Initial study on the possible mechanisms involved in the effects of high doses of perfluorooctane sulfonate (PFOS) on prolactin secretion

Salgado, Renato M.; Pereiro, Natividad; López-Doval, S.; Lafuente, A.

doi:10.1016/j.fct.2015.05.013

Cited by 17 publications

(7 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a study by Salgado et al (2015), adult male rats were treated with 3 or 6 mg PFOS/kg bw daily for 28 days. At the end of the treatment, the serum levels of prolactin and oestradiol were measured, as well as the concentrations of dopamine and its metabolites (DOPAC and HVA), and GABA in the anterior and mediobasal hypothalamus.…”

Section: Pfosmentioning

confidence: 99%

Risk to human health related to the presence of perfluorooctane sulfonic acid and perfluorooctanoic acid in food

Knutsen¹,

Alexander²,

Barregård³

et al. 2018

EFS2

189

199

View full text Add to dashboard Cite

The European Commission asked EFSA for a scientific evaluation on the risks to human health related to the presence of perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) in food. Regarding PFOS and PFOA occurrence, the final data set available for dietary exposure assessment contained a total of 20,019 analytical results (PFOS n = 10,191 and PFOA n = 9,828). There were large differences between upper and lower bound exposure due to analytical methods with insufficient sensitivity. The CONTAM Panel considered the lower bound estimates to be closer to true exposure levels. Important contributors to the lower bound mean chronic exposure were 'Fish and other seafood', 'Meat and meat products' and 'Eggs and egg products', for PFOS, and 'Milk and dairy products', 'Drinking water' and 'Fish and other seafood' for PFOA. PFOS and PFOA are readily absorbed in the gastrointestinal tract, excreted in urine and faeces, and do not undergo metabolism. Estimated human half-lives for PFOS and PFOA are about 5 years and 2-4 years, respectively. The derivation of a health-based guidance value was based on human epidemiological studies. For PFOS, the increase in serum total cholesterol in adults, and the decrease in antibody response at vaccination in children were identified as the critical effects. For PFOA, the increase in serum total cholesterol was the critical effect. Also reduced birth weight (for both compounds) and increased prevalence of high serum levels of the liver enzyme alanine aminotransferase (ALT) (for PFOA) were considered. After benchmark modelling of serum levels of PFOS and PFOA, and estimating the corresponding daily intakes, the CONTAM Panel established a tolerable weekly intake (TWI) of 13 ng/kg body weight (bw) per week for PFOS and 6 ng/kg bw per week for PFOA. For both compounds, exposure of a considerable proportion of the population exceeds the proposed TWIs.

show abstract

Section: Pfosmentioning

confidence: 99%

Risk to human health related to the presence of perfluorooctane sulfonic acid and perfluorooctanoic acid in food

Knutsen¹,

Alexander²,

Barregård³

et al. 2018

EFS2

189

199

View full text Add to dashboard Cite

show abstract

“…Multiple studies that evaluated PFOS exposure in adult rats reported highly reproducible increases in norepinephrine and increases in other monoamines such as dopamine and serotonin in the hypothalamus. ,,, The consistency of these results is likely because the studies were conducted in the same species and were dosed at the same life stage, the same brain region was sampled, and the same PFAS was used in all studies. The final notable alteration in the neurotransmitters was increased glutamate in the hippocampus of mice exposed to PFOS during adulthood or development. , Similar to the changes in neurotransmitters in the hypothalamus, the same species and PFAS were used in both studies.…”

Section: Pfas Effects On Neurotransmittersmentioning

confidence: 95%

“…There is growing evidence that PFOS, PFOA, and PFAS mixtures lead to changes in neurotransmitter levels, ,− alter neurotransmitter receptor and transporter expression and function, ,,,,,− and change neurotransmitter metabolism. ,− ,,,,,,,,,, Although the major focus for the evaluation of PFAS neurotoxicity has been on PFAS developmental neurotoxicity, ,,,− ,− ,,,,,,,,− PFAS exposure during both development and adulthood may change neurotransmitter levels in a brain region-specific manner (Table ). Lifelong exposure of humans to PFAS may result in dynamic changes in neurological function resulting from PFAS accumulation over time.…”

