RESUMEN

Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant and accumulated in the liver of mammals. PFOS exposure is closely associated with the development of pyroptosis. Nevertheless, the underlying mechanism is unclear. We found here that PFOS induced pyroptosis in the mice liver and L-02 cells as demonstrated by activation of the NOD-like receptor protein 3 inflammasome, gasdermin D cleavage and increased release of interleukin-1ß and interleukin-18. The level of cytoplasmic calcium was accelerated in hepatocytes upon exposure to PFOS. The phosphorylated/activated form of calcium/calmodulin-dependent protein kinase II (CaMKII) was augmented by PFOS in vivo and in vitro. PFOS-induced pyroptosis was relieved by CaMKII inhibitor. Among various CaMKII subtypes, we identified that CaMKIIγ was activated specifically by PFOS. CaMKIIγ interacted with Smad family member 3 (Smad3) under PFOS exposure. PFOS increased the phosphorylation of Smad3, and CaMKII inhibitor or CaMKIIγ siRNA alleviated PFOS-caused phosphorylation of Smad3. Inhibiting Smad3 activity was found to alleviate PFOS-induced hepatocyte pyroptosis. This study puts forward that CaMKIIγ-Smad3 is the linkage between calcium homeostasis disturbance and pyroptosis, providing a mechanistic explanation for PFOS-induced pyroptosis.

RESUMEN

Perfluorooctane sulfonate (PFOS) is one of the most widely used perfluorinated compounds, and as an environmental endocrine disruptor and environmental persistent pollutant, the threat of PFOS to human health is of increasing concern. Exposure to PFOS has been shown to be closely associated with liver disease, but the intrinsic molecular targets and mechanisms of PFOS-induced liver damage are not well understood. This study was conducted to explore whether the Wnt/ß-Catenin signaling pathway and the endoplasmic reticulum stress signaling pathway are involved in damage of PFOS to the liver. In this study, we used the CCK-8 method to detect cell viability, a microscope and DAPI staining to observe cell morphology, flow cytometry to detect cell ROS and apoptosis levels; and Western blot to detect the expressions of proteins in the WNT/ß-Catenin, endoplasmic reticulum stress and apoptosis-related pathways. We found that PFOS activated WNT/ß-Catenin and endoplasmic reticulum stress-related pathways in L-02 cells and could lead to the development of oxidative stress and apoptosis. Our findings showed that PFOS could cause damage to L-02 cells, and the WNT/ß-Catenin signaling and endoplasmic reticulum stress pathways were involved in the changes caused by PFOS to L-02 cells, which provided a new theoretical basis for studying the hepatotoxicity and mechanism of PFOS. PFOS can lead to increased intracellular ROS levels, causing oxidative stress, endoplasmic reticulum stress and activation of the WNT/ß-catenin signaling pathway. Our experimental results showed that PFOS can cause damage to L-02 cells, and the WNT/ß-Catenin signaling pathway and endoplasmic reticulum stress pathway are involved in the process of damage caused by PFOS to L-02 cells.

RESUMEN

Microplastics (MPs) and perfluorooctane sulfonate (PFOS) are emerging pollutants that are ubiquitously present in the environment and can cause series of ecotoxicological effects on aquatic animals. This study examined how the expression of genes related to insulin growth factor (igf1, igf2a, igf2b, igfra, and igfrb) and growth hormone (ghrh, gh1, ghra, and ghrb) changes during the development of zebrafish embryos exposed to 8 µm polyethylene microplastics (PE-MPs) and perfluorooctane sulfonate (PFOS) individually and in combination for 72 h. Our findings revealed that both low-concentrations of MP (50 µg/L) and PFOS (0.02 µg/L) treatments could significantly activate gene expression within a short period. High concentrations of MPs (500 µg/L) and PFOS (0.1 µg/L) not only rapidly activated gene expression but also sustained high expression levels for a longer duration. During combined exposures, peak gene expression in the low concentration groups (50 µg/L MPs and 0.02 µg/L PFOS; 50 µg/L MPs and 0.1 µg/L PFOS) primarily occurred within 12 h after treatment. In the high concentration groups (500 µg/L MPs and 0.02 µg/L PFOS), peak expression was also observed within 12 h. Notably, the combined exposure groups exhibited more pronounced effects on gene expression than the individual exposure groups. The activation of gene expression was both more significant and longer-lasting in the combined exposure, indicating a synergistic regulatory effect of MPs and PFOS. Overall, our study suggests that zebrafish embryo development can be significantly impacted by exposure to MPs, PFOS, and their combination, with combined exposures having a more lasting and profound effect on gene regulation compared to single exposures.

