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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
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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
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ABSTRACT: The severe incident of Fukushima Daiichi Nuclear Power Station has caused radioactive contamination of environment including drinking water. Radioactive iodine, cesium, strontium, barium and zirconium are hazardous fission products because of the high yield and/or relatively long half-life. In the present study, 4 pot-type water purifiers and several adsorbents were examined for the removal effects on these elements from drinking water. Iodide, iodate, cesium and barium were removed by all water purifiers with efficiencies about 85%, 40%, 75-90% and higher than 85%, respectively. These efficiencies lasted for 200 l, which is near the recommended limits for use of filter cartridges, without decay. Strontium was removed with initial efficiencies from 70% to 100%, but the efficiencies were slightly decreased by use. Zirconium was removed by two models, but hardly removed by the other models. Synthetic zeolite A4 efficiently removed cesium, strontium and barium, but had no effect on iodine and zirconium. Natural zeolite, mordenite, removed cesium with an efficiency as high as zeolite A4, but the removal efficiencies for strontium and barium were far less than those of zeolite A4. Activated carbon had little removal effects on these elements. In case of radioactive contamination of tap water, water purifiers may be available for convenient decontamination of drinking water in the home.
The Journal of Toxicological Sciences 01/2011; 36(6):829-34. · 1.52 Impact Factor
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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
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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
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ABSTRACT: Perfluorooctanoic acid (PFOA) has similar characteristics to perfluorooctane sulfonate (PFOS) in reproduction toxicity featured by neonatal death. We found that PFOS exposure to mice during pregnancy led to intracranial blood vessel dilatation of fetuses accompanied by severe lung collapse which caused neonatal mortality. Thus, we adopted the corresponding experimental design to PFOS in order to characterize the neonatal death by PFOA. Pregnant ICR mice were given 1, 5 and 10 mg/kg PFOA daily by gavage from gestational day (GD) 0 to 17 and 18 for prenatal and postnatal evaluations, respectively. Five to nine dams per group were sacrificed on GD 18 for prenatal evaluation; other 10 dams were left to give birth. No maternal death was observed. The liver weight increased dose-dependently, with hepatocellular hypertrophy, necrosis, increased mitosis and mild calcification at 10 mg/kg. PFOA at 10 mg/kg increased serum enzyme activities (GGT, ALT, AST and ALP) with hypoproteinemia and hypolipidemia. PFOA treatment reduced the fetal body weight at 5 and 10 mg/kg. Teratological evaluation showed delayed ossification of the sternum and phalanges and delayed eruption of incisors at 10 mg/kg, but did not show intracranial blood vessel dilatation. Postnatal evaluation revealed that PFOA reduced the neonatal survival rate at 5 and 10 mg/kg. At 5 mg/kg pups were born alive and active and 16% died within 4 days observation, while all died within 6 hr after birth at 10 mg/kg without showing intracranial blood vessel dilatation. The cause of neonatal death by PFOA may be different from PFOS.
The Journal of Toxicological Sciences 08/2010; 35(4):527-33. · 1.52 Impact Factor
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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
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ABSTRACT: To determine the optimum timing of partial hepatectomy (PH) in a previously developed mouse liver micronucleus test (Igarashi and Shimada, 1997), the relation between DNA damage and micronucleus was examined using the in vivo alkaline comet assay and the micronucleus test on the liver of the same individual mouse. Five genotoxic carcinogens, 1-nitropyrene (1-NP) (125 mg/kg), cyclophosphamide (CP) (50 mg/kg), methylmethan sulfonate (MMS) (80 mg/kg), mitomycin C (MMC) (2 mg/kg) and diethylnitrosamine (DEN) (50 mg/kg) were intraperitoneally dosed to each group consisting of 4 male ddY mice. The mice were subjected to PH 3, 8 or 24 hr after dosing of each carcinogen, and comet assay was performed using the removed liver. The regenerated hepatocyte was sampled five days after PH, and the incidence of micronucleus was measured. CP, MMS, MMC and DEN induced DNA damage at 8 and 24 hr after dosing, while 1-NP induced DNA damage only 8 hr after dosing. All five carcinogens induced micronuclei whenever PH was performed. In the case of CP, the peak of DNA damage was 24 hr after dosing and the timing of PH did not remarkably affect the incidence of micronuclei. The other 4 carcinogens showed peak DNA damage at 8 hr and the highest incidence of micronuclei when PH was operated 24 hr after dosing. In conclusion, we are the first to show the relation of induction between DNA damage and micronucleus in the liver from the same mouse, and tentatively showed the optimal timing of PH as 24 hr after dosing.
