ID 105960
Author
Sun, Yuanzhi Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Enkhjargal, Molomjamts Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Sugihara, Aya Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Yamada, Saki Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Chen, Xiaohui Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Miura, Yukari Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Fukunaga, Eri Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima
Satoh, Masaya Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Oyama, Yasuo Laboratory of Cellular Signaling, Graduate School of Integrated Arts and Sciences, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
triclocarban
thymocytes
membrane potential
flow cytometer
Content Type
Departmental Bulletin Paper
Description
The effect of triclocarban (TCC), an environmental pollutant from household items and health care products, on membrane potential of rat thymocytes was examined by a flow cytometry with a fluorescent probe sensitive to membrane potential, bis-(1,3-dibutylbarbituric acid)trimethine oxonol, because TCC changes intracellular ionic circumstance that may affect the membrane potential. TCC at 0.3 μM or more (up to 3 μM) depolarized the membranes. This TCC-induced phenomenon was against our prediction because TCC increases intracellular Ca2+ concentration that activates Ca2+-dependent K+ channels, resulting in a hyperpolarization. The depolarization was still observed under Ca2+-free condition, but not under Na+-free condition. Furthermore, TCC hyperpolarized the membranes under Ca2+- and Na+-free condition. To see if TCC inhibits Ca2+-dependent hyperpolarization, the effect of A23187, a calcium ionophore, on the membrane potential was examined in the cells treated with TCC. A23187 induced large depolarization in the cells treated with 0.3–3 μM TCC. The A23187-induced depolarization in the presence of TCC was greatly attenuated under Na+-free or Ca2+-free condition whereas A23187 elicited hyperpolarization in the cells treated with 0.3–3 μM TCC under Ca2+- and Na+-free condition. Results suggest that 0.3–3 μM TCC increases membrane permeability of Na+ and Ca2+, resulting in the depolarization. Large depolarization induced by TCC in the presence of external Ca2+ and Na+ may mask the hyperpolarization elicited via the increase in intracellular Ca2+ concentration by TCC. Thus, there is a possibility that TCC depolarizes membranes of lymphocytes, resulting in alteration of cellular functions of lymphocytes.
Journal Title
徳島大学総合科学部自然科学研究 = Natural Science Research, The University of Tokushima
ISSN
09146385
NCID
AN10065859
Volume
27
Issue
4
Start Page
53
End Page
59
Sort Key
53
Published Date
2013-10
Remark
P.59のページ付に誤植(P.57と表記)
EDB ID
FullText File
language
eng
TextVersion
Publisher
departments
Bioscience and Bioindustry