Asunto(s)

Ácidos Alcanesulfónicos , Desarrollo Embrionario , Fluorocarburos , Microplásticos , Contaminantes Químicos del Agua , Pez Cebra , Animales , Fluorocarburos/toxicidad , Ácidos Alcanesulfónicos/toxicidad , Contaminantes Químicos del Agua/toxicidad , Desarrollo Embrionario/efectos de los fármacos , Microplásticos/toxicidad , Biomarcadores/metabolismo , Somatomedinas/metabolismo , Somatomedinas/genética , Hormona del Crecimiento/genética , Hormona del Crecimiento/metabolismo , Embrión no Mamífero/efectos de los fármacos , Expresión Génica/efectos de los fármacos

RESUMEN

Per- and polyfluoroalkyl substances (PFAS) are pervasive environmental pollutants frequently detected in drinking water worldwide. Reports linking PFAS exposure to cardiovascular disease have increased significantly in recent years. Furthermore, women appear to be more susceptible to the adverse effects of PFAS. However, the potential role of ovaries in the increased vulnerability of females to PFAS-related health effects remains unknown. In this study, we investigated the impact of perfluorooctane sulfonate (PFOS), a prominent PFAS, on the cardiovascular function in female rats with intact ovaries and ovariectomized (OVX) females. Bilateral OVX or sham surgeries were performed in 8-week-old female SD rats. Following recovery from surgeries, the rats were given drinking water containing 50 µg/mL of PFOS for 3 weeks. Control groups received PFOS-free water. PFOS exposure significantly reduced body weight but increased blood pressure similarly in both intact and OVX rats. Echocardiography analysis revealed that PFOS exposure decreased cardiac output, end-systolic volume, and end-diastolic volume in intact but not OVX rats. Vascular function studies demonstrated that PFOS equally reduced endothelium-dependent and -independent relaxation responses in intact and OVX rats. The endothelium-independent contractile responses were more pronounced in both intact and OVX rats. eNOS protein levels were similarly decreased in both intact and OVX rats. In conclusion, PFOS affects cardiac function through hormone-dependent mechanisms, while vascular function is impaired independent of ovarian status, indicating an intricate interplay between PFOS exposure, ovarian status, and cardiovascular function.

RESUMEN

Given environmental persistence, potential for bioaccumulation, and toxicity of Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), the scientific community has increasingly focused on researching their toxicology and degradation methods. This paper presents a survey of recent research advances in the toxicological effects and degradation methods of PFOA and PFOS. Their adverse effects on the liver, nervous system, male reproductive system, genetics, and development are detailed. Additionally, the degradation techniques of PFOA and PFOS, including photochemical, photocatalytic, and electrochemical methods, are analyzed and compared, highlighted the potential of these technologies for environmental remediation. The biotransformation pathways and mechanisms of PFOA and PFOS involving microorganisms, plants, and enzymes are also presented. As the primary green degradation pathway for PFOA and PFOS, Biodegradation uses specific microorganisms, plants or enzymes to remove PFOA and PFOS from the environment through redox reactions, enzyme catalysis and other pathways. Currently, there has been a paucity of research conducted on the biodegradation of PFOA and PFOS. However, this degradation technology is promising owing to its specificity, cost-effectiveness, and ease of implementation. Furthermore, novel materials/methods for PFOA and PFOS degradation are presented in this paper. These novel materials/methods effectively improve the degradation efficiency of PFOA and PFOS and provide new ideas and tools for the degradation of PFOA and PFOS. This information can assist researchers in identifying flaws and gaps in the field, which can facilitate the formulation of innovative research ideas.

Asunto(s)

Ácidos Alcanesulfónicos , Biodegradación Ambiental , Caprilatos , Fluorocarburos , Fluorocarburos/metabolismo , Caprilatos/metabolismo , Ácidos Alcanesulfónicos/metabolismo , Ácidos Alcanesulfónicos/toxicidad , Contaminantes Ambientales/metabolismo , Contaminantes Ambientales/toxicidad , Animales , Tecnología Química Verde/métodos

RESUMEN

As a persistent organic pollutant, perfluorooctane sulfonate (PFOS) has a serious detrimental impact on human health. It has been suggested that PFOS is associated with liver inflammation. However, the underlying mechanisms are still unclear. Here, PFOS was found to elevate the oligomerization tendency of voltage-dependent anion channel 1 (VDAC1) in the mice liver and human normal liver cells L-02. Inhibition of VDAC1 oligomerization alleviated PFOS-induced nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome activation. Cytoplasmic membrane VDAC1 translocated to mitochondria was also observed in response to PFOS. Therefore, the oligomerization of VDAC1 occurred mainly in the mitochondria. VDAC1 was found to interact with the ATP synthase beta subunit (ATP5B) under PFOS treatment. Knockdown of ATP5B or immobilization of ATP5B to the cytoplasmic membrane alleviated the increased VDAC1 oligomerization and NLRP3 inflammasome activation. Therefore, our results suggested that PFOS induced NLRP3 inflammasome activation through VDAC1 oligomerization, a process dependent on ATP5B to transfer VDAC1 from the plasma membrane to the mitochondria. The findings offer novel perspectives on the activation of the NLRP3 inflammasome, the regulatory mode on VDAC1 oligomerization, and the mechanism of PFOS toxicity.

