Home CUSTOMERS General Physiology and Biophysics 2012 General Physiology and Biophysics Vol.31, No.1, p.1–10, 2012

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.31, No.1, p.1–10, 2012

Title: Biologic effects of SMF and paclitaxel on K562 human leukemia cells
Author: Run-Guang Sun, Wen-Fang Chen, Hao Qi, Kun Zhang, Ting Bu, Ying Liu, Shu-Rui Wang

Abstract: In this study, we evaluated the ability of 8.8 mT static magnetic fields (SMF) to enhance the in vitro action of a chemotherapeutic agent, paclitaxel, against K562 human leukemia cells. We analyzed the cell proliferation, cell cycle distribution, DNA damage and alteration of cell surface and cell organelle ultrastructure after K562 cells were exposed to paclitaxel in the presence or absence of 8.8 mT SMF. The results showed that in the presence of SMF, the efficient concentration of paclitaxel on K562 cells was decreased from 50 to 10 ng/ml. Cell cycle analysis indicated that K562 cells treated with SMF plus paclitaxel were arrested at the G2 phase, which was mainly induced by paclitaxel. Through comet assay, we found that the cell cycle arrest effect of paclitaxel with or without SMF on K562 cells was correlated with DNA damage. The results of atomic force microscopy and transmission electron microscopy observation showed that the cell ultrastructure was altered in the group treated with the combination of SMF and paclitaxel, holes and protuberances were observed, and vacuoles in cytoplasm were augmented. Our data indicated that the potency of the combination of SMF and paclitaxel was greater than that of SMF or paclitaxel alone on K562 cells, and these effects were correlated with DNA damage induced by SMF and paclitaxel. Therefore, the alteration of cell membrane permeability may be one important mechanism underlying the effects of SMF and paclitaxel on K562 cells.

Keywords: Biologic effects of SMF and paclitaxel on K562 human leukemia cells
Published online: 01-Feb-2012
Year: 2012, Volume: 31, Issue: 1 Page From: 1, Page To: 10
doi:10.4149/gpb_2012_002


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