The Journal of Toxicological Sciences 01/2010; 35(6):881-9. · 1.52 Impact Factor
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ABSTRACT: Several appliance manufacturers have recently released new type air purifiers that can disinfect bacteria, fungi and viruses by diffusing reactive oxygen species (ROS) into the air. In this study, mice were exposed to the outlet air from each of 3 air purifiers from different manufacturers (A, B, C), and the lung was examined for DNA damage, lipid peroxidation and histopathology to confirm the safety of these air purifiers. Neither abnormal behavior during exposure nor gross abnormality at necropsy was observed. No histopathological changes were also observed in the lung. However, significant increase of DNA damage was detected by the comet assay in the lung immediately after the direct exposure for 48 hr to models A and B, and for 16 hr to model B. As for model B, DNA migration was also increased by 2 hr exposure in a 1 m(3) plastic chamber but not by 48 hr exposure in a room (12.6 m(3)). Model C did not cause DNA damage. Lipid peroxidation and 8-hydroxy deoxyguanosine (8-OH-dG) was not increased under the conditions DNA damage was detected by the comet assay. The present results revealed that some models of air purifiers that diffuse ROS potentially cause DNA damage in the lung although the mechanism was left unsolved.
The Journal of Toxicological Sciences 01/2010; 35(6):929-33. · 1.52 Impact Factor
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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
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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
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ABSTRACT: There is a great concern about global contamination with persistent fluoroorganic compounds including perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA), however, few data are available on the environmental levels of these chemicals in China. In the present study, therefore, environmental or tap water samples collected from various regions of China were assayed for PFOS and PFOA by solid phase extraction and liquid chromatography-mass spectrometry technique. Median concentrations (maximum concentration) of PFOS and PFOA in environmental water were 0.4 (2.4) and 0.1 (1.3) ngL(-1) for the remote area (n=13), 4.0 (14.1) and 3.9 (30.8) ngL(-1) for the urban area (n=22), respectively. Systematic survey was also conducted in the Hun River (n=11) and the Yangtze River (n=34). In the Hun River, the median of PFOS concentration was 4.9ngL(-1), while PFOA was below the limit of quantitation (0.1ngL(-1)) at many of the sampling sites. The Yangtze River was moderately contaminated with both chemicals: median concentration was 4.2ngL(-1) for PFOS and 5.4ngL(-1) for PFOA. Remarkably high concentration of PFOA was found at 2 sampling sites of the Yangtze River (110.6 and 297.5ngL(-1)), but the concentration had declined to the average level at the next sampling site in both cases. Many cities provided tap water with low levels of PFOS and PFOA, however, tap water in Guangzhou and Shenzhen exceeded 10ngL(-1) for both chemicals. This study revealed obvious presence of perfluorinated compounds spread out the entire territory of China, and the levels in urban area of China were almost comparable to those in the US, Europe and Japan.