Asunto(s)

Ácidos Alcanesulfónicos , Fluorocarburos , Inflamasomas , Proteína con Dominio Pirina 3 de la Familia NLR , Canal Aniónico 1 Dependiente del Voltaje , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/genética , Animales , Ácidos Alcanesulfónicos/toxicidad , Inflamasomas/metabolismo , Inflamasomas/efectos de los fármacos , Canal Aniónico 1 Dependiente del Voltaje/metabolismo , Canal Aniónico 1 Dependiente del Voltaje/genética , Fluorocarburos/toxicidad , Humanos , Ratones , ATPasas de Translocación de Protón Mitocondriales/metabolismo , Línea Celular , Ratones Endogámicos C57BL , Hígado/efectos de los fármacos , Hígado/metabolismo , Contaminantes Ambientales/toxicidad , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Hepatocitos/efectos de los fármacos , Hepatocitos/metabolismo

RESUMEN

The potential association between colorectal cancer (CRC) and environmental pollutants is worrisome. Previous studies have found that some perfluoroalkyl acids, including perfluorooctane sulfonate (PFOS), induced colorectal tumors in experimental animals and promoted the migration of and invasion by CRC cells in vitro, but the underlying mechanism is unclear. Here, we investigated the effects of PFOS on the proliferation and migration of CRC cells and the potential mechanisms involving activating the PI3K/Akt-NF-κB signal pathway and epithelial-mesenchymal transition (EMT). It was found that PFOS promoted the growth and migration of HCT116 cells at non-cytotoxic concentrations and increased the mRNA expression of the migration-related angiogenic cytokines vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8). In a mechanistic investigation, the up-stream signal pathway PI3K/Akt-NF-κB was activated by PFOS, and the process was suppressed by LY294002 (PI3K/Akt inhibitor) and BAY11-7082 (NF-κB inhibitor) respectively, leading to less proliferation of HCT116 cells. Furthermore, matrix metalloproteinases (MMP) and EMT-related markers were up-regulated after PFOS exposure, and were also suppressed respectively by LY294002 and BAY11-7082. Moreover, the up-regulation of EMT markers was suppressed by a MMP inhibitor GM6001. Taken together, our results indicated that PFOS promotes colorectal cancer cell migration and proliferation by activating the PI3K/Akt-NF-κB signal pathway and epithelial-mesenchymal transition. This could be a potential toxicological mechanism of PFOS-induced malignant development of colorectal cancer.

Asunto(s)

Ácidos Alcanesulfónicos , Movimiento Celular , Neoplasias Colorrectales , Transición Epitelial-Mesenquimal , Fluorocarburos , Fluorocarburos/toxicidad , Ácidos Alcanesulfónicos/toxicidad , Transición Epitelial-Mesenquimal/efectos de los fármacos , Neoplasias Colorrectales/patología , Humanos , Movimiento Celular/efectos de los fármacos , Fosfatidilinositol 3-Quinasas/metabolismo , Transducción de Señal/efectos de los fármacos , Contaminantes Ambientales/toxicidad , Células HCT116 , Proteínas Proto-Oncogénicas c-akt/metabolismo , FN-kappa B/metabolismo , Proliferación Celular/efectos de los fármacos , Línea Celular Tumoral

RESUMEN

Epidemic and animal studies have reported that perfluoroalkyl and polyfluoroalkyl substances (PFASs) are strongly associated with liver injury; however, to date, the effects of PFASs on the hepatic microenvironment remain largely unknown. In this study, we established perfluorooctane sulfonic acid (PFOS)-induced liver injury models by providing male and female C57BL/6 mice with water containing PFOS at varying doses for 4 weeks. Hematoxylin and eosin staining revealed that PFOS induced liver injury in both sexes. Elevated levels of serum aminotransferases including those of alanine aminotransferase and aspartate transaminase were detected in the serum of mice treated with PFOS. Female mice exhibited more severe liver injury than male mice. We collected the livers from female mice and performed single-cell RNA sequencing. In total, 36,529 cells were included and grouped into 10 major cell types: B cells, granulocytes, T cells, NK cells, monocytes, dendritic cells, macrophages, endothelial cells, fibroblasts, and hepatocytes. Osteoclast differentiation was upregulated and the T cell receptor signaling pathway was significantly downregulated in PFOS-treated livers. Further analyses revealed that among immune cell clusters in PFOS-treated livers, Tcf7+CD4+T cells were predominantly downregulated, whereas conventional dendritic cells and macrophages were upregulated. Among the fibroblast subpopulations, hepatic stellate cells were significantly enriched in PFOS-treated female mice. CellphoneDB analysis suggested that fibroblasts interact closely with endothelial cells. The major ligand-receptor pairs between fibroblasts and endothelial cells in PFOS-treated livers were Dpp4_Cxcl12, Ackr3_Cxcl12, and Flt1_complex_Vegfa. These genes are associated with directing cell migration and angiogenesis. Our study provides a general framework for understanding the microenvironment in the livers of female mice exposed to PFOS at the single-cell level.

