150
Electromagnetic Fields in Biological Systems
In this context, the relationship between magnetic fields and oxidative stress has also
been investigated in vitro (see also Section 3.3.1.9).
Hao et al. (2011) investigated whether SMFs (8.8 mT, for 12 hours) can enhance the
killing effect of adriamycin (ADM) in human leukemia cells (K562). The authors showed
that the 8.8-mT SMF enhanced the cytotoxity potency of ADM on K562 cells and suggested that the decrease in P-glycoprotein expression may be one reason underlying this
effect.
Sarvestani et al. (2010) evaluated the influence of an SMF (15 mT, for 5 hours) on
the progression of cell cycle in rat BMSCs. The cells were divided into two groups. One
group was exposed to SMF alone, whereas the other group was exposed to X-rays before
SMF exposure. The population of cells did not show any significant difference in the first
group, but the second group exposed to acute radiation before SMF exposure showed a
significant increase in the number of cells in the G 2 /M phase. The SMF intensified the
effects of X-ray exposure, whereas SMF alone did not have any detectable influence on
cell cycle.
Schwenzer et al. (2007) reported that there was no effect of an SMF alone (3.0 T, for
2 hours) on clonogenic ability, proliferation, and cell cycle in eugenic human lung fibroblasts (Hel 299).
Kimura et al. (2008) examined the effect of 3- or 5-T SMF on gene expression in the
experimental model metazoan Caenorhabditis elegans. In addition, transient induction
of hps12 family genes was observed after SMF exposure. The small-hps gene hps16 was
also induced but to a much lesser extent, and the lacZ-stained population of hps16-1::lacZ
transgenic worms did not significantly increase after SMF exposure with or without a
second stressor, mild heat shock. Several genes encoding apoptotic cell death activators
and secreted surface proteins were upregulated after ionizing radiation (IR), but they
were not induced by SMF. The RT-PCR analyses for 12 of these genes confirmed the
expression differences between worms exposed to SMF and those exposed to IR. In contrast to IR, exposure to high SMFs did not induce DNA double-strand breaks or germ
line cell apoptosis during meiosis. These results suggest that the response of C. elegans
to high SMFs is unique and capable of adjustment during long exposure, and that this
treatment may be less hazardous than other invasive treatments and drugs.
Lupke et al. (2006) examined the cell-activating capacity of an ELF-EMF (50 Hz,
1.0 mT) on human umbilical cord blood–derived monocytes. The results confirmed
the previous findings of cell-activating capacity of ELF-EMFs in human monocytes,
which was detected as an increased ROS release. Furthermore, gene expression profiling (human UniGene RZPD-2 cDNA array) was performed to achieve a comprehensive
view of the genes involved in the cell activation process after 45 minutes of exposure.
These results indicated alteration of 986 genes involved in metabolism, cellular physiological processes, signal transduction, and immune response. Significant regulations
could be analyzed for five genes (expression greater than twofold or less than 0.5-fold):
(1) IL 15RA (receptor α chain); (2) EPS15R (epidermal growth factor receptor pathway
substrate 15-like 1); (3) DNMT3A (hypothetical protein MGC16121); (4) DNMT3A (DNA
[cytosine-5] methyltransferase 3 α); and (5) one gene with no match to known genes,
DKFZP586J1624. Real-time RT-PCR analysis of the expression kinetics of IL15RA, and
IL10RA during the 45-minute exposure indicated the regulation of cell activation via
Electromagnetic Fields in Biological Systems
In this context, the relationship between magnetic fields and oxidative stress has also
been investigated in vitro (see also Section 3.3.1.9).
Hao et al. (2011) investigated whether SMFs (8.8 mT, for 12 hours) can enhance the
killing effect of adriamycin (ADM) in human leukemia cells (K562). The authors showed
that the 8.8-mT SMF enhanced the cytotoxity potency of ADM on K562 cells and suggested that the decrease in P-glycoprotein expression may be one reason underlying this
effect.
Sarvestani et al. (2010) evaluated the influence of an SMF (15 mT, for 5 hours) on
the progression of cell cycle in rat BMSCs. The cells were divided into two groups. One
group was exposed to SMF alone, whereas the other group was exposed to X-rays before
SMF exposure. The population of cells did not show any significant difference in the first
group, but the second group exposed to acute radiation before SMF exposure showed a
significant increase in the number of cells in the G 2 /M phase. The SMF intensified the
effects of X-ray exposure, whereas SMF alone did not have any detectable influence on
cell cycle.
Schwenzer et al. (2007) reported that there was no effect of an SMF alone (3.0 T, for
2 hours) on clonogenic ability, proliferation, and cell cycle in eugenic human lung fibroblasts (Hel 299).
Kimura et al. (2008) examined the effect of 3- or 5-T SMF on gene expression in the
experimental model metazoan Caenorhabditis elegans. In addition, transient induction
of hps12 family genes was observed after SMF exposure. The small-hps gene hps16 was
also induced but to a much lesser extent, and the lacZ-stained population of hps16-1::lacZ
transgenic worms did not significantly increase after SMF exposure with or without a
second stressor, mild heat shock. Several genes encoding apoptotic cell death activators
and secreted surface proteins were upregulated after ionizing radiation (IR), but they
were not induced by SMF. The RT-PCR analyses for 12 of these genes confirmed the
expression differences between worms exposed to SMF and those exposed to IR. In contrast to IR, exposure to high SMFs did not induce DNA double-strand breaks or germ
line cell apoptosis during meiosis. These results suggest that the response of C. elegans
to high SMFs is unique and capable of adjustment during long exposure, and that this
treatment may be less hazardous than other invasive treatments and drugs.
Lupke et al. (2006) examined the cell-activating capacity of an ELF-EMF (50 Hz,
1.0 mT) on human umbilical cord blood–derived monocytes. The results confirmed
the previous findings of cell-activating capacity of ELF-EMFs in human monocytes,
which was detected as an increased ROS release. Furthermore, gene expression profiling (human UniGene RZPD-2 cDNA array) was performed to achieve a comprehensive
view of the genes involved in the cell activation process after 45 minutes of exposure.
These results indicated alteration of 986 genes involved in metabolism, cellular physiological processes, signal transduction, and immune response. Significant regulations
could be analyzed for five genes (expression greater than twofold or less than 0.5-fold):
(1) IL 15RA (receptor α chain); (2) EPS15R (epidermal growth factor receptor pathway
substrate 15-like 1); (3) DNMT3A (hypothetical protein MGC16121); (4) DNMT3A (DNA
[cytosine-5] methyltransferase 3 α); and (5) one gene with no match to known genes,
DKFZP586J1624. Real-time RT-PCR analysis of the expression kinetics of IL15RA, and
IL10RA during the 45-minute exposure indicated the regulation of cell activation via