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Chen BF, Tsai MC, Jow GM.
Biochem Biophys Res Commun.
2006 Feb 3;340(1):134-9
Induction of calcium influx from extracellular fluid by beauvericin in human
leukemia cells.
School of Medicine, Fu Jen Catholic University, 510 Chung-Cheng Rd., Hsin-Chuang,
Taipei, Hsien 24205, Taiwan.
Beauvericin, a cyclic hexadepsipeptide, is a mycotoxin that can induce cell
death in human lymphoblastic leukemia CCRF-CEM cells. Our previous data have
shown that beauvericin induces cell death in CCRF-CEM cells in a dose- and
time-dependent manner, and that this beauvericin-induced cell death can be
prevented by administration of intracellular calcium chelator-BAPTA. Therefore,
the intracellular Ca2+ concentration ([Ca2+]i) may play an important role in
beauvericin-induced cell death in CCRF-CEM cells. In this study, the effect of
beauvericin on [Ca2+]i and the possible mechanism responsible for the changes of
[Ca2+]i in CCRF-CEM cells were investigated. Beauvericin caused a rapid and
sustained [Ca2+]i rise in a dose-dependent manner. Excess extracellular Ca2+
facilitated beauvericin-induced [Ca2+]i rise by adding 1 mM CaCl2 in the bathing
medium. On the other hand, beauvericin-induced [Ca2+]i rise was prevented in
Ca2+-free Tyrode's solution by 200 microM EGTA. In addition, beauvericin-induced
[Ca2+]i rise was also attenuated by intracellular Ca2+ chelator-BAPTA/AM. It is
worthy to note that neither the voltage-dependent Ca2+ channel blocker,
nimodipine, nor depletion of intracellular Ca2+ with thapsigargin, an
endoplasmic reticulum Ca2+ pump inhibitor, has any effect on beauvericin-induced
[Ca2+]i rise. The data from present study indicate that beauvericin acts as a
potent Ca2+ mobilizer by stimulating extracellular Ca2+ influx CCRF-CEM cells.
PMID: 16343425
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