Asunto(s)

Ácidos Alcanesulfónicos , Fluorocarburos , Ratones Endogámicos C57BL , Animales , Fluorocarburos/toxicidad , Ácidos Alcanesulfónicos/toxicidad , Femenino , Ratones , Masculino , Enfermedad Hepática Inducida por Sustancias y Drogas/genética , Transcriptoma/efectos de los fármacos , Hígado/efectos de los fármacos , Análisis de la Célula Individual , Contaminantes Ambientales/toxicidad

RESUMEN

The incidence of nonalcoholic steatohepatitis (NASH) is related with perfluorooctane sulfonate (PFOS), yet the mechanism remains ill-defined. Mounting evidence suggests that ferroptosis plays a crucial role in the initiation of NASH. In this study, we used mice and human hepatocytes L-02 to investigate the role of ferroptosis in PFOS-induced NASH and the effect and molecular mechanism of PFOS on liver ferroptosis. We found here that PFOS caused NASH in mice, and lipid accumulation and inflammatory response in the L-02 cells. PFOS induced hepatic ferroptosis in vivo and in vitro, as evidenced by the decrease in glutathione peroxidase 4 (GPX4), and the increases in cytosolic iron, acyl-CoA synthetase long-chain family member 4 (ACSL4) and lipid peroxidation. In the PFOS-treated cells, the increases in the inflammatory factors and lipid contents were reversed by ferroptosis inhibitor. PFOS-induced ferroptosis was relieved by autophagy inhibitor. The expression of mitochondrial calcium uniporter (MCU) was accelerated by PFOS, leading to subsequent mitochondrial calcium accumulation, and inhibiting autophagy reversed the increase in MCU. Inhibiting mitochondrial calcium reversed the variations in GPX4 and cytosolic iron, without influencing the change in ACSL4, induced by PFOS. MCU interacted with ACSL4 and the siRNA against MCU reversed the changes in ACSL4，GPX4 and cytosolic iron systemically. This study put forward the involvement of hepatic ferroptosis in PFOS-induced NASH and identified MCU as the mediator of the autophagy-dependent ferroptosis.

Asunto(s)

Ácidos Alcanesulfónicos , Autofagia , Calcio , Coenzima A Ligasas , Ferroptosis , Fluorocarburos , Enfermedad del Hígado Graso no Alcohólico , Ferroptosis/efectos de los fármacos , Fluorocarburos/toxicidad , Animales , Ácidos Alcanesulfónicos/toxicidad , Ratones , Enfermedad del Hígado Graso no Alcohólico/inducido químicamente , Enfermedad del Hígado Graso no Alcohólico/patología , Autofagia/efectos de los fármacos , Coenzima A Ligasas/metabolismo , Humanos , Calcio/metabolismo , Canales de Calcio/metabolismo , Masculino , Ratones Endogámicos C57BL , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Línea Celular , Hepatocitos/efectos de los fármacos

RESUMEN

Perfluorooctane sulfonate (PFOS) is a pervasive organic toxicant that damages body organs, including heart. Isosakuranetin (ISN) is a plant-based flavonoid that exhibits a broad range of pharmacological potentials. The current investigation was conducted to evaluate the potential role of ISN to counteract PFOS-induced cardiac damage in rats. Twenty-four albino rats (Rattus norvegicus) were distributed into four groups, including control, PFOS (10 mg/kg) intoxicated, PFOS + ISN (10 mg/kg + 20 mg/kg) treated, and ISN (20 mg/kg) alone supplemented group. It was revealed that PFOS intoxication reduced the expressions of Nrf-2 and its antioxidant genes while escalating the expression of Keap-1. Furthermore, PFOS exposure reduced the activities of glutathione reductase (GSR), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), Heme oxygenase-1 (HO-1) and glutathione (GSH) contents while upregulating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Besides, PFOS administration upregulated the levels of creatine kinase-MB (CK-MB), troponin I, creatine phosphokinase (CPK), and lactate dehydrogenase (LDH). Moreover, the levels of tumor necrosis factor-alpha (TNF-α), nuclear factor kappa-B (NF-κB), interleukin-6 (IL-6), and interleukin-1ß (IL-1ß) were increased after PFOS intoxication. Additionally, PFOS exposure downregulated the expression of Bcl-2 while upregulating the expressions of Bax and Caspase-3. Furthermore, PFOS administration disrupted the normal architecture of cardiac tissues. Nonetheless, ISN treatment remarkably protected the cardiac tissues via regulating aforementioned dysregulations owing to its antioxidative, anti-inflammatory, and antiapoptotic properties.

