| Autor: |
Albers JL; Department of Fisheries and Wildlife, Michigan State University, East Lansing, Michigan 48824, United States., Ivan LN; Department of Fisheries and Wildlife, Michigan State University, East Lansing, Michigan 48824, United States., Clark BW; Office of Research and Development, Center for Environmental Measurement and Modeling, Atlantic Coastal Environmental Sciences Division, U.S. Environmental Protection Agency, Narragansett, Rhode Island 02882, United States., Nacci DE; Office of Research and Development, Center for Environmental Measurement and Modeling, Atlantic Coastal Environmental Sciences Division, U.S. Environmental Protection Agency, Narragansett, Rhode Island 02882, United States., Klingler RH; School of Freshwater Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53204, United States., Thrash A; Biocomputing and Biotechnology, Institute for Genomics, Mississippi State University, Starkville, Mississippi 39759, United States., Steibel JP; Department of Fisheries and Wildlife, Michigan State University, East Lansing, Michigan 48824, United States., Vinas NG; Environmental Laboratory, US Army Engineer Research and Development Center, U.S. Army Corps of Engineers, Vicksburg, Mississippi 39180, United States., Carvan MJ; School of Freshwater Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53204, United States., Murphy CA; Department of Fisheries and Wildlife, Michigan State University, East Lansing, Michigan 48824, United States. |
| Abstrakt: |
Molecular, cellular, and organismal alterations are important descriptors of toxic effects, but our ability to extrapolate and predict ecological risks is limited by the availability of studies that link measurable end points to adverse population relevant outcomes such as cohort survival and growth. In this study, we used laboratory gene expression and behavior data from two populations of Atlantic killifish Fundulus heteroclitus [one reference site (SCOKF) and one PCB-contaminated site (NBHKF)] to inform individual-based models simulating cohort growth and survival from embryonic exposures to environmentally relevant concentrations of neurotoxicants. Methylmercury exposed SCOKF exhibited brain gene expression changes in the si:ch211-186j3.6, si:dkey-21c1.4, scamp1, and klhl6 genes, which coincided with changes in feeding and swimming behaviors, but our models simulated no growth or survival effects of exposures. PCB126-exposed SCOKF had lower physical activity levels coinciding with a general upregulation in nucleic and cellular brain gene sets (BGS) and downregulation in signaling, nucleic, and cellular BGS. The NBHKF, known to be tolerant to PCBs, had altered swimming behaviors that coincided with 98% fewer altered BGS. Our models simulated PCB126 decreased growth in SCOKF and survival in SCOKF and NBHKF. Overall, our study provides a unique demonstration linking molecular and behavioral data to develop quantitative, testable predictions of ecological risk. |