Chemosphere 09/2009; 77(5):605-11. · 3.21 Impact Factor
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ABSTRACT: Effects of perfluorooctane sulfonate (PFOS) on maleic dialdehyde (MDA) content, superoxide dismutase (SOD) activity and total antioxidation capability (T-AOC) were compared in mice at different postnatal developmental stages, and concentrations and distributions of PFOS in different tissues were measured simultaneously. The male and female mice at postnatal day (PD) 7, PD 14, PD 21, PD 28 and PD 35 were distributed randomly to dosage group (50 mg/kg body weight) and control group (0 mg/kg body weight). Mice were administered with PFOS by once subcutaneous injection. Subsequently, after 24 hr, MDA content, SOD activity and T-AOC in brain and liver were analyzed. The PFOS concentrations in blood, brain and liver were determined by high-performance liquid chromatography negative electrospray tandem mass spectrometry (LC-MS). PFOS induced degression of the body weights of mice evidently and increase of relative weights of liver. Meanwhile, it depressed the SOD activity and T-AOC in brain and liver. The concentrations and distribution percentages of PFOS in blood, brain and liver of mice were significantly different at various postnatal developmental stages. Achieved results in this study indicate that younger mice pups were more sensitive to PFOS exposure. In addition, significant distinctions in concentrations and distribution percentages of PFOS in various tissues were demonstrated in this study. The gender difference observed was greater in the older mice. Thus it is worth giving attention especially to adverse effects of PFOS on foetus and children.
The Journal of Toxicological Sciences 07/2009; 34(3):245-54. · 1.52 Impact Factor
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ABSTRACT: Samples of precipitation events (snow and rain) in Dalian, a typical coastal town in China, were analyzed for perfluorosulfonates (PFSAs) and perfluorocarboxylates (PFCAs) to investigate atmospheric contamination by these compounds. In the snow event on December 16, 2006, samples were collected from 21 different sites and in another 6 precipitation events, samples were collected from a single location. Four PFSAs (C4, C6, C8, C10) and seven PFCAs (C6-12) were analyzed. Among the homologues, perfluorooctane sulfonate (PFOS) concentrations were the highest with a geometric mean (GM) of 145 ng/L (n=21) during the snow event on December 16, 2006, followed by perfluorooctanoate (PFOA) with a GM of 24.7 ng/L (n=21). Concentrations of perfluorobutane sulfonate (PFBS), perfluorohexane sulfonate (PFHxS) and perfluoroheptanoate (PFHpA) were more than two orders of magnitude lower than that of PFOS. Other PFSAs and PFCAs were found to be below the limit of detection in all the samples. In other 6 precipitation events, PFSAs and PFCAs were detected approximately in the same order of magnitude in both snow and rain. The results indicate that wet deposition may be a potential transport mechanism of perfluorinated chemicals in the environment.
Environment international 06/2009; 35(4):737-42. · 4.79 Impact Factor
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ABSTRACT: DNA is damaged by reactive oxygen species (ROS) and such damage is age-dependent. Blood chemical parameters also change age-dependently. Glutathione (GSH) plays an important role as an antioxidant. However, the effects of GSH on DNA damage and blood chemistry are unclear. Therefore, this study was aimed to evaluate GSH contribution to DNA damage and changes of blood chemical parameters in aged and young rats. The GSH content in the livers and kidneys of aged rats (20 months) were lower than that in young rats (9 weeks of age) with higher DNA damage detected by a comet assay. There was a negative correlation between the GSH content and the DNA damage in the liver and kidney. L-buthionine (S,R)-sulfoximine (BSO; 0, 5, 20 mM), which inhibits GSH synthesis, was administered in drinking water for 28 days to young and aged rats (8 weeks and 19 months of age at the start of the administration). The treatment significantly decreased GSH levels in the heart, liver, lung and kidney of either the young or aged rats without causing DNA damage in those organs. When compared with young rats, aged rats showed higher levels in aspartate aminotransferase, alanine aminotransferase, total bilirubin, total cholesterol, globulin, creatinine, sodium and chloride and lower levels in alkaline phosphatase, triglyceride, albumin/globulin and inorganic phosphorus. However, BSO did not change these parameters in young or aged rats. These results showed that there was a negative correlation between GSH and DNA damage during aging, but the BSO-induced GSH depletion did not affect DNA damage or blood chemistry levels in young and aged rats under these study conditions.
