-
[show abstract]
[hide abstract]
ABSTRACT: The anoxic-oxic (A/O) process has been extensively applied for simultaneous removal of organic contaminants and nitrogen in wastewater treatment. However, very little is known about its ability to remove toxic materials. Municipal wastewater contains various kinds of pollutants, some of which have recalcitrant genotoxicity and may cause potential threat to environment, and even can lead to extinction of many species. In this study, we have selected three municipal wastewater treatment plants (WWTPs) employing anoxic-oxic (A/O) process to evaluate their ability to remove acute toxicity and genotoxicity of wastewater. Mortality rate of zebrafish (Danio rerio) was used to evaluate acute toxicity, while micronucleus (MN) and comet assays were used to detect genotoxicity. Results showed that in this process the acute toxicity was completely removed as the treatment proceeded along with decrease in chemical oxygen demand (COD) (<50mgL(-1)) in the effluent. However, in these treatment processes the genotoxicity was not significantly reduced, but an increase in genotoxicity was observed. Both MN and comet assays showed similar results. The eliminated effluent may pose genotoxic threaten although its COD level has met the Chinese Sewage Discharge Standard. This study suggests that further treatment of the wastewater is required after the A/O process to remove the genotoxicity and minimize the ecotoxicological risk.
Chemosphere 12/2012; · 3.21 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Proteomic analysis allows detection of changes of proteins expression in organisms exposed to environmental pollutants, leading to the discovery of biomarkers of exposure and understanding of the action mechanism of toxicity. In the present study, we applied iTRAQ labeling quantitative proteomic technology for global characterization of the liver proteome in mice exposed to perfluorooctane sulfonate (PFOS). This successfully identified and quantified 1038 unique proteins. Seventy-one proteins showed a significant expression change in the treated groups (1.0, 2.5, 5.0 mg/kg of body weight) compared with the control group, and 16 proteins displayed strong dose-dependent changes. Gene ontology analysis showed that these differential proteins were significantly enriched and mainly involved in lipid metabolism, transport, biosynthetic processes, and response to stimulus. We detected significantly increased expression levels of enzymes regulating peroxisomal β-oxidation-including long-chain acyl-CoA synthetase, acyl-CoA oxidase 1, bifunctional enzyme, and 3-ketoacyl-CoA thiolase A. PFOS also significantly induced cytochrome P450s and glutathione S-transferases that are responsible for the metabolism of xenobiotic compounds. The expressions of several proteins with important biological functions-such as cysteine sulfinic acid decarboxylase, aldehyde dehydrogenase, and apolipoprotein A-I, also correlated with PFOS exposure. Together, the present results provide insight into the molecular mechanism and biomarkers for PFOS-induced effects.
Environmental Science & Technology 10/2012; · 4.80 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are two typical perfluorinated compounds (PFCs), found
in a wide range of environmental media and organisms, including humans. Human biomonitoring studies of body fluids have revealed
that in many areas of the world the general population has been exposed to background levels of PFOS and PFOA. Fingernail
has been suggested as a promising biopsy material for assessment of PFCs environmental exposure. In the present study, PFOS
and PFOA were quantified using high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) in fingernails
of urban and rural children (N=93) aged 6–12 years. A questionnaire was conducted to determine factors that could influence the PFOS and PFOA levels in
the children. The levels of PFOS in urban children were significantly higher (geometric mean (GM)=328 ng/g) than those in
rural children (GM=27 ng/g). In contrast, PFOA levels were significantly lower in the urban children compared with the rural
children. Significant positive correlation (R=0.53, P<0.05 for urban areas; R=0.71; P<0.001 for rural areas) between the PFOS and PFOA concentrations indicated they had similar sources. The PFOS and PFOA levels
were higher in fingernail samples from children aged <9 years than in children aged ⩾9 years. In addition, females had higher
PFOA levels than males, in both regions. Other factors that significantly influenced PFOS and PFOA levels were dietary habits
and socio-economic background. The results of this study indicate fingernails are a suitable material for biomonitoring of
PFCs environmental exposure. However, the levels determined in the fingernail samples need to be first evaluated with regard
to the levels determined in other samples, such as human serum.
