Effects of perfluorooctane sulfonate (PFOS) on swimming behavior and membrane potential of paramecium caudatum
Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were distributed widely in the global. PFOS (15 µM or higher) caused backward swimming of paramecia. The Triton-extracted paramecia, where the membrane was disrupted and the externa...
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| Published in | Journal of toxicological sciences Vol. 33; no. 2; pp. 155 - 161 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Japan
The Japanese Society of Toxicology
01.05.2008
Japan Science and Technology Agency |
| Subjects | |
| Online Access | Get full text |
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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 µM 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 µM Ca2+ in the medium and backward swimming at about 0.2 µM 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. |
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| AbstractList | 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. Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were distributed widely in the global. PFOS (15 [mu]M 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 [mu]M Ca super(2+) in the medium and backward swimming at about 0.2 [mu]M and higher. PFOS (0.1 mM) did not change the relationship between the swimming directions and free Ca super(2+) 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 Ca super(2+) 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 Ca super(2+) 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 Ca super(2+) into the cilia through voltage-gated Ca super(2+) channels. The Ca super(2+) channels are most probably activated by the depolarizing receptor potentials resulted from the PFOS-induced activation of chemoreceptors. Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were distributed widely in the global. PFOS (15 µM 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 µM Ca2+ in the medium and backward swimming at about 0.2 µM 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. 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.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. |
| Author | Saito, Norimitsu Jin, Yihe Kawamoto, Kosuke Oami, Kazunori Sato, Itaru Tsuda, Shuji Nishikawa, Yasuo |
| Author_xml | – sequence: 1 fullname: Kawamoto, Kosuke organization: Laboratory of Veterinary Public Health, Department of Veterinary Medicine, Faculty of Agriculture, Iwate University – sequence: 2 fullname: Nishikawa, Yasuo organization: Laboratory of Veterinary Public Health, Department of Veterinary Medicine, Faculty of Agriculture, Iwate University – sequence: 3 fullname: Oami, Kazunori organization: Graduate School of Life and Environmental Sciences, University of Tsukuba – sequence: 4 fullname: Jin, Yihe organization: Department of Environmental Science and Technology, Dalian University of Technology – sequence: 5 fullname: Sato, Itaru organization: Laboratory of Veterinary Public Health, Department of Veterinary Medicine, Faculty of Agriculture, Iwate University – sequence: 6 fullname: Saito, Norimitsu organization: Research Institute for Environmental Sciences and Public Health of Iwate Prefecture – sequence: 7 fullname: Tsuda, Shuji organization: Laboratory of Veterinary Public Health, Department of Veterinary Medicine, Faculty of Agriculture, Iwate University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18544907$$D View this record in MEDLINE/PubMed |
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| References_xml | – reference: Lau, C., Thibodeaux, J.R., Hanson, R.G., Rogers, J.M., Grey, B.E., Stanton, M.E., Butenhoff, J.L. and Stevenson, L.A. (2003): Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. II: postnatal evaluation. Toxicol. Sci., 74, 382-392. – reference: Hu, W.Y., Jones, P.D., DeCoen, W., King, L., Fraker, P., Newsted, J. and Giesy, J.P. (2003): Alterations in cellmembrane properties caused by perfluorinated compounds. Comp. Biochem. Physiol. C Toxicol. Pharmacol., 135, 77-88. – reference: Lau, C., Butenhoff, J.L. and Rogers, J.M. (2004): The developmental toxicity of perfluoroalkyl acids and their derivatives. Toxicol. Appl. Pharmacol., 198, 231-241. – reference: Martin, J.W., Smithwick, M.M., Braune, B.M., Hoekstra, P.F., Muir, D.C. and Mabury, S.A. (2004): Identification of long-chain perfluorinated acids in biota from the Canadian Arctic. Environ. Sci. Technol., 38, 373-380. – reference: Oami, K. 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| Snippet | Persistent perfluorinated organic compounds such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) were distributed widely in the global.... |
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| SubjectTerms | Alkanesulfonic Acids - toxicity Animals Behavioral mutant Caprylates - toxicity Cells, Cultured Fluorocarbons - toxicity Hemolysis Membrane Potentials - drug effects Mice Paramecium Paramecium caudatum Paramecium caudatum - physiology PFOS Surface-Active Agents - pharmacology Swimming Triton-extracted model Water Pollutants, Chemical - toxicity |
| Title | Effects of perfluorooctane sulfonate (PFOS) on swimming behavior and membrane potential of paramecium caudatum |
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