The Journal of Toxicological Sciences 11/2008; 33(4):421-9. · 1.52 Impact Factor
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ABSTRACT: Pregnant mice exposure to perfluorooctane sulfonate (PFOS) causes neonatal death. Ten pregnant ICR mice per group were given 1, 10 or 20 mg/kg PFOS daily by gavage from gestational day (GD) 0 to the end of the study. Five dams per group were sacrificed on GD 18 for prenatal evaluation, the others were left to give birth. Additional studies were conducted for histopathological examination of lungs and heads of fetuses and neonates at birth. PFOS treatment (20 mg/kg) reduced the maternal weight gain and feed intake but increased the water intake. The liver weight increased in a dose-dependent manner accompanied by hepatic hypertrophy at 20 mg/kg. PFOS reduced the fetal body weight in a dose-dependent manner and caused a bilateral enlargement in the neck region in all fetuses at 20 mg/kg and mild enlargement in some fetuses at 10 mg/kg, in addition to skeletal malformations. Almost all fetuses at 20 mg/kg were alive on GD18 and showed normal lung structure; but at parturition, all neonates were inactive and weak, showed severe lung atelectasis and severe dilatation of intracranial blood vessel, and died within a few hours. At 10 mg/kg, all neonates were born alive, 27% showed slight lung atelectasis, all of them had mild to severe dilatation of the intracranial blood vessel, and 45% of neonates died within 24 hr. The cause of neonatal death in mice exposed to PFOS may be attributed either to the intracranial blood vessel dilatation or to respiratory dysfunction. The former might be a cause of the latter.
The Journal of Toxicological Sciences 06/2008; 33(2):219-26. · 1.52 Impact Factor
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ABSTRACT: Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were distributed widely in the global. PFOS (15 microM or higher) caused backward swimming of paramecia. The Triton-extracted paramecia, where the membrane was disrupted and the externally applied chemicals are freely accessible to the ciliary apparatus, showed forward swimming up to 0.1 microM Ca2+ in the medium and backward swimming at about 0.2 microM and higher. PFOS (0.1 mM) did not change the relationship between the swimming directions and free Ca2+ concentrations. Effects of various surfactants including PFOS and PFOA on the swimming direction of paramecia were compared with the hemolysis of mouse erythrocytes as an indicator of surfactant activities. The hemolysis did not correlate with their swimming behavior. PFOS caused triphasic membrane potential changes both in the wild-type paramecia and caudatum non-reversal (CNR) mutants, the latter is defective in voltage-gated Ca2+ channels. An action potential of the wild-type specimen was induced at lower current intensity when PFOS was present in the medium. Voltage-clamp study indicated that PFOS had no effect on the depolarization-induced Ca2+ influx responsible for the action potential. The membrane potential responses obtained were similar to those obtained by the application of some bitter substances such as quinine that activate chemoreceptors of paramecia. Since the CNR specimens did not exhibit PFOS-induced backward swimming at concentrations examined, the backward swimming is attributable to the influx of Ca2+ into the cilia through voltage-gated Ca2+ channels. The Ca2+ channels are most probably activated by the depolarizing receptor potentials resulted from the PFOS-induced activation of chemoreceptors.
The Journal of Toxicological Sciences 06/2008; 33(2):155-61. · 1.52 Impact Factor
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ABSTRACT: Isotopic dilution with stable zinc and chelation with DTPA are recommended for removal of radioactive zinc from the body; however, it is unclear which method is more effective. In the present study, the efficacies of these methods were compared in order to determine which treatment should be selected in case of internal contamination with radioactive zinc. Intraperitoneal administration of stable zinc dose-dependently removed 65Zn from the mouse body. However, the dose could not be increased above 3 mg/kg due to its toxicity. Oral administration of zinc was less effective than intraperitoneal administration at the same dose. Our results suggest that the recommended dose of stable zinc (2-3 mg/kg, p.o.) has little efficacy. The efficacies of Ca-DTPA and Zn-DTPA were strongly dependent on the elapsed time after 65Zn exposure. Zn-DTPA was more effective than Ca-DTPA, and its recommended dose (30 micromol/kg) significantly removed 65Zn. Therefore, chelation therapy with Zn-DTPA should be started as soon as possible after internal contamination with radiozinc.