Keywordsperfluorooctane sulfonate-perfluorooctanoic acid-fingernails-biomarker-environmental exposure
Chinese Science Bulletin 04/2012; 55(33):3755-3762. · 1.32 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorosulfonates (PFSAs) and perfluorocarboxylates (PFCAs) in precipitation collected from Shenyang, China were determined.
Snow samples were collected in the snow event on March 4, 2007 from 34 sites involving both the urban and suburban areas in
Shenyang. The snowmelt was preconcentrated by solid phase extraction and analyzed using LC-MS method. Measurable amounts of
perfluoroalkyl acids (PFAS) were found in precipitation samples from Shenyang, demonstrating that wet deposition is one possible
pathway for the removing of the selected PFAS chemicals from atmosphere. Major PFAS detected were PFOS (<0.38–51 ng/L), PFOA
(0.82–13 ng/L) and PFHpA (0.76–11 ng/L), with their mean concentration of 5.4, 3.3 and 2.9 ng/L, respectively. Other PFSAs
and PFCAs were detected at much lower frequency or below the limit of detection in all the samples. The work presented here
offers some basis for the investigation on the environmental behavior and the evaluation of human exposure to PFAS.
Chinese Science Bulletin 04/2012; 54(14):2440-2445. · 1.32 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Textile industries are important sources of toxic discharges and contribute enormously to water deterioration, while little attention has been paid to the toxicity of textile effluents in discharge regulation. Bioassays with zebrafish were employed to evaluate the toxicity of wastewater samples collected from different stages at a textile factory and sewage treatment plants (STPs). Physico-chemical parameters, acute toxicity, genotoxicity and oxidative stress biomarkers were analyzed. The wastewater samples from bleaching, rinsing and soaping of the textile factory exhibited high acute toxicity and genotoxicity. The coexisting components of dye compounds, as assistants and oxidants, seemed to cause some effect on the toxic response. After treatment employing the anoxic-oxic (A/O) process in STPs, the color and the chemical oxygen demand (COD) were reduced by 40% and 84%, respectively, falling within the criteria of the Chinese Sewage Discharge Standard. In contrast, increases in acute toxicity and genotoxicity were observed in the anaerobic tank, indicating the formation of toxic intermediates. The genotoxicity of the effluent of the STP was not significantly different from that of the influent, suggesting the wastewater treatment processes were not effective in removing the genotoxicity of the dye wastewater. Results indicated that the effluent contains pro-oxidants since the activities of glutathione (GSH), malondialdehyde (MDA), and total anti-oxidation capacity (T-AOC) were all elevated. In addition, decreases in superoxide dismutase (SOD) and glutathione-S transferase (GST) activities observed can be interpreted as a cytotoxicity sign due to an over-production of reactive oxygen species (ROS). The results of the present study suggest that the STPs were not capable of reducing the toxicity of wastewater sufficiently. Further treatment is needed to remove the potential risks posed by textile effluent to ecosystems and human health, and employing a toxicity index is necessary for discharge regulation.
Journal of Environmental Sciences 01/2012; 24(11):2019-27. · 1.66 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are anthropogenic compounds manufactured since the 1950s and are distributed worldwide. Now, the pollutants are being challenged by entering into the brain and the toxic effect on the central nervous system due to calcium disorder, mainly through channels on cell membrane. However, little is known about the role of calcium store in PFOS- and PFOA-evoked abnormal calcium increase. In the present study, PFOA and PFOS were measured in primary cultures of rat hippocampal neurons by LC/MS/MS analysis. Flow cytometry was used to examine altered calcium patterns in neurons labeled with fluo-3/AM and to disclose the mechanism by which PFOS and PFOA induced calcium increase in cultured neurons. The results indicate that both PFOS and PFOA can accumulate in cultured neurons and elevate calcium concentrations via release of intracellular calcium stores. Furthermore, inositol 1,4,5-trisphosphate receptors (IP(3)Rs) and ryanodine receptors (RyRs) were found to take part in PFOS or PFOA inducing calcium release from calcium stores. IP(3)Rs seem to serve a predominant role in PFOS-induced calcium release. Calcium release from intracellular stores may partially account for the perturbation of calcium homeostasis caused by PFOS or PFOA.
