145
Static, Low-Frequency, and Pulsed Magnetic Fields
new avenues of research in vascular therapies by promoting endothelial cell growth and
by enhancing the healing response of endothelium.
Furthermore, the same authors (Martino, Portelli, et al. 2010) showed that reduction
of the geomagnetic field inhibits the growth rates of model cancer cell lines. In particular, a reduced field of 0.2–0.5 μT led to a decrease in the viable number of fibrosarcoma
cells (HT1080) compared with the geomagnetic field level of 45 μT. The authors speculated that although the underlying mechanism is unclear, this change as assessed by cell
number is not a result of apoptosis, necrosis, or cell cycle alterations.
Potenza et al. (2010) described the effects of a gradient SMF (B max of 300 mT; for 4,
24, 48, and 72 hours) on cell growth and mitochondrial DNA integrity of HUVEC. The
SMF was shown to be significant after 4 hours of exposure, inducing damage at both the
nuclear and mitochondrial levels, reducing mitochondrial content, and increasing ROS
levels. Twenty-four hours of exposure increased mitochondrial DNA content as well as
expression of one of the main genes related to mitochondrial biogenesis. No significant
differences between exposed and sham cultures were found after exposures of 48 and
72 hours. The results suggested that a 300-mT SMF does not cause permanent DNA
damage in HUVECs and that it stimulates a transient mitochondrial biogenesis.
Sullivan, Balin, and Allen (2011) reported that SMF (230–250 mT) exposure stimulates ROS production in human fetal lung cells (WI-38) during the first 18-hour period
when cells are attaching to the culture vessel. These results support the hypothesis that
increased ROS formation may account for SMF effects on cell attachment. However,
SMF decreases growth in WI-38 cells long after the increase in ROS has abated, suggesting that other mechanisms account for SMF effects on cell growth.
Chiu et al. (2007) tested the effects of an SMF (400 mT) on osteoblasts differentiation
in MG63 osteoblast-like cells. The results showed that the SMF increased ALP activity
and extracellular matrix release in MG63 cells. In contrast, SMF-exposed cells exhibited significant increase in fluorescence anisotropy at 6 hours, with significant reduction
in the proliferation effects of growth factors noted at 24 hours. The authors suggested
that one of the possible mechanisms by which SMF affects osteoblastic maturation is
increasing the membrane rigidity and reducing the proliferation-promoting effects of
growth factors at the membrane domain. The same research group also investigated
the effects of an SMF (400 mT, for 5 days) on the differentiation of MG63 cells cultured
on the surface of poly-L-lactide (PLLA) substrates by MTT assay (Feng et al. 2010). The
SMF-exposed cells exhibited decreased MTT values after 1 and 3 days of culture. In
addition, SMF promoted the expression of extracellular matrix in MG63 cells on the
PLLA substrate. After 1 day, the ALP-specific activity of SMF-exposed MG63 cells was
significantly increased by 1.5-fold. These results showed that MG63 cells seeded on a
PLLA disc and treated with SMF had a more differentiated phenotype.
Wang et al. (2009) investigated the effect of SMF (230–280 mT) on cellular signaling pathways in human embryonic cells. The SMF-mediated responses were manifest
at the cellular level as morphological changes and biochemical markers indicative of
pre-oligodendrocyte differentiation. This study provides a framework describing how
SMF exposure is transduced from a plausible molecular biosensor (lipid membranes)
to cell-level responses that include differentiation toward neural lineages. In addition, the authors suggested that SMF might be involved in new relationships between
Static, Low-Frequency, and Pulsed Magnetic Fields
new avenues of research in vascular therapies by promoting endothelial cell growth and
by enhancing the healing response of endothelium.
Furthermore, the same authors (Martino, Portelli, et al. 2010) showed that reduction
of the geomagnetic field inhibits the growth rates of model cancer cell lines. In particular, a reduced field of 0.2–0.5 μT led to a decrease in the viable number of fibrosarcoma
cells (HT1080) compared with the geomagnetic field level of 45 μT. The authors speculated that although the underlying mechanism is unclear, this change as assessed by cell
number is not a result of apoptosis, necrosis, or cell cycle alterations.
Potenza et al. (2010) described the effects of a gradient SMF (B max of 300 mT; for 4,
24, 48, and 72 hours) on cell growth and mitochondrial DNA integrity of HUVEC. The
SMF was shown to be significant after 4 hours of exposure, inducing damage at both the
nuclear and mitochondrial levels, reducing mitochondrial content, and increasing ROS
levels. Twenty-four hours of exposure increased mitochondrial DNA content as well as
expression of one of the main genes related to mitochondrial biogenesis. No significant
differences between exposed and sham cultures were found after exposures of 48 and
72 hours. The results suggested that a 300-mT SMF does not cause permanent DNA
damage in HUVECs and that it stimulates a transient mitochondrial biogenesis.
Sullivan, Balin, and Allen (2011) reported that SMF (230–250 mT) exposure stimulates ROS production in human fetal lung cells (WI-38) during the first 18-hour period
when cells are attaching to the culture vessel. These results support the hypothesis that
increased ROS formation may account for SMF effects on cell attachment. However,
SMF decreases growth in WI-38 cells long after the increase in ROS has abated, suggesting that other mechanisms account for SMF effects on cell growth.
Chiu et al. (2007) tested the effects of an SMF (400 mT) on osteoblasts differentiation
in MG63 osteoblast-like cells. The results showed that the SMF increased ALP activity
and extracellular matrix release in MG63 cells. In contrast, SMF-exposed cells exhibited significant increase in fluorescence anisotropy at 6 hours, with significant reduction
in the proliferation effects of growth factors noted at 24 hours. The authors suggested
that one of the possible mechanisms by which SMF affects osteoblastic maturation is
increasing the membrane rigidity and reducing the proliferation-promoting effects of
growth factors at the membrane domain. The same research group also investigated
the effects of an SMF (400 mT, for 5 days) on the differentiation of MG63 cells cultured
on the surface of poly-L-lactide (PLLA) substrates by MTT assay (Feng et al. 2010). The
SMF-exposed cells exhibited decreased MTT values after 1 and 3 days of culture. In
addition, SMF promoted the expression of extracellular matrix in MG63 cells on the
PLLA substrate. After 1 day, the ALP-specific activity of SMF-exposed MG63 cells was
significantly increased by 1.5-fold. These results showed that MG63 cells seeded on a
PLLA disc and treated with SMF had a more differentiated phenotype.
Wang et al. (2009) investigated the effect of SMF (230–280 mT) on cellular signaling pathways in human embryonic cells. The SMF-mediated responses were manifest
at the cellular level as morphological changes and biochemical markers indicative of
pre-oligodendrocyte differentiation. This study provides a framework describing how
SMF exposure is transduced from a plausible molecular biosensor (lipid membranes)
to cell-level responses that include differentiation toward neural lineages. In addition, the authors suggested that SMF might be involved in new relationships between