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    Please use this identifier to cite or link to this item: https://ir.fy.edu.tw:8080/ir/handle/987654321/9512

    Title: Cytotoxicity studies of 2-hydroxymethyl-1-naphthol diacetate on K+ currents in neoplastic plasma cells.
    Authors: Ai-Yu Shen;Hui-Fang Li;Shih I. Lu
    Contributors: 輔英科技大學 物理治療系
    Keywords: myeloma cells;voltage-activated K+ current;Ca2+-activated K+ current;2-hydroxymethyl-1-naphthol diacetate
    Date: 1999-06-01
    Issue Date: 2010-11-10 09:42:39 (UTC+8)
    Abstract: The present study investigated the effects of 2-hydroxymethyl-1-naphthol diacetate (TAC) on cell proliferation and K+ currents in RPMI-8226 human myeloma cells. In cells with intracellular Ca2+ concentration ([Ca2+]i) = 10 nM, depolarizing square pulses from a holding potential of –80 mV elicited instantaneous outward current with slow inactivation, corresponding to voltage-activated K+ current. TAC (1–100 μM) inhibited IK(V) in a concentration-dependent manner. A23187 (1 μM), a Ca2+ ionophore, can potentiate Ca2+-activated K+ current (IK(Ca)). Tetraethylammonium chloride (10 mM) caused a small decrease in the amplitude of IK(Ca) elicited by A23187, whereas TAC (30 μM) and quinidine (10 μM) decreased IK(Ca) more effectively. The present results show that TAC directly blocks voltage- and Ca2+-activated K+ currents in human myeloma cells. TAC inhibited both cell proliferation and voltage-activated K+ current with an effective dose inducing half-maximum effects at 3.8 ± 0.8 μM and 10 ± 1.5 μM, respectively. The present study suggests that the cytotoxic effect of TAC in cancer cells may be partially explained by blockade of K+ channels. The delocalization energy of TAC and other analogs was employed to compare their ability to block the voltage-activated K+ channel in myeloma cells. It was found that naphthol derivatives-mediated blockade of voltage-activated K+ channel might relate to the level of delocalization energy and molecular volume.
    Relation: Drug Dev. Res. 47(1),1-8
    Appears in Collections:[物理治療系] 期刊論文

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