Toxicology in Vitro 05/2011; 25(7):1294-301. · 2.78 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS) and 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) are two persistent environmental contaminants that are toxic to developing nervous systems, particularly via their disruption of thyroid hormone (TH) function. To investigate whether an interaction existed between PFOS and BDE-47 on TH-mediated pathways, adult female Wistar rats were exposed to 3.2 and 32 mg/kg of PFOS or BDE-47 in their diet and co-exposed to a combination of each chemical (3.2 mg/kg) from gestational day 1 to postnatal day (PND) 14. Serum and brain tissues from both male and female neonates were collected on PNDs 1, 7, and 14 to examine TH-regulated gene and protein expression. The results revealed that (1) a significant accumulation difference occurred between the two chemicals; (2) On a equimolar basis, BDE-47 and PFOS affected serum total triiodothyronine and total thyroxine differently in adults and offspring; (3) there were region-specific and exposure- and time-dependent alterations in TH concentrations and tested gene and protein expression levels; and (4) interaction for the combined chemicals was only observed for brain-derived neurotrophic factor (BDNF), which exhibited a synergistic effect on PND 1 in the cortex and an antagonistic effect on PND 14 in the hippocampus. Our results suggest a complex TH-mediated gene and protein response to BDE-47 and/or PFOS exposure that seems little related to TH homeostasis and that little combined interaction of co-exposures was observed except on BDNF. The underlying mechanisms remain uncertain but seem to involve more actions than just TH-regulated pathway.
Toxicological Sciences 03/2011; 121(2):279-91. · 4.65 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Extensive human exposure to perfluoroalkyl compounds (PFAA) together with their persistence and various toxicities have arisen increasing concern. A noninvasive method would improve exposure assessment for large population, especially the children susceptible to contaminants. The aim of the study was to assess the use of PFAA measurements in human nails as a biomarker of exposure to PFAAs. Fingernail, toenail, and blood samples were collected from 28 volunteers. The PFAA concentrations were determined by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Six PFAA were detected in nails, with perfluorooctane sulfonate (PFOS) being the compound with the highest median concentration (33.5 and 26.1 ng/g in fingernail and toenail, respectively). Followed was perfluorononanoate (PFNA), with the median concentrations of 20.4 and 16.8 ng/g, respectively, in fingernail and toenail. Other PFAA detected were perfluorooctanoate (PFOA), perfluorodecanoate (PFDA), perfluorododecanoate (PFDoA), and perfluorotetradecanoate (PFTA), with median levels ranging between 0.19 and 8.94 ng/g. PFOS and PFNA concentrations in fingernail significantly correlated with those in serum. Fingernail PFOS and PFNA levels were 2.8 and 24.4 times, respectively, higher than the serum levels. The accumulation of PFAA in nails, together with its advantages in noninvasive sampling and ability of reflecting long-term exposure, made nails PFAA an attractive biomarker of exposure.
Environmental Science & Technology 03/2011; 45(19):8144-50. · 4.80 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS) is one of the persistent organic pollutants distributed widely in the global environment. We have found that a single oral administration of PFOS induced tonic convulsion in mice and rats when a brief ultrasonic stimulus was applied to the animals. The aim of this study is to examine whether the neurotoxicity is caused by subchronic dietary exposure to PFOS. Rats were treated with dietary PFOS at 0, 2, 8, 32 and 128 ppm for 13 weeks. Animals were carefully observed for pharmacotoxic signs and responses to the ultrasonic stimulus applied biweekly. PFOS increased liver weight and decreased food consumption and body weight. PFOS concentrations in the serum, brain, liver and kidney were increased almost proportional to its total dose, although the ratios of PFOS concentrations in tissues to total doses in the group treated with the highest concentration were a little lower. The ranges of relative concentrations in the brain, liver and kidney to serum concentration were 0.13 to 0.24, 2.7 to 6.3 and 0.82 to 1.6, respectively. PFOS alone did not cause any neurotoxic symptoms; however, 5 rats out of 6 showed tonic convulsion in the 6th week when ultrasonic stimulus was applied to the 128 ppm rats with the total PFOS dose of 338 mg/kg. The ultrasonic stimulus did not cause convulsion in the other groups. Histopathological examination including electron microscopic examination could not detect any abnormality in the brain. Because the acute oral dose of PFOS causing the convulsion was 250 mg/kg (Sato et al., 2009), the convulsion induced by PFOS seemed to depend on its total dose regardless of treatment schedule.