Asunto(s)

Ácidos Alcanesulfónicos , Apoptosis , Fluorocarburos , Proteína 1 Asociada A ECH Tipo Kelch , Factor 2 Relacionado con NF-E2 , Animales , Ratas , Ácidos Alcanesulfónicos/farmacología , Ácidos Alcanesulfónicos/toxicidad , Apoptosis/efectos de los fármacos , Factor 2 Relacionado con NF-E2/metabolismo , Fluorocarburos/farmacología , Proteína 1 Asociada A ECH Tipo Kelch/metabolismo , Masculino , Inflamación/tratamiento farmacológico , Inflamación/metabolismo , Inflamación/inducido químicamente , Inflamación/patología , Flavonas/farmacología

RESUMEN

The European honey bee (Apis mellifera) is an important crop pollinator threatened by multiple stressors, including exposure to contaminants. Perfluorooctane sulfonate (PFOS) is a persistent global contaminant that accumulates and biomagnifies in food chains and is detected in honey. Even sublethal exposure to PFOS is detrimental to bee health, but exposure routes are unclear and nothing is known about bee response (detection, avoidance, or attraction) to PFOS. Using Y-mazes, we studied the response of individual bees to PFOS-spiked sugar syrup at four concentrations, 0.02, 30, 61 and 103 µg L-1. Bee activity, choice behavior, and drink duration for unspiked and spiked sugar syrup was recorded for 10 min in the Y-maze system. Most bees (≥80%) tasted and then drank the sugar syrup solutions, including the PFOS-contaminated syrup. Only at 61 and 103 µg L-1 did bees significantly avoid drinking PFOS-spiked syrup, and only when given a choice with unspiked syrup. When the choice of consuming unspiked syrup was removed, the bees drank PFOS-spiked syrup at all the PFOS concentrations tested, and avoidance was not evident. Avoidance was not observed in any treatment at 0.02 or 30 µg L-1 PFOS, concentrations that are frequently reported in environmental waters in contaminated areas. These findings confirm that bees will access PFOS-contaminated resources at concentrations detrimental to the colony health, and provide evidence of potential exposure pathways that may threaten crop pollination services and also human health via food chain transfer in PFOS-contaminated areas. Environ Toxicol Chem 2024;43:1638-1647. © 2024 SETAC.

Asunto(s)

Ácidos Alcanesulfónicos , Fluorocarburos , Abejas/efectos de los fármacos , Fluorocarburos/toxicidad , Fluorocarburos/análisis , Ácidos Alcanesulfónicos/toxicidad , Animales , Contaminantes Ambientales/toxicidad , Contaminantes Ambientales/análisis , Conducta Animal/efectos de los fármacos

RESUMEN

Perfluorooctane sulfonate (PFOS), an officially listed persistent organic pollutant, is a widely distributed perfluoroalkyl substance. Epidemiological studies have shown that PFOS is intimately linked to the occurrence of insulin resistance (IR). However, the detailed mechanism remains obscure. In previous studies, we found that mitochondrial calcium overload was concerned with hepatic IR induced by PFOS. In this study, we found that PFOS exposure noticeably raised lysosomal calcium in L-02 hepatocytes from 0.5 h. In the PFOS-cultured L-02 cells, inhibiting autophagy alleviated lysosomal calcium overload. Inhibition of mitochondrial calcium uptake aggravated the accumulation of lysosomal calcium, while inhibition of lysosomal calcium outflowing reversed PFOS-induced mitochondrial calcium overload and IR. Transient receptor potential mucolipin 1 (TRPML1), the calcium output channel of lysosomes, interacted with voltage-dependent anion channel 1 (VDAC1), the calcium intake channel of mitochondria, in the PFOS-cultured cells. Moreover, we found that ATP synthase F1 subunit beta (ATP5B) interacted with TRPML1 and VDAC1 in the L-02 cells and the liver of mice under PFOS exposure. Inhibiting ATP5B expression or restraining the ATP5B on the plasma membrane reduced the interplay between TRPML1 and VDAC1, reversed the mitochondrial calcium overload and deteriorated the lysosomal calcium accumulation in the PFOS-cultured cells. Our research unveils the molecular regulation of the calcium crosstalk between lysosomes and mitochondria, and explains PFOS-induced IR in the context of activated autophagy.

Asunto(s)

Ácidos Alcanesulfónicos , Autofagia , Calcio , Fluorocarburos , Resistencia a la Insulina , Hígado , Lisosomas , Mitocondrias , ATPasas de Translocación de Protón Mitocondriales , Ácidos Alcanesulfónicos/toxicidad , Fluorocarburos/toxicidad , Animales , Lisosomas/efectos de los fármacos , Lisosomas/metabolismo , Autofagia/efectos de los fármacos , Calcio/metabolismo , Ratones , ATPasas de Translocación de Protón Mitocondriales/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Masculino , Canal Aniónico 1 Dependiente del Voltaje/metabolismo , Línea Celular , Hepatocitos/efectos de los fármacos , Hepatocitos/metabolismo , Contaminantes Ambientales/toxicidad , Canales Catiónicos TRPM/metabolismo , Ratones Endogámicos C57BL

