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Assessing the effects of dietary exposure to PPARα agonists in mummichogs (Fundulus heteroclitus)
Citation:
Clark, B., N. McNabb, I. Kirby, J. Bishop, D. Champlin, A. Whitehead, AND D. Nacci. Assessing the effects of dietary exposure to PPARα agonists in mummichogs (Fundulus heteroclitus). Pollutant Responses in Marine Organisms, Charleston, South Carolina, May 19 - 22, 2019.
Impact/Purpose:
Some persistent compounds found in the environment cause toxicity through the peroxisome proliferator-activated receptor (PPAR) pathway, but these effects are not well understood in wild organisms. This presentation describes studies that will contribute to our understanding of the ecological risks associated with persistent pollutants that act through these toxic mechanisms. Here we fed fish two model chemicals that act through this pathway and assessed their growth, energy reserves, reproduction, and gene expression changes. The results demonstrate the value of integrating chemical, biological, and molecular techniques to assess the effects and mechanisms of chemical stress in wild fish populations. Ultimately these studies will contribute to improved understanding by managers and scientists of mechanisms connecting human activities, ecological stressors, and ecosystem condition.
Description:
Perfluorinated compounds (PFCs), including per- and polyfluoroalkyl substances (PFASs), are a large family of structurally related surfactants used in a wide variety of consumer products, food packaging, fire-fighting foams, and stain-proof coatings. PFASs have generated increasing concern due to this widespread use and environmental persistence, so there is a need to better understand the toxicity and mechanisms of action of PFASs, especially in ecological organisms such as fish. Effects of PFASs on growth, reproduction, and metabolic homeostasis in mammals and fish may be mediated in part by activation of peroxisome proliferator-activated receptor (PPAR) pathways. To better understand these toxicity pathways, we are conducting a series of dietary studies with an estuarine fish (Fundulus heteroclitus, mummichog). In this study, we examined the effects of the polybrominated diphenyl ether BDE99 and the human therapeutic clofibric acid (CLA) as model compounds for toxic actions expected with some PFASs. Although data are limited, both compounds interact with the PPARα pathway in fish and produce a variety of adverse effects, including alterations in metabolic homeostasis. Wild-caught adult mummichog from Jerusalem, RI were individually tagged and placed in tanks receiving flowing seawater at 23 °C. Fish in four replicate tanks/treatment (2 male, 2 female/tank) were fed diets amended with acetone (control), BDE99 (75, 150, 375, or 750 ng/g fish ww/day), or CLA (80 µg/g fish ww/day) for 38 days. Weight and length was monitored throughout, and breeding was assessed by manual strip-spawning. On days 10 and 39, ½ the fish were sacrificed, and fish weight/length and wet weight of gonad, liver, abdominal fat, and brains were recorded. Tissues were archived for molecular and chemical analyses. Energetic reserves (fat and liver) were affected in a dose-responsive manner by day 39. At day 10, fish in all treatments but CLA were reproductive, but by day 39 only control females were (~30 eggs/female in control vs <5 eggs/female in others). Assessment of transcriptomic responses and bioaccumulation is ongoing. These results will aid in our understanding of the mechanisms of toxicity of these compounds and provide insight for future studies with PFASs. Ultimately, the output of these studies will be used to inform ecological models, including bioenergetic and population models.