The Journal of Toxicological Sciences 01/2011; 36(1):55-62. · 1.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The toxicity of perfluorooctane sulfonate (PFOS), a persistent organic compound, is of great concern. Several studies have reported that PFOS decreases circulating thyroid hormone (TH) concentrations. However, the mechanisms involved remain to be determined. Female rats were exposed to (1) vehicle; (2) PFOS (0.2, 1.0, and 3.0 mg/kg); (3) propylthiouracil (PTU, 10 mg/kg); or (4) PTU (10 mg/kg) + PFOS (3.0 mg/kg) by gavage once a day for 5 consecutive days. Parameters including contents of total T4 (TT4) and total T3 (TT3) in both serum and bile, serum concentrations of transthyretin and thyroglobulin, as well as transcripts of transporters involved in hepatic uptake and efflux of T4 were determined in control and PFOS-exposed groups. TT4 and TT3 were also analyzed in PTU and PTU + PFOS groups in order to reflect the different hormone effects between PFOS, PTU, and PFOS + PTU. Results showed that serum TT4 and TT3 decreased, while bile TT4 and TT3 remained stable following PFOS exposure. Exposure to 3.0 mg/kg of PFOS significantly enhanced hepatic organic anion transporter OATP2 mRNA expression (1.43 times of control). Treatment with PFOS increased hepatic expression of multidrug resistance--associated protein MRP2, approximately 1.80 and 1.69 times of control in 1.0 and 3.0 mg/kg groups, respectively. Spearman's correlation coefficients revealed that MRP2 mRNA expression correlated well with serum TT4 level (r = -0.528, P = 0.012). Serum thyroglobulin and transthyretin levels remained stable. Serum TT3, bile TT4, and bile TT3 were significantly different between PFOS and PTU groups. No significant differences of TT4 and TT3 in both serum and bile were observed between PTU and PTU + PFOS (P > 0.05). In conclusion, PFOS increased hepatic expression of OAPT2, which could possibly enhance hepatic uptake and metabolism of T4 in rats. PFOS-induced TT4 deficiency is mainly due to the extrathyroidal metabolism of T4, which is probably different from the classic goitrogen, PTU.
Archive für Toxikologie 11/2010; 85(6):613-21. · 4.67 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A fluorochemical industrial park was built in 2004 in Fuxin, China, for the production of polytetrafluoroethylene (PTFE) and perfluorobutane sulfonate (PFBS). Yet little is known about the distribution of fluorochemicals in the environment and in people living in and around the park. In this study, environmental samples were collected from 22 sites in Fuxin to investigate the extent of perfluorinated compound (PFC) contamination in the environment around the park, and in drinking water from the public water supply system and groundwater in shallow aquifers from private wells near the park. Serum samples were also collected from nonoccupationally exposed residents living in Fuxin to determine the PFC load of local residents. As the dominant contaminant of eight target PFCs, the maximum concentrations of perfluorooctanoic acid (PFOA) in sediment and river water of the River Xi along the industrial park were 48 ng/g dry weight and 668 ng/L, respectively; the highest PFOA concentration in groundwater beneath the park was 524 ng/L; and the PFOA levels in drinking water from the public water supply system ranged between 1.3 and 2.7 ng/L. In human serum, PFOA had the geometric mean at 4.3 ng/mL, ranging from 0.02 to 93 ng/mL. This study serves to document what should be the beginning of a long-term surveillance effort to minimize potential exposure of residents living in Fuxin.
Environmental Science & Technology 10/2010; 45(19):8075-80. · 4.80 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorinated compounds (PFCs) have been determined in various matrices within China including water bodies, precipitations, biota and non-occupationally PFCs-exposed populations in recent years, yet little attention has been focused on the distributions of PFCs in urban river sediments from Chinese major metropolises such as Guangzhou and Shanghai so far. In this study, sediment samples of 0-2 cm were collected from 13 sites in the Zhujiang River across Guangzhou and nine sites in the Huangpu River across Shanghai. PFCs analysis on these sediments via high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) system was implemented targeting eight analytes involving perfluorobutane sulfonate (PFBS), perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorododecanoic acid (PFDoA) and perfluorotetradecanoic acid (PFTA). According to the analytical results, total concentrations of PFCs ([summation operator]PFCs) in sediments from the Zhujiang River were between 0.09 and 3.6 ng/g dry weight (dw), with PFOS being the dominant PFC contaminant in the river ranged from below LOD to 3.1 ng/g dw; while [summation operator]PFCs in sediments from the Huangpu River were between 0.25 and 1.1 ng/g dw, with PFOA being the main PFC contaminant in the river determined in the levels of 0.20-0.64 ng/g dw. Additionally, an overall decreasing trend of PFCs contaminations with depth was observed in both of two 60 cm sediment cores from the Zhujiang River and the Huangpu River each.