RESUMEN

BACKGROUND: Endocrine disruptors (EDs) have emerged as potential contributors to the development of type-2 diabetes. Perfluorooctane sulfonate (PFOS), is one of these EDs linked with chronic diseases and gathered attention due to its widespread in food. OBJECTIVE: To assess at baseline and after 1-year of follow-up associations between estimated dietary intake (DI) of PFOS, and glucose homeostasis parameters and body-mass-index (BMI) in a senior population of 4600 non-diabetic participants from the PREDIMED-plus study. METHODS: Multivariable linear regression models were conducted to assess associations between baseline PFOS-DI at lower bound (LB) and upper bound (UB) established by the EFSA, glucose homeostasis parameters and BMI. RESULTS: Compared to those in the lowest tertile, participants in the highest tertile of baseline PFOS-DI in LB and UB showed higher levels of HbA1c [ß-coefficient(CI)] [0.01 %(0.002 to 0.026), and [0.06 mg/dL(0.026 to 0.087), both p-trend ≤ 0.001], and fasting plasma glucose in the LB PFOS-DI [1.05 mg/dL(0.050 to 2.046),p-trend = 0.022]. Prospectively, a positive association between LB of PFOS-DI and BMI [0.06 kg/m2(0.014 to 0.106) per 1-SD increment of energy-adjusted PFOS-DI was shown. Participants in the top tertile showed an increase in HOMA-IR [0.06(0.016 to 0.097), p-trend = 0.005] compared to participants in the reference tertile after 1-year of follow-up. DISCUSSION: This is the first study to explore the association between DI of PFOS and glucose homeostasis. In this study, a high baseline DI of PFOS was associated with a higher levels of fasting plasma glucose and HbA1c and with an increase in HOMA-IR and BMI after 1-year of follow-up.

Asunto(s)

Ácidos Alcanesulfónicos , Glucemia , Fluorocarburos , Homeostasis , Ácidos Alcanesulfónicos/sangre , Humanos , Fluorocarburos/sangre , Masculino , Femenino , Anciano , Glucemia/análisis , Persona de Mediana Edad , Índice de Masa Corporal , Diabetes Mellitus Tipo 2 , Disruptores Endocrinos , Dieta/estadística & datos numéricos , Anciano de 80 o más Años , Estudios Prospectivos , Contaminantes Ambientales/sangre

RESUMEN

Perfluorooctane sulfonate (PFOS) is a persistent chemical that has long been a threat to human health. However, the molecular effects of PFOS on various organs are not well studied. In this study, male Sprague-Dawley rats were treated with various doses of PFOS through gavage for 21 days. Subsequently, the liver, lung, heart, kidney, pancreas, testis, and serum of the rats were harvested for lipid analysis. We applied a focusing lipidomic analytical strategy to identify key lipid responses of phosphorylcholine-containing lipids, including phosphatidylcholines and sphingomyelins. Partial least squares discriminant analysis revealed that the organs most influenced by PFOS exposure were the liver, kidney, and testis. Changes in the lipid profiles of the rats indicated that after exposure, levels of diacyl-phosphatidylcholines and 22:6-containing phosphatidylcholines in the liver, kidney, and testis of the rats decreased, whereas the level of 20:3-containing phosphatidylcholines increased. Furthermore, levels of polyunsaturated fatty acids-containing plasmenylcholines decreased. Changes in sphingomyelin levels indicated organ-dependent responses. Decreased levels of sphingomyelins in the liver, nonmonotonic dose responses in the kidney, and irregular responses in the testis after PFOS exposure are observed. These lipid responses may be associated with alterations pertaining to phosphatidylcholine synthesis, fatty acid metabolism, membrane properties, and oxidative stress in the liver, kidney, and testis. Lipid responses in the liver could have contributed to the observed increase in liver to body weight ratios. The findings suggest potential toxicity and possible mechanisms associated with PFOS in multiple organs.

Asunto(s)

Ácidos Alcanesulfónicos , Fluorocarburos , Riñón , Hígado , Ratas Sprague-Dawley , Testículo , Animales , Ácidos Alcanesulfónicos/toxicidad , Fluorocarburos/toxicidad , Masculino , Ratas , Hígado/efectos de los fármacos , Hígado/metabolismo , Riñón/efectos de los fármacos , Riñón/metabolismo , Testículo/efectos de los fármacos , Testículo/metabolismo , Contaminantes Ambientales/toxicidad , Esfingomielinas , Fosfatidilcolinas , Metabolismo de los Lípidos/efectos de los fármacos , Lipidómica , Pulmón/efectos de los fármacos , Pulmón/metabolismo