Journal of Veterinary Medical Science 04/2008; 70(3):213-6. · 0.85 Impact Factor
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ABSTRACT: To evaluate the effects of aging on DNA damage, spontaneous and chemical-induced DNA damage and its repair were examined using comet assays at pH 9, 12.1 and 13, and an 8-OH-dG assay in the liver and kidney of young (9-week-old) and aged (20-month-old) rats. Additionally, blood chemistry was examined to investigate any correlation between vital functions and age-dependent DNA damage. DNA migration at pH 13 and 8-OH-dG levels increased in the liver and/or kidney of aged rats, but DNA migration did not increase at pH 9 or 12.1; that is, alkali-labile sites and 8-OH-dG were concomitantly accumulated in aged rats. These results suggest that 8-OH-dG production caused by reactive oxygen species exceeded glycosylation and that the glycosylation activity is far more than the AP endonucleation in aged rats. Methyl methanesulfonate (MMS, 80 mg/kg, i.p.) increased DNA migration at pH 12.1 and 13 in the liver and kidney at 3 and 24 hr after treatment in young and aged rats. The DNA damage in aged rats was less and decreased more slowly compared with young rats. The pictures of MMS-induced DNA migrations at pH 12.1 and 13 were very similar to each other. These results suggest that the adduct glycosylation and repair of the single-strand breaks (SSBs) of aged rats are less than those of young rats, although AP endonucleation is sufficient to remove the AP sites. N-nitrosodiethylamine (160 mg/kg, i.p.) increased DNA migration at pH 12.1 and 13 in the liver and kidney at 3 and 24 hr in young rats and at pH 12.1 and 13 in the kidney at 24 hr in aged rats. These results showed that SSBs were predominantly detected as chemical-induced DNA damage and DNA repairs such as N-glycosylase, DNA polymerase and DNA ligase, and that the metabolic activation declined in aged rats. Aspartate aminotransferase, alanine aminotransferase, total bilirubin, total cholesterol, total protein, globulin, creatinine and chloride age-dependently increased and alkaline phosphates, albumin/globulin ratio, inorganic phosphorus and potassium age-dependently decreased, and these changes were correlated with the DNA migration at pH 13 and/or 8-OH-dG. These results suggest that the activity of DNA repair and metabolic activation enzymes declines in aged rats and that the accumulation of spontaneous DNA damage may affect vital functions.
The Journal of Toxicological Sciences 09/2007; 32(3):249-59. · 1.52 Impact Factor
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ABSTRACT: Japanese horse chestnut (Aesculus turbinata) seed extract inhibits the activity of cyclooxygenase (COX), but its active constituents have not been identified. In the present study, COX inhibitors were isolated from the hexane extract of this seed by means of 4 steps of liquid chromatography and were identified by gas chromatography/mass spectrometry and nuclear magnetic resonance. The COX inhibitors in the extract of Japanese horse chestnut seeds were identified as linoleic acid, linolenic acid, and oleic acid. Their efficacies were in the following order: linolenic acid = linoleic acid > oleic acid. These active constituents are C18 unsaturated fatty acids; stearic acid, a C18 saturated fatty acid, had no activity. Linolenic acid and linoleic acid had high selectivity toward COX-2 (selectivity index = 10), whereas oleic acid had no selectivity. Considering the efficacy and yield of each fatty acid, linoleic acid may be the principal COX inhibitor in this seed.
Journal of Veterinary Medical Science 07/2007; 69(7):709-12. · 0.85 Impact Factor
