149
Static, Low-Frequency, and Pulsed Magnetic Fields
and in intracellular free calcium concentrations, were observed in CD4 + CD45RA − T cells
compared with CD4 + CD45RA + T cells in either of the magnetic fields. The results suggested that exposure to either magnetic field induces a delay in the response to stimulants
and that modifications are rapidly reversible, at least after a short exposure.
Blackman (2006) commented that because calcium ion release is a measure of neurotransmitter activity, calcium ion release can be chosen as a simple method for studying EMF effects on cells. Dose-response curves show responses at two levels of exposure
with a flat response to doses between these two dose peaks. These two levels are known
as intensity windows.
Zhang et al. (2010) studied the effects of an ELF-EMF (50 Hz, 0.8 mT) on intracellular
calcium ion ([Ca 2+ ] i ). Osteoblastic cells were used as a model both to test the hypothesis
that ELF-EMFs can alter the concentrations of [Ca 2+ ] i and to examine the predicted window effect. The results demonstrated that ELF-EMFs can induce the uptake of [Ca 2+ ] i as
the empirical evidence of the specified window effects of [Ca 2+ ] i in osteoblasts.
Morabito et al. (2010) examined the effects of short-term exposure to ELF-EMF
(50 Hz, 0.1 and 1.0 mT, for 30 minutes) on muscle cell differentiation and function in
C2C12 cells. The focus was on markers of oxidative stress and Ca 2+ handling. The data
revealed that an ELF-EMF of 1.0 mT induced ROS production in myoblasts and myotubes with a concomitant decrease in mitochondrial membrane potential; activated the
cellular detoxification system, increasing catalase and GSH peroxidase (GPx) activities; and altered intracellular Ca 2+ homeostasis, increasing the spontaneous activity of
myotubes and enhancing cellular reactivity to a depolarizing agent (KCl) or an agonist
(caffeine) of intracellular store Ca 2+ channels. In conclusion, the results suggested a possible link between exposure to an ELF-EMF and modification of the cellular redox state,
which in turn could increase the level of intracellular Ca 2+ and thus modulate the metabolic activity of C2C12 cells.
For PEMF effects, Li et al. (2006) compared the effects of ultrasound (US) on osteoblast proliferation with those of a PEMF (7.5 Hz, 2 mV/cm) by using different signal
transduction pathway inhibitors. The cells were stimulated for 15 minutes under US
or for 2 hours under PEMF exposure. The results showed that there are different transduction pathways for US and PEMF stimulation that lead to an upgrade of osteoblast
proliferation, although their pathways all lead to an increase in cytocolic Ca 2+ and the
activation of calmodulin. These findings offered a biochemical mechanism to support
the process of US- and PEMF-induced enhanced healing of bone fractures.
Martino et al. (2008) investigated the effects of a repetitive pulse burst PEMF (15 Hz,
0.9 mT/10 μs, 9 mV/cm) on the cellular activity of SaOS-2 osteoblast-like cells. The PEMF
stimulation did not affect metabolic activity and cell number. However, the ALP activity
of SaOS-2 cells and mineral nodule formation increased significantly after PEMF stimulation. These observations suggested that PEMF does not affect cellular metabolism;
however, it may play a role in the enhancement of SaOS-2 cell mineralization.
3.3.2.3 In Vitro Genotoxicity
It has been known for several years that oxidative stress damages lipids, proteins, and
nucleic acids, resulting in cell membrane and synaptic disorganization, neural cell
signaling dysfunction following apoptotic or necrotic events, or both (Cui et al. 2004).
Static, Low-Frequency, and Pulsed Magnetic Fields
and in intracellular free calcium concentrations, were observed in CD4 + CD45RA − T cells
compared with CD4 + CD45RA + T cells in either of the magnetic fields. The results suggested that exposure to either magnetic field induces a delay in the response to stimulants
and that modifications are rapidly reversible, at least after a short exposure.
Blackman (2006) commented that because calcium ion release is a measure of neurotransmitter activity, calcium ion release can be chosen as a simple method for studying EMF effects on cells. Dose-response curves show responses at two levels of exposure
with a flat response to doses between these two dose peaks. These two levels are known
as intensity windows.
Zhang et al. (2010) studied the effects of an ELF-EMF (50 Hz, 0.8 mT) on intracellular
calcium ion ([Ca 2+ ] i ). Osteoblastic cells were used as a model both to test the hypothesis
that ELF-EMFs can alter the concentrations of [Ca 2+ ] i and to examine the predicted window effect. The results demonstrated that ELF-EMFs can induce the uptake of [Ca 2+ ] i as
the empirical evidence of the specified window effects of [Ca 2+ ] i in osteoblasts.
Morabito et al. (2010) examined the effects of short-term exposure to ELF-EMF
(50 Hz, 0.1 and 1.0 mT, for 30 minutes) on muscle cell differentiation and function in
C2C12 cells. The focus was on markers of oxidative stress and Ca 2+ handling. The data
revealed that an ELF-EMF of 1.0 mT induced ROS production in myoblasts and myotubes with a concomitant decrease in mitochondrial membrane potential; activated the
cellular detoxification system, increasing catalase and GSH peroxidase (GPx) activities; and altered intracellular Ca 2+ homeostasis, increasing the spontaneous activity of
myotubes and enhancing cellular reactivity to a depolarizing agent (KCl) or an agonist
(caffeine) of intracellular store Ca 2+ channels. In conclusion, the results suggested a possible link between exposure to an ELF-EMF and modification of the cellular redox state,
which in turn could increase the level of intracellular Ca 2+ and thus modulate the metabolic activity of C2C12 cells.
For PEMF effects, Li et al. (2006) compared the effects of ultrasound (US) on osteoblast proliferation with those of a PEMF (7.5 Hz, 2 mV/cm) by using different signal
transduction pathway inhibitors. The cells were stimulated for 15 minutes under US
or for 2 hours under PEMF exposure. The results showed that there are different transduction pathways for US and PEMF stimulation that lead to an upgrade of osteoblast
proliferation, although their pathways all lead to an increase in cytocolic Ca 2+ and the
activation of calmodulin. These findings offered a biochemical mechanism to support
the process of US- and PEMF-induced enhanced healing of bone fractures.
Martino et al. (2008) investigated the effects of a repetitive pulse burst PEMF (15 Hz,
0.9 mT/10 μs, 9 mV/cm) on the cellular activity of SaOS-2 osteoblast-like cells. The PEMF
stimulation did not affect metabolic activity and cell number. However, the ALP activity
of SaOS-2 cells and mineral nodule formation increased significantly after PEMF stimulation. These observations suggested that PEMF does not affect cellular metabolism;
however, it may play a role in the enhancement of SaOS-2 cell mineralization.
3.3.2.3 In Vitro Genotoxicity
It has been known for several years that oxidative stress damages lipids, proteins, and
nucleic acids, resulting in cell membrane and synaptic disorganization, neural cell
signaling dysfunction following apoptotic or necrotic events, or both (Cui et al. 2004).