Chemosphere 06/2010; 80(2):123-30. · 3.21 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS) is a persistent and bio-accumulative pollutant ubiquitous in wildlife and humans, which receives many concerns on the fate, transport, distribution, and toxicity. Studies have shown that PFOS-induced neurotoxicity in experimental animals; however, little is known about the potential mechanism of PFOS exposure on the central nervous system (CNS). Ca(2+)/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha), cAMP-response element binding protein (CREB), c-fos, and c-jun, which are important down-stream molecules of calcium signaling in describing neuron cells structure and function in the CNS, were examined in the paper with the purpose to evaluate the effect of PFOS exposure on brain and approach the molecular mechanisms involved in the neurotoxicity induced by PFOS. Adult male Sprague-Dawley rats were administered with PFOS at dosages of 1.7, 5.0, and 15.0 mg/L in drinking water for 91 consecutive days. LC/MS was used for PFOS analysis in brain tissues, and western blot was employed to determine the expression of CaMKIIalpha and pCREB in the isolated cortex and hippocampus. The expression of c-fos and c-jun was detected by real-time reverse transcription polymerase chain reaction. The results showed that the expression of CaMKIIalpha and pCREB exhibits a significant increase in cortex and hippocampus after treatment with PFOS, compared with the control. The transcription factor c-fos was up-regulated in hippocampus, and c-jun was elevated both in cortex and hippocampus in PFOS-treated groups. These results indicated that, at least in part, the neurotoxic effect induced by PFOS is mediated by the Ca(2+)-dependent molecules in calcium signaling.
Archive für Toxikologie 06/2010; 84(6):471-9. · 4.67 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Higher blood levels of perfluorooctane sulfonate (PFOS) in males than the females have been observed in many human biomonitoring studies, which is not well explained yet. The effects of gestation and regular bleeding on blood PFOS level in mice were investigated to evaluate the potential factors that could result in the sex difference. The mice were exposed to PFOS via drinking water at a concentration of 50 mug/l. After 6 weeks of pre-exposure and the gestation period, the blood PFOS concentrations in the gestagenic mice were significantly lower than the control non-gestagenic mice with a ratio of 0.45. Significant lower blood PFOS concentrations in the male mice treated by regular artificial bleeding were observed compared with those from the control male. However, such difference was not observed for the females. The sex difference in the effect of regular artificial bleeding on the blood PFOS level may be caused by the different accumulation and elimination rate in the female and male mice. In addition, the effect of intermittent exposure to PFOS on blood level was evaluated. Each single exposure caused a significant increase in blood PFOS level in both females and males, suggesting the acute exposure to PFOS occurred before the blood sampling, e.g. exposure to PFOS-contaminated foods or drinks, would affect the biomonitoring data to some extent depending on the background blood level. Thus serial blood monitoring is required to obtain accurate body burden.
The Journal of Toxicological Sciences 06/2010; 35(3):309-16. · 1.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS), a persistent and bioaccumulative compound, is widely distributed in the environment. To explore the molecular mechanism of neonatal neurotoxic effects, we evaluated the transcriptional effects of prenatal and neonatal exposure to PFOS in developing rat brain by performing gene expression profiling in the cerebral cortex. Dams received 3.2 mg/kg PFOS in their feed from gestational day 1 (GD1) to weaning (PND 21). Pups then had free access to treated feed until PND 35. Six Illumina RatRef-12 Expression BeadChips were used to identify gene expression changes on postnatal days (PNDs) 1, 7, and 35. Significantly affected genes (P < 0.05) were involved in neuroactive ligand-receptor interaction, calcium signaling pathways, cell communication, long-term potentiation/depression, the cell cycle, and peroxisome proliferator-activated receptor (PPAR) signaling. To compare prenatal and lactational exposure contributions to transcriptional effects, a subset of altered genes obtained from the gene-profile study that represented neurobiological functions was analyzed using RT-PCR in a follow-up cross-foster study lasting from PND1 to 21. Prenatal and postnatal exposure to PFOS caused potential neurotoxicity as demonstrated by developmentally different global transcriptional changes. Prenatal exposure was more effective in altering expression of several genes. Also, transcriptional effects of PFOS exposure on neurodevelopment occurred primarily by disrupting the neuroendocrine system.