RESUMEN

UV/Fe3+ and persulfate are two promising advanced oxidative degradation systems for in situ remediation of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), yet a lack of comprehensive understanding of the degradation mechanisms. For the first time, we used density functional theory (DFT) to calculate the entire reaction pathways of the degradation of PFOA/PFOS in water by UV/Fe3+ and persulfate. In addition, we have deeply explored the different attack pathways driven by •OH and SO4-•, and found that SO4-• determines PFOA/PFOS to obtain PFOA/PFOS free radicals through single electron transfer to initiate the degradation reaction, while •OH determines the speed of PFOA/PFOS degradation reaction. Both degradation reactions were thermodynamically advantageous and kinetically feasible under calculated conditions. Based on the thermodynamic data, persulfate was found to be more favorable for the advanced oxidative degradation of Perfluorinated compounds (PFCs). Moreover, for SO4-• and •OH co-existing in the persulfate system, pH will affect the presence and concentration of these two types of free radicals, and low pH is not necessary for the degradation of PFOA/PFOS in the persulfate system. These results can considerably advance our understanding of the PFOA/PFOS degradation process in advanced oxidation processes (AOPs), which is driven by •OH and SO4-•. This study provides a DFT calculation process for the mechanism calculation of advanced oxidation degradation of other types of PFCs pollutants, hoping to elucidate the future development of PFCs removal. Further research should focus on determining the advanced oxidation degradation pathways of other types of PFCs, to support the development of computational studies on the advanced oxidation degradation of PFCs.

Asunto(s)

Ácidos Alcanesulfónicos , Caprilatos , Fluorocarburos , Oxidación-Reducción , Contaminantes Químicos del Agua , Fluorocarburos/química , Caprilatos/química , Cinética , Contaminantes Químicos del Agua/química , Ácidos Alcanesulfónicos/química , Rayos Ultravioleta , Sulfatos/química , Teoría Funcional de la Densidad , Termodinámica , Restauración y Remediación Ambiental/métodos , Hierro/química

RESUMEN

Per- and polyfluoroalkyl substances (PFAS) are persistent, bioaccumulative, and toxic synthetic chemicals of concern, which have been detected in nearly all environmental compartments. The present study provides a data analysis on PFAS concentrations in the Dutch inland and coastal national waters and fish sampled from 2008 to 2022 and 2015 to 2022, respectively. Although the fish database is relatively small, the water database is unique because of its temporal dimension. It appears that PFAS are omnipresent in Dutch water and fish, with relatively small spatial differences in absolute and relative concentrations (fingerprints) and few obvious temporal trends. Only perfluorooctanoic acid and perfluorooctanesulfonic acid (PFOS) aqueous concentrations in the rivers Rhine and Scheldt have substantially decreased since 2012. Still, PFOS concentrations exceed the European water quality standards at all and fish standards at many locations. Masses of PFAS entering the country and the North Sea are roughly 3.5 tonnes/year. Generally, the data suggest that most PFAS enter the Dutch aquatic environment predominantly through diffuse sources, yet several major point sources of specific PFAS were identified using fingerprints and monthly concentration profiles as identification tools. Finally, combining concentrations in fish and water, 265 bioaccumulation factors were derived, showing no statistically significant differences between freshwater and marine fish. Overall, the analysis provides new insights into PFAS bioaccumulation and spatiotemporal trends, mass discharges, and sources in The Netherlands. Environ Toxicol Chem 2024;43:965-975. © 2024 The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC.

Asunto(s)

Monitoreo del Ambiente , Peces , Fluorocarburos , Contaminantes Químicos del Agua , Países Bajos , Contaminantes Químicos del Agua/metabolismo , Contaminantes Químicos del Agua/análisis , Fluorocarburos/metabolismo , Fluorocarburos/análisis , Peces/metabolismo , Animales , Ácidos Alcanesulfónicos/análisis , Ácidos Alcanesulfónicos/metabolismo , Bioacumulación , Ríos/química , Caprilatos/metabolismo

RESUMEN

Perfluorooctane sulfonate (PFOS) exerts adverse effects on neuronal development in young population. Limited evidences have shown that early-life PFOS exposure holds a potential risk for developing age-related neurodegenerative diseases such as Alzheimer's disease later in life. The present study investigated the effects of lactational PFOS exposure on cognitive function using one-year-old mice. Dams were exposed to PFOS (1 mg/kg body weight) through lactation by gavage. Male offspring were used for the behavior test battery to assess cognitive function. Western blot analysis was conducted to measure the levels of proteins related to the pathogenesis of Alzheimer's disease. PFOS-exposed mice displayed a mild deficiency in social recognition. In the hippocampus, the expression of tau protein was significantly increased. These results underline a mild effect of developing PFOS exposure on cognitive function and neurodegeneration. The present study presents the long-lasting effects of PFOS in middle-aged period and warrants a potential aftermath.

