in these small fish species to better understand resultant phenotypes and to correlate structural alteration with molecular biological studies. In this way we are anchoring phenotypes with gene expression. In individual fish where specific genes have been mutated (Collaboration with Dr. Keith Cheng, Hershey Medical Center, Hershey, PA) or in individuals exposed to organic substances of known or expected toxicity, structural analysis at various levels of biological organization enables integration across all levels of biological organization enabling whole body phenomics. Special projects include The Duke Superfund Research Center, 2P42-ESO10356-10A2, supported by NIH/NIEHS. Studies investigate responses of fish to polycyclic aromatic hydrocarbons and include early life stages and multigenerational effects. Contaminated and reference sites are included in these investigations of feral fish. Also, we receive funding as part of theme 2 of the Center for Environmental Implications of Nano Technology (CEINT). Our studies seek to determine whether there are specific toxic consequences upon exposure to nano silver (Ag NPs) versus exposure to conventional silver. We hosted Na Zheng (Angie), Visiting Investigator, Associate Professor, Northeast Institute of Geography and Agricultural Ecology, Chinese Academy of Sciences. She was the recipient of a K.C. Wong award supporting her role as visiting investigator. Together, we investigated metals mixtures and embryo toxicity. We collaborate with Stella Marinakos, Pratt School and CEINT on the synthesis and refinement of nanoselenium. This complements work done over the past year with seleno-methionine and sodium selenite in parental and embryo exposures. We continue to investigate ways to assess whole body responses of aquarium model fish and to link phenotype to genotype. Collaboration with the Stapleton laboratory has investigated alterations in embryo and larval zebrafish exposed to flame retardant compounds and selected metabolites. Here our morphologic investigations have helped to differentiate between delayed development and toxicity in the developing eye.
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