Environmental Science and Technology 02/2010; 44(5):1847-53. · 5.23 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are distributed widely in the global environment including wildlife and human. In this study, we investigated the genotoxicity of PFOS and PFOA using the novel in vivo comet assay developed for Paramecium caudatum. For the comet assay, large nuclei squeezed out of the paramecia with 0.25 M sucrose containing 0.6% Triton X-100 were embedded in a layer of agarose gel placed over the slide glass. N-methyl-N´-nitro-N-nitrosoguanidine (MNNG) and 2-aminoanthracene (2-AA) were successfully used for positive controls. Productions of 8-hydroxydeoxyguanosine (8-OH-dG) and intracellular reactive oxygen species (ROS) were also measured in paramecia. PFOS did not cause DNA damage on any conditions examined. On the other hand, 12 and 24 hr exposure to PFOA (100 µM) increased DNA migration in electrophoresis condition at pH 13, but not at pH 12.1, suggesting that the DNA damage may be alkali labile site (such as apurinic/apyrimidinic (AP) site). Exposure of paramecia to 100 µM PFOA for 1, 3 and 24 hr and to 10 µM PFOA for 24 hr significantly increased intracellular ROS. Under the same condition, however, 8-OH-dG level was not affected by PFOA. The PFOA-induced DNA damage was not abolished by the application of 100 µM GSH which completely inhibited the increase of intracellular ROS. In conclusion, the PFOA-induced in vivo DNA damage was first shown in paramecia, and the DNA damage might not be directly attributable to increase in intracellular ROS.
The Journal of Toxicological Sciences 01/2010; 35(6):835-41. · 1.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS), an environmentally persistent organic pollutant, has been reported to be transferred to the developing organisms via both placenta and breast milk. A cross-foster model was used to determine whether prenatal or postnatal exposure to PFOS alone can disturb the TH homeostasis in rat pups, and if so, which kind of exposure is a major cause of TH level alteration. Pregnant rats were fed standard laboratory rodent diet containing 0 (control) or 3.2 mg PFOS/kg throughout gestation and lactation period. On the day of birth, litters born to treated and control dams were cross-fostered, resulting in the following groups: unexposed control (CC), pups exposed only prenatally (TC), only postnatally (CT) or both prenatally and postnatally (TT). Serum and liver PFOS concentrations, serum total thyroxine (T4), total triiodothyronine (T3), reverse T3 (rT3) levels, and hepatic expression of genes involved in TH transport, metabolism, and receptors were evaluated in pups at the age of postnatal days (PNDs) 0, 7, 14, 21, or 35. PFOS body burden level in pups in group CT increased, while those in group TC dropped as they aged. Neither total T3 nor rT3 in pups was affected by PFOS exposure. Gestational exposure to PFOS alone (TC) significantly (p < 0.05) decreased T4 level in pups on PNDs 21 and 35, 20.3 and 19.4% lower than the control on the same PND, respectively. Postnatal exposure to PFOS alone (CT) also induced T4 depression on PNDs 21 and 35, 28.6 and 35.9% lower than controls, respectively. No significant difference in T4 level (p > 0.05) was observed between TC and CT on these two time points. None of the selected TH related transcripts was affected by PFOS in pups on PND 0. Only transcript level of transthyretin, TH binding protein, in group TT significantly increased to 150% of the control on PND 21. The results showed that prenatal PFOS exposure and postnatal PFOS exposure induced hypothyroxinemia in rat pups to a similar extent, which suggested that in utero PFOS exposure and postnatal PFOS accumulation, especially though maternal milk, are matters of great concern.