Asunto(s)

Ácidos Alcanesulfónicos , Enfermedad de Alzheimer , Fluorocarburos , Masculino , Femenino , Animales , Ratones , Lactancia , Fluorocarburos/toxicidad , Hipocampo

RESUMEN

Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are persistent anthropogenic chemicals that are widely distributed in the environment and pose significant risks to human health. Foam fractionation has emerged as a promising method to recover PFOS/PFOA from water. However, PFOS/PFOA concentrations in wastewater are often inadequate to generate stable foams due to their high critical micelle concentrations and the addition of a cosurfactant is necessary. In this study, we developed whey soy protein (WSP) as a green frother and collector derived from soybean meal (SBM), which is an abundant and cost-effective agro-industrial residue. WSP exhibited excellent foaming properties across a wide pH range and demonstrated strong collection capabilities that enhanced the recovery of PFOS/PFOA. The mechanism underlying this collection ability was elucidated through various methods, revealing the involvement of electrostatic attraction, hydrophobic interaction, and hydrogen bonding. Furthermore, we designed a double plate internal to improve the enrichment of PFOS/PFOA by approximately 2.3 times while reducing water recovery. Under suitable conditions (WSP concentration: 300 mg/L, pH: 6.0, air flowrate: 300 mL/min), we achieved high recovery percentages of 94-98% and enrichment ratios of 7.5-12.8 for PFOS/PFOA concentrations ranging from 5 to 20 mg/L. This foam fractionation process holds great promise for the treatment of PFOS/PFOA and other per- and polyfluoroalkyl substances.

Asunto(s)

Ácidos Alcanesulfónicos , Fluorocarburos , Contaminantes Químicos del Agua , Humanos , Agua , Proteínas de Soja , Suero Lácteo/química , Proteína de Suero de Leche , Fluorocarburos/análisis , Caprilatos/análisis , Ácidos Alcanesulfónicos/análisis , Contaminantes Químicos del Agua/análisis

RESUMEN

The perfluoalkyl substance (PFASs) perfluorooctane sulfonate (PFOS) has been widely used in industry. However, PFOS is a persistent organic pollutant and has been gradually replaced by its short-chain analogs, perfluorohexane sulfonate (PFHxS) and perfluorobutane sulfonate (PFBS). PFASs are extremely persistent and are very frequently detected among the general population. The aim of the study was to determine the effect of selected PFASs on peripheral blood mononuclear cells (PBMCs) and the mechanisms of their action. PBMCs were exposed to PFOS, PFBS and PFHxS at concentrations ranging from 0.02 to 400 µM for 24 h, they were then tested for viability, apoptosis (changes in cytosolic calcium ions level and caspase-3, -8 and -9 activation), ferroptosis (changes in chelatable iron ions level and lipid peroxidation), and autophagy (LC3-II and Raptor level assay). PFOS exposure decreased cell viability, increased calcium ion level and caspase-8 activation; it also enhanced lipid peroxidation and increased the intracellular pool of chelatable iron ions as well as LC3-II protein content. In contrast, short-chain PFBS and PFHxS induced significant changes in the markers of apoptosis but had no substantial impact on ferroptosis or autophagy markers over a wide range of concentrations. Our results indicate that only PFOS demonstrated pro-ferroptotic and pro-autophagic potential but observed changes occurred at relatively high exposure. A short-chain substitute (PFBS) exhibited strong pro-apoptotic potential at concentrations related to occupational exposure. While the short-chain PFASs strongly affected the mitochondrial pathway of apoptosis, apoptosis itself was only induced by PFBS via the intrinsic and extrinsic pathways. It seems that the length of the carbon chain in PFASs appears to determine the cell death mechanisms activated in human PBMCs following exposure. Our findings provide a new insight into the immune toxicity mechanism induced by these compounds.

Asunto(s)

Ácidos Alcanesulfónicos , Fluorocarburos , Ácidos Sulfónicos , Humanos , Calcio , Leucocitos Mononucleares , Ácidos Alcanesulfónicos/toxicidad , Ácidos Alcanesulfónicos/metabolismo , Fluorocarburos/toxicidad , Fluorocarburos/metabolismo , Alcanosulfonatos , Apoptosis , Iones , Hierro

RESUMEN

Microplastics (MPs) and Perfluorooctane sulfonate (PFOS) are two hard-biodegradable pollutants widely existing in the waste streams treated by anaerobic digestion. However, their synergistic effect on methanogenic metabolism is still unknown. This study investigated the impact of polyethylene terephthalate (PET) MPs alone and co-existing with PFOS on CO2 conversion to CH4 in a thermophilic biogas upgrading system. The results showed that either PET MPs addition alone or coexisting with PFOS improved the ultimate CH4 percentage and increased CO2 utilization rate. When Fe0 was added into the reactors with PET to enhance the interspecies electron transfer, a potential defluorination was observed with a defluorination rate of 15.88 ± 1.53%. Exposure of the reactor to PFOS of 300 µg/L could change the methanogenic pathway, resulting in a newly emerged Methanomassiliicoccus with dominance of 16%. Furthermore, under the exposure of PFOS, the number of predicted genes regulating enzymes in methanogenic steps from CO2 increased. These results suggest that the co-existence of PET MPs and PFOS will not inhibit the activity of hydrotrophic methanogenes, and a portion of PFOS may be biodegraded during the methanogenesis under Fe0 regulation.

Asunto(s)

Ácidos Alcanesulfónicos , Euryarchaeota , Fluorocarburos , Microplásticos , Microplásticos/toxicidad , Plásticos , Biocombustibles , Tereftalatos Polietilenos , Dióxido de Carbono/metabolismo , Euryarchaeota/metabolismo