Section: Pfas Effects On Neurotransmittersmentioning

confidence: 99%

“…Recent studies have been evaluating metabolism-related mechanisms to explain PFAS-induced changes in neurotransmitter levels. The monoamine neurotransmitters include norepinephrine, dopamine, and serotonin and share metabolic enzymes and precursors. , There is evidence in the animal data that PFAS exposure changes monoamine metabolism. ,− ,,,,,,, Multiple studies demonstrated PFOS-treated male rats had decreased dopamine or serotonin turnover in the hypothalamus , and hippocampus . Studies that developmentally exposed northern leopard frog tadpoles to PFOS or PFOA found no changes in whole-brain serotonin levels or serotonin turnover. , This suggests that the effects of PFAS on monoamine metabolism may depend on the species and brain region.…”

Section: Pfas Effects On Neurotransmittersmentioning

confidence: 99%

“…Ongoing research has identified that the PFAS’s neurotoxic targets for neurotransmission alter neurotransmitter levels, ,− synaptic protein expression and function, ,,,,,− and calcium signaling. − ,,− This Review aims to critically analyze the state of PFAS neurotoxicity with focus on neurotransmission-related end points and to reveal PFAS’s potential targets of neurological disease that require epidemiological evaluation in the future. Recent reviews have broadly focused on brain accumulation and neurotoxicity. ,,− This critical analysis of the field focuses specifically on neurotransmission targets, which may underlie adverse neurological outcomes.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Neurotransmission Targets of Per- and Polyfluoroalkyl Substance Neurotoxicity: Mechanisms and Potential Implications for Adverse Neurological Outcomes

Brown-Leung

Cannon

2022

Chem. Res. Toxicol.

View full text Add to dashboard Cite

Per- and polyfluoroalkyl substances (PFAS) are a group of persistent environmental pollutants that are ubiquitously found in the environment and virtually in all living organisms, including humans. PFAS cross the blood–brain barrier and accumulate in the brain. Thus, PFAS are a likely risk for neurotoxicity. Studies that measured PFAS levels in the brains of humans, polar bears, and rats have demonstrated that some areas of the brain accumulate greater amounts of PFAS. Moreover, in humans, there is evidence that PFAS exposure is associated with attention-deficit/hyperactivity disorder (ADHD) in children and an increased cause of death from Parkinson’s disease and Alzheimer’s disease in elderly populations. Given possible links to neurological disease, critical analyses of possible mechanisms of neurotoxic action are necessary to advance the field. This paper critically reviews studies that investigated potential mechanistic causes for neurotoxicity including (1) a change in neurotransmitter levels, (2) dysfunction of synaptic calcium homeostasis, and (3) alteration of synaptic and neuronal protein expression and function. We found growing evidence that PFAS exposure causes neurotoxicity through the disruption of neurotransmission, particularly the dopamine and glutamate systems, which are implicated in age-related psychiatric illnesses and neurodegenerative diseases. Evaluated research has shown there are highly reproduced increased glutamate levels in the hippocampus and catecholamine levels in the hypothalamus and decreased dopamine in the whole brain after PFAS exposure. There are significant gaps in the literature relative to the assessment of the nigrostriatal system (striatum and ventral midbrain) among other regions associated with PFAS-associated neurologic dysfunction observed in humans. In conclusion, evidence suggests that PFAS may be neurotoxic and associated with chronic and age-related psychiatric illnesses and neurodegenerative diseases. Thus, it is imperative that future mechanistic studies assess the impact of PFAS and PFAS mixtures on the mechanism of neurotransmission and the consequential functional effects.

show abstract

PFAS: exploration of neurotoxicity and environmental impact

Nannaware,

Mayilswamy,

Kandasubramanian

2024

Environ Sci Pollut Res

View full text Add to dashboard Cite

Initial study on the possible mechanisms involved in the effects of high doses of perfluorooctane sulfonate (PFOS) on prolactin secretion

Cited by 17 publications

References 75 publications

Risk to human health related to the presence of perfluorooctane sulfonic acid and perfluorooctanoic acid in food

Risk to human health related to the presence of perfluorooctane sulfonic acid and perfluorooctanoic acid in food

Neurotransmission Targets of Per- and Polyfluoroalkyl Substance Neurotoxicity: Mechanisms and Potential Implications for Adverse Neurological Outcomes

PFAS: exploration of neurotoxicity and environmental impact

Contact Info

Product

Resources

About