Carcinogenic potency of perfluorooctane sulfonate (PFOS) on Syrian hamster embryo (SHE) cells

Jacquet, N.; Maire, Marie-Aline; Landkocz, Yann; Vasseur, Paule

doi:10.1007/s00204-011-0752-8

Cited by 36 publications

(21 citation statements)

References 38 publications

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“…Therefore, in the current study we attempted to investigate the consequences of a possible imbalance in the expression of PPARs caused by PFOS during early development. Interestingly, in contrast to previous in vitro studies showing activation of PPARα in kidney Cos-1 cells (Shipley et al, 2004) or PPARβ/δ in Syrian hamster embryo cells after exposure to PFOS (Jacquet et al, 2011), we found no changes in the expression of these two receptor isoforms. Instead, we detected a significant upregulation of PPARγ mRNA after exposure to 50 nM PFOS.…”

Section: Discussioncontrasting

confidence: 99%

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Perfluorooctane sulfonate induces neuronal and oligodendrocytic differentiation in neural stem cells and alters the expression of PPARγ in vitro and in vivo

Ibrahim

Tofighi

Onishchenko

et al. 2013

Toxicology and Applied Pharmacology

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Perfluorinated compounds are ubiquitous chemicals of major concern for their potential adverse effects on the human population. We have used primary rat embryonic neural stem cells (NSCs) to study the effects of perfluorooctane sulfonate (PFOS) on the process of NSC spontaneous differentiation. Upon removal of basic fibroblast growth factor, NSCs were exposed to nanomolar concentrations of PFOS for 48 h, and then allowed to differentiate for additional 5 days. Exposure to 25 or 50 nM concentration resulted in a lower number of proliferating cells and a higher number of neurite-bearing TuJ1-positive cells, indicating an increase in neuronal differentiation. Exposure to 50 nM also significantly increased the number of CNPase-positive cells, pointing to facilitation of oligodendrocytic differentiation. PPAR genes have been shown to be involved in PFOS toxicity. By q-PCR we detected an upregulation of PPARγ with no changes in PPARα or PPARδ genes. One of the downstream targets of PPARs, the mitochondrial uncoupling protein 2 (UCP2) was also upregulated. The number of TuJ1- and CNPase-positive cells increased after exposure to PPARγ agonist rosiglitazone (RGZ, 3 μM) and decreased after pre-incubation with the PPARγ antagonist GW9662 (5 μM). RGZ also upregulated the expression of PPARγ and UCP2 genes. Meanwhile GW9662 abolished the UCP2 upregulation and decreased Ca²⁺ activity induced by PFOS. Interestingly, a significantly higher expression of PPARγ and UCP3 genes was also detected in mouse neonatal brain after prenatal exposure to PFOS. These data suggest that PPARγ plays a role in the alteration of spontaneous differentiation of NSCs induced by nanomolar concentrations of PFOS.

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Section: Discussioncontrasting

confidence: 99%

“…Slotkin et al (2008) reported that PFOS influences differentiation of PC12 cells. Exposure of Syrian hamster embryo cells revealed the transforming potential of PFOS in parallel with an increased expression of peroxisome proliferator-activated receptor (PPAR) genes (Jacquet et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Perfluorooctane sulfonate induces neuronal and oligodendrocytic differentiation in neural stem cells and alters the expression of PPARγ in vitro and in vivo

Ibrahim

Tofighi

Onishchenko

et al. 2013

Toxicology and Applied Pharmacology

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“…No genotoxicity in SHE cells was seen via the COMET assay, nor was DNA breakage increased in benzo-α-pyrene initiated cells. The data reported herein and that reported by Jacquet et al [38] demonstrate a lack of cell transformation potential in vitro to be associated with PFOA.…”

Section: Discussionsupporting

confidence: 73%

Evaluation of perfluorooctanoate for potential genotoxicity

Butenhoff

Kennedy

Jung³

et al. 2014

Toxicology Reports

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Perfluorooctanoate (PFOA) is a fully fluorinated eight-carbon fatty acid analog with exceptional stability toward degradation that has been used as an industrial surfactant and has been detected in environmental and biological matrices. Exposures to PFOA in the workplace and in the environment have continuously stimulated investigations into its potential human health hazards. In this article, the results of fifteen unpublished genotoxicity assays conducted with perfluorooctanoate (as either the linear or linear/branched ammonium salt (APFO) or the linear/branched sodium salt) are reported and include: seven mutation assays (three in vitro reverse mutation assays with histidine auxotrophic strains of Salmonella typhimurium, two in vitro reverse mutation assays with the tryptophan auxotrophic Escherichia coli WP2uvr strain, one in vitro mitotic recombination (gene conversion) assay with Saccharomyces cerevisiae D4, and an in vitro Chinese hamster ovary (CHO) HGPRT forward mutation assay); seven studies to assess potential for chromosomal damage (three in vitro CHO chromosomal aberration studies, an in vitro human whole blood lymphocyte chromosomal aberration study, and three in vivo mouse micronucleus assays); and an in vitro C3H 10T1/2 cell transformation assay. Although PFOA has not been demonstrated to be metabolized, all in vitro assays were conducted both in the presence and in the absence of a mammalian hepatic microsomal activation system. These assays were originally described in twelve contract laboratory reports which have been available via the United States Environmental Protection Agency public docket (Administrative Record 226) for over a decade; however, the details of these assays have not been published previously in the open scientific literature. With the exception of limited positive findings at high and cytotoxic concentrations in some assay trials which reflected the likely consequence of cytotoxic disruption of normal cellular processes and not a specific genotoxic effect, the results of the studies presented in this paper and other published results clearly demonstrate the absence of direct mutagenic or genotoxic risk associated with PFOA. This finding is consistent with the physical/chemical characteristics of PFOA and is supported by other published genotoxicity studies.

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“…PFOS increased mutation frequencies at redBA/gam gene loci in gpt delta transgenic mouse embryonic fibroblasts (Wang et al., ). PFOS failed to induce DNA strand breaks in SHE cells (Jacquet et al., ) and DNA strand breaks or micronuclei in human HepG2 cells (Eriksen et al., ; Florentin et al., ). In another HepG2 study, concomitantly with increased ROS production, a non‐dose‐dependent increase in strand breaks was observed (Wielsøe et al., ).…”

Section: Assessmentmentioning

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

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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.

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Carcinogenic potency of perfluorooctane sulfonate (PFOS) on Syrian hamster embryo (SHE) cells

Cited by 36 publications

References 38 publications

Perfluorooctane sulfonate induces neuronal and oligodendrocytic differentiation in neural stem cells and alters the expression of PPARγ in vitro and in vivo

Perfluorooctane sulfonate induces neuronal and oligodendrocytic differentiation in neural stem cells and alters the expression of PPARγ in vitro and in vivo

Evaluation of perfluorooctanoate for potential genotoxicity

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

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