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.
"Sun et al.  evaluated the ability of 8.8 mT SMFs to enhance the in vitro action of a chemotherapeutic agent, paclitaxel, against K562 human leukemia cells. The authors 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 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. "
[Show abstract][Hide abstract] ABSTRACT: The interaction of static magnetic fields (SMFs) with living organisms is a rapidly growing field of investigation. The magnetic fields (MFs) effect observed with radical pair recombination is one of the well-known mechanisms by which MFs interact with biological systems. Exposure to SMF can increase the activity, concentration, and life time of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis. Current evidence suggests that cell proliferation can be influenced by a treatment with both SMFs and anticancer drugs. It has been recently found that SMFs can enhance the anticancer effect of chemotherapeutic drugs; this may provide a new strategy for cancer therapy. This review focuses on our own data and other data from the literature of SMFs bioeffects. Three main areas of investigation have been covered: free radical generation and oxidative stress, apoptosis and genotoxicity, and cancer. After an introduction on SMF classification and medical applications, the basic phenomena to understand the bioeffects are described. The scientific literature is summarized, integrated, and critically analyzed with the help of authoritative reviews by recognized experts; international safety guidelines are also cited.
[Show abstract][Hide abstract] ABSTRACT: Our results demonstrate that the addition of cisplatin after paclitaxel-induced mitotic arrest was more effective than individual treatment on gastric adenocarcinoma cells (MKN45). However, the treatment did not induce benefits in cells derived from lymph node metastasis (ST2957). Time-lapse microscopy revealed that cell death was caused by mitotic catastrophe and apoptosis induction, as the use of the caspase inhibitor z-VAD-fmk decreased cell death. We propose that the molecular mechanism mediating this cell fate is a slippage suffered by these cells, given that our Western blot (WB) analysis revealed premature cyclin B degradation. This resulted in the cell exiting from mitosis without undergoing DNA damage repair, as demonstrated by the strong phosphorylation of H2AX. A comet assay indicated that DNA repair was impaired, and Western blotting showed that the Chk2 protein was degraded after sequential treatment (paclitaxel-cisplatin). Based on these results, the modulation of cell death during mitosis may be an effective strategy for gastric cancer therapy.
[Show abstract][Hide abstract] ABSTRACT: The present study investigates the role of leukocyte transfer in the induction of kidney damage from mice that have undergone a severe renal ischemia-reperfusion insult into the intact recipient mice. First, Balb/c (inbred) mice were subjected to either sham operation (Sham donors) or bilateral renal IR injury (60 min ischemia-3 h reperfusion, IR donors). Leukocytes were isolated from blood and were transferred to two recipient groups: intact recipient mice received leukocytes from Sham donor group (Sham recipient) or from IR donor group (IR recipient). After 24 h, recipient mice were anesthetized for sample collections. Renal malondialdehyde increased and total glutathione concentration and superoxide dismutase activity decreased significantly in the IR recipient group compared to the Sham recipient group. BUN and plasma creatinine were significantly different between donor groups, but these parameters were not significantly different in the two recipient groups. In the IR donor group, there have been extensive changes in renal tissues comparing to Sham including severe destruction of the tubules, necrosis and tubular obstruction plus tubular flattening. IR recipient kidneys showed significant differences from their corresponding Sham group, demonstrating some degrees of injury including loss of brush borders from proximal tubules, cellular vacuolation and flattening of the tubules. However, less tissue damage was seen in this group comparing to IR donor kidneys. These findings showed that leucocytes transferred from post-ischemic mice induced oxidative stress and consequent damage to native kidneys, suggesting a role of leucocytes in the oxidative processes of reperfusion injury.
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