Embryonic exposure to PFAS causes long-term, compound-specific behavioral alterations in zebrafish.
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2023-05
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Per- and polyfluoroalkyl substances (PFAS) are commonly used as surfactants and coatings for industrial processes and consumer products. These compounds have been increasingly detected in drinking water and human tissue, and concern over their potential effects on health and development is growing. However, relatively little data are available for their potential impacts on neurodevelopment and the degree to which different compounds within this class may differ from one another in their neurotoxicity. The present study examined the neurobehavioral toxicology of two representative compounds in a zebrafish model. Zebrafish embryos were exposed to 0.1-100uM perfluorooctanoic acid (PFOA) or 0.01-1.0uM perfluorooctanesulfonic acid (PFOS) from 5 to 122 h post-fertilization. These concentrations were below threshold for producing increased lethality or overt dysmorphologies, and PFOA was tolerated at a concentration 100× higher than PFOS. Fish were maintained to adulthood, with behavioral assessments at 6 days, 3 months (adolescence) and 8 months of age (adulthood). Both PFOA and PFOS caused behavioral changes in zebrafish, but PFOS and PFOS produced strikingly different phenotypes. PFOA was associated with increased larval motility in the dark (100uM), and enhanced diving responses in adolescence (100uM) but not adulthood. PFOS was associated with a reversed light-dark response in the larval motility test (0.1-1uM), whereby the fish were more active in the light than the dark. PFOS also caused time-dependent changes in locomotor activity in the novel tank test during adolescence (0.1-1.0uM) and an overall pattern of hypoactivity in adulthood at the lowest concentration (0.01uM). Additionally, the lowest concentration of PFOS (0.01uM) reduced acoustic startle magnitude in adolescence, but not adulthood. These data suggest that PFOS and PFOA both produce neurobehavioral toxicity, but these effects are quite distinct from one another.
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Hawkey, Andrew B, Mikayla Mead, Sarabesh Natarajan, Anas Gondal, Olivia Jarrett and Edward D Levin (2023). Embryonic exposure to PFAS causes long-term, compound-specific behavioral alterations in zebrafish. Neurotoxicology and teratology, 97. p. 107165. 10.1016/j.ntt.2023.107165 Retrieved from https://hdl.handle.net/10161/29472.
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Edward Daniel Levin
Dr. Levin is Chief of the Neurobehavioral Research Lab in the Psychiatry Department of Duke University Medical Center. His primary academic appointment is as Professor in the Department of Psychiatry and Behavioral Sciences. He also has secondary appointments in the Department Pharmacology and Cancer Biology, the Department of Psychological and Brain Sciences and the Nicholas School of the Environment at Duke. His primary research effort is to understand basic neural interactions underlying cognitive function and addiction and to apply this knowledge to better understand cognitive dysfunction and addiction disorders and to develop novel therapeutic treatments.
The three main research components of his laboratory are focused on the themes of the basic neurobiology of cognition and addiction, neurobehavioral toxicology and the development of novel therapeutic treatments for cognitive dysfunction and substance abuse. Currently, our principal research focus concerns nicotine. We have documented the basic effects of nicotine on learning memory and attention as well as nicotine self-administration. We are continuing with more mechanistic studies in rat models using selective lesions, local infusions and neurotransmitter interaction studies. We have found that nicotine improves memory performance not only in normal rats, but also in rats with lesions of hippocampal and basal forebrain connections. We are concentrating on alpha7 and alpha4beta2 nicotinic receptor subtypes in the hippocampus, amygdala , thalamus and frontal cortex and how they interact with dopamine D1 and D2 and glutamate NMDA systems with regard to memory and addiction. I am also conducting studies on human cognitive behavior. We have current studies to assess nicotine effects on attention, memory and mental processing speed in schizophrenia, Alzheimer's Disease and Attention Deficit Hyperactivity Disorder. In the area of neurobehavioral toxicology, I have continuing projects to characterize the adverse effects of prenatal and adolescent nicotine exposure. Our primary project in neurobehavioral toxicology focuses on the cognitive deficits caused by the marine toxins. The basic and applied aims of our research complement each other nicely. The findings concerning neural mechanisms underlying cognitive function help direct the behavioral toxicology and therapeutic development studies, while the applied studies provide important functional information concerning the importance of the basic mechanisms under investigation.
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