Neonatal exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) causes neurobehavioural defects in adult mice

Johansson, Niclas; Fredriksson, Anders; Eriksson, Per

doi:10.1016/j.neuro.2007.10.008

Cited by 400 publications

(279 citation statements)

References 74 publications

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“…Rodent studies show that a NOAEL of 1 mg/kg/day and a LOAEL of 5 mg/kg/day for developmental toxicity (36). Johansson et al (37) reported that neonatal exposure (1.4 or 21 µmol/kg) of PFOS (∼1.4 or 21 µM) caused irreversible neurobehavioral defects such as reduced and/or lack of habituation and hyperactivity in adult mice. Our data demonstrated PFOS (10 µM and above) induced a robust augmentation of mPSC frequency ( Figure 1B), which may cause excessive excitability in neurons.…”

Section: Discussionmentioning

confidence: 99%

Acute Enhancement of Synaptic Transmission and Chronic Inhibition of Synaptogenesis Induced by Perfluorooctane Sulfonate through Mediation of Voltage-Dependent Calcium Channel

Liao

et al. 2008

Environ. Sci. Technol.

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Perfluorooctane sulfonate (PFOS) is a persistent and bioaccumulative pollutant ubiquitous in wildlife and humans. Although the distribution and fate of PFOS have been widely studied, its potential neurotoxicity remains largely unknown. In the present study, the acute and chronic effects of PFOS on the development and synaptic transmission of hippocampal neurons was examined. Perfusion with PFOS markedly increased the frequency of miniature postsynaptic currents (mPSCs) and slightly elevated the amplitude of mPSCs in cultured hippocampal neurons. Perfusion with PFOS also increased the amplitude of field excitatory postsynaptic potentials (fEPSPs) recorded in the CA1 region of hippocampal slices. Both of these effects were largely blocked by the L-type Ca 2+ channel antagonist nifedipine. Further studies showed that PFOS enhanced inward Ca 2+ currents and increased intracellular Ca 2+ in cultured neurons; these effects were also substantially inhibited by nifedipine. Moreover, prolonged treatment with PFOS moderately inhibited neurite growth and dramatically suppressed synaptogenesis in cultured neurons in a nifedipine-sensitive manner. Thus, through enhancement of Ca 2+ channels, PFOS may exhibit both acute excitotoxic effects on synaptic function and chronically inhibit synaptogenesis in the brain.

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Section: Discussionmentioning

confidence: 99%

Acute Enhancement of Synaptic Transmission and Chronic Inhibition of Synaptogenesis Induced by Perfluorooctane Sulfonate through Mediation of Voltage-Dependent Calcium Channel

Liao

et al. 2008

Environ. Sci. Technol.

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“…Recent studies on PFAAs in rodents have found that neonatal exposure to PFOS or PFOA can cause disruption to the central nervous system, resulting in abnormal development of motor neurons and significant changes in gene expression, including genes responsible for calcium signaling pathways, peroxisome proliferator-activated receptor signaling, cell communication, and the cell cycle [25]. Other symptoms included deranged spontaneous behavior, hyperactivity that worsened with age, changes in exploratory behavior, and reduced muscle strength in males [26]. The toxicity of these compounds has been examined in multiple studies, although the mechanisms behind these toxic effects are still poorly understood.…”

Section: Possible Toxicological Implicationsmentioning

confidence: 99%

“…In the brain, PFOS has been detected following laboratory animal exposure [25], demonstrating its ability to cross the BBB. Recent studies with rodents have found that neonatal exposure to PFOS or PFOA can cause disruption to the central nervous system, resulting in abnormal development of motor neurons and significant changes in gene expression [25,26]. Furthermore, in vitro PFOS and FOSA exposure in both differentiated and undifferentiated PC12 cells showed that both compounds were disruptive to DNA synthesis [27].…”

Section: Introductionmentioning

confidence: 99%

Brain region distribution and patterns of bioaccumulative perfluoroalkyl carboxylates and sulfonates in East Greenland polar bears (Ursus maritimus)

Greaves

Letcher

Sonne

et al. 2013

Enviro Toxic and Chemistry

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Abstract-The present study investigated the comparative accumulation of perfluoroalkyl acids (PFAAs) in eight brain regions of polar bears (Ursus maritimus, n ¼ 19) collected in 2006 from Scoresby Sound, East Greenland. The PFAAs studied were perfluoroalkyl carboxylates (PFCAs, C 6 -C 15 chain lengths) and sulfonates (C 4 , C 6 , C 8 , and C 10 chain lengths) as well as selected precursors including perfluorooctane sulfonamide. On a wet-weight basis, blood-brain barrier transport of PFAAs occurred for all brain regions, although inner regions of the brain closer to incoming blood flow (pons/medulla, thalamus, and hypothalamus) contained consistently higher PFAA concentrations compared to outer brain regions (cerebellum, striatum, and frontal, occipital, and temporal cortices). For pons/medulla, thalamus, and hypothalamus, the most concentrated PFAAs were perfluorooctane sulfonate (PFOS), ranging from 47 to 58 ng/g wet weight, and perfluorotridecanoic acid, ranging from 43 to 49 ng/g wet weight. However, PFOS and the longer-chain PFCAs (C 10 -C 15 ) were significantly (p < 0.002) positively correlated with lipid content for all brain regions. Lipid-normalized PFOS and PFCA (C 10 -C 15 ) concentrations were not significantly (p > 0.05) different among brain regions. The burden of the sum of PFCAs, perfluoroalkyl sulfonates, and perfluorooctane sulfonamide in the brain (average mass, 392 g) was estimated to be 46 mg. The present study demonstrates that both PFCAs and perfluoroalkyl sulfonates cross the blood-brain barrier in polar bears and that wet-weight concentrations are brain region-specific. Environ. Toxicol. Chem. 2013;32:713-722. # 2012 SETAC

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“…PFAAs can cause a number of toxic effects in the liver, immune system, and nervous system. They are especially toxic during development and reproduction and have induced cancer (Lau et al, 2007;Johansson et al, 2008). Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are the two primary PFAA components with C 8 chain lengths.…”

Section: Introductionmentioning

confidence: 99%

Induction of oxidative stress and related transcriptional effects of perfluorononanoic acid using an in vivo assessment

Yang

Liu²,

Ren

et al. 2014

Comparative Biochemistry and Physiology Part C: Toxicology &

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Neonatal exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) causes neurobehavioural defects in adult mice

Cited by 400 publications

References 74 publications

Acute Enhancement of Synaptic Transmission and Chronic Inhibition of Synaptogenesis Induced by Perfluorooctane Sulfonate through Mediation of Voltage-Dependent Calcium Channel

Acute Enhancement of Synaptic Transmission and Chronic Inhibition of Synaptogenesis Induced by Perfluorooctane Sulfonate through Mediation of Voltage-Dependent Calcium Channel

Brain region distribution and patterns of bioaccumulative perfluoroalkyl carboxylates and sulfonates in East Greenland polar bears (Ursus maritimus)

Induction of oxidative stress and related transcriptional effects of perfluorononanoic acid using an in vivo assessment

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