Environmental Science and Technology 11/2009; 43(21):8416-22. · 5.23 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are widely used in industrial fields and consumer products, and are ubiquitously found in the environment and animal tissues. In the present study, their neurotoxicity was examined using rats and mice by means of neurobehavioral observation, histopathological inspection and chemical assays. PFOS and PFOA alone did not cause any neurotoxic symptoms up to their sublethal doses (PFOS: 500 mg/kg, PFOA: 1,000 mg/kg). However, tonic convulsions were caused in the PFOS-treated rats (> or = 250 mg/kg) and mice (> or = 125 mg/kg) when ultrasonic stimulus was applied to the animals. The same ultrasonic stimulus never induced convulsions in the control animals and in the animals treated with PFOA. Concentration of PFOS in the brain was considerably lower than in other tissue, but it seemed to increase gradually with time after exposure. No morphological changes were detected by histopathological examination of the brain. There were also no changes in concentrations of norepinephrine, dopamine, serotonin, glycine, 4-aminobutylic acid and glutamic acid in the brain. The present study revealed neurotoxic effects of PFOS in animals. Convulsive effect of PFOS may not be attributed to the quantitative alterations of neurotransmitters or lesions of nerve cells in the brain, although the mechanism of its neurotoxicity has not been cleared.
The Journal of Toxicological Sciences 10/2009; 34(5):569-74. · 1.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorooctanesulfonate (PFOS) is an environmental contaminant found in human and animal tissues worldwide. The developing nervous system is thought to be particularly sensitive to PFOS by the fact that PFOS can cross blood-brain and placental barriers. Effect of gestational and lactational exposure to PFOS on central nervous system (CNS) in Wistar rats was investigated by the cross-foster model built with PFOS at 0 or 3.2 mg/kg food. Real-time reverse transcription-polymerase chain reaction was employed to evaluate the gene expression of calcium-dependent signaling molecules in rats' hippocampus which are critical to the function of CNS. The expression of calcium-related signaling molecules, such as N-methyl-D-aspartate receptor subtype-2B (NR2B), calmodulin (CaM), Ca2+/calmodulin-dependent kinase II alpha (CaMKIIalpha) and cAMP-response element-binding (CREB) were increased in the PFOS exposure group at postnatal day 1 (PND 1). The decreased NR2B in the prenatal PFOS exposure group, the decreased CaM in the pre-/postnatal PFOS exposure group, the increased CaMKIIalpha in the whole-life PFOS exposure group and the increased CREB in the prenatal/whole-life PFOS exposure group was observed at PND 7. At PND 35, rats exhibited the decreased NR2B in the pre-/postnatal and the whole-life PFOS exposure group, and the decreased CaM in the postnatal PFOS group. The results indicate that perinatal exposure to PFOS during the critical period of development of the brain may have neurotoxic effect on CNS by mediating the molecules of calcium signaling pathway.
Archive für Toxikologie 09/2009; 84(1):71-9. · 4.67 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Perfluorinated compounds (PFCs) have received much attention on their distributions in various matrixes of different areas globally, however, little is known about their existences in river sediments of China. In this study, eight target PFCs including perfluorobutane sulfonate (PFBS), perfluorohexane sulfonate (PFHxS), perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluorododecanoic acid (PFDoA) and perfluorotetradecanoic acid (PFTA) were determined based upon the upper 10cm surface sediment samples collected from eleven sites covering three main streams of the Daliao River system in northeast China, which received huge amount of industrial and domestic wastewater annually from the neighbouring areas. Analytical results indicated that total concentrations of PFCs were determined in the range of 0.29-1.03ngg(-1) dry weight in sediments from this river system. As the dominant PFCs contaminants in sediment samples, concentrations of PFOS and PFOA were ranged between <LOQ and 0.37ngg(-1) dry weight and from <LOQ to 0.17ngg(-1) dry weight, respectively, while those of the other six target analytes relating to PFBS, PFHxS, PFNA, PFDA, PFDoA and PFTA were below their LOQs at most of the sampling sites. Additional analyses on vertical variations of total PFCs concentrations in sectioned sediment core samples from three main streams of this river system presented overall decreasing trends of PFCs contaminations with depth in the top 10cm surface sediments of these rivers.
Chemosphere 09/2009; 77(5):652-7. · 3.21 Impact Factor
