151
Static, Low-Frequency, and Pulsed Magnetic Fields
the alternative pathway, whereas the delayed gene expression of FOS, IL2RA, and the
melatonin-synthesizing enzyme HIOMT suggested the suppression of inflammatory
processes. Accordingly, the authors suggested that ELF-EMF activates human monocytes via the alternative pathway. The same research group further demonstrated that
ELF-EMFs (50 Hz, 0.05–1.0 mT, for 48 hours) significantly elevated phagocytic activity,
free radical release, and IL-1β production and concluded that ELF-EMFs did not induce
any genotoxic effect (Frahm et al. 2006).
Simkó (2007) hypothesized that ELF-EMFs can modify the activity of an organism by
changing ROS levels leading to oxidative stress, because free radicals can interact with
DNA resulting in single-strand breaks. The author reviewed several studies on oxidative
stress, as well as the changes in oxidant and antioxidant content after ELF-EMF exposure. Finally, the author concluded that modulations of the oxidant and antioxidant levels through ELF-EMF exposure can play a causal role in cancer development. However,
the mechanisms of ELF-EMF-induced genotoxicity are not yet clear.
Koyama et al. (2008) investigated the effects of an ELF-EMF (60 Hz, 5 mT, for
24 hours) on cell functions. The number of apurinic/apyrimidinic (AP) sites in human
glioma A172 cells was measured following ELF-EMF exposure. The cells were exposed
to an ELF-EMF, to genotoxic agents, to methyl methane sulfonate (MMS), and to hydrogen peroxide (H 2 O 2 ) alone, or to an ELF-EMF with the genotoxic agents. There was no
difference in the number of AP sites between ELF-EMF-exposed cells and sham controls. With MMS or H 2 O 2 alone, the number of AP sites increased with longer treatment times. The exposure to ELF-EMF in combination with genotoxic agents increased
AP-site levels compared with exposure to genotoxic agents alone. These results suggested that the number of AP sites induced by MMS or H 2 O 2 is enhanced by exposure to
ELF-EMFs. The authors postulated that ELF-EMFs can enhance the activity or lengthen
the lifetime of radical pairs.
Di Loreto et al. (2009) investigated the effects of ELF-EMF (50 Hz, 0.1 and 1 mT)
on oxidative damage. The authors showed that ELF-EMFs increased cell viability and
reduced the levels of apoptotic death in rat neuronal primary cultures, with no significant effects on the main antioxidative defenses. Linear regression analysis suggested
a positive correlation between reduced GSH and ROS levels in 1-mT EMF-exposed
cells. They assumed that GSH plays an important role in antioxidant defense toward
the ELF-EMF-induced redox challenge. Moreover, the GSH-based cellular response was
achieved together with an overexpression of a brain-derived neurotrophic factor as well
as with the IL-1β-dependent regulation of prosurvival signaling pathways after ELFEMF exposure.
Focke et al. (2010) confirmed that intermittent exposure of human primary fibroblasts to an ELF-EMF (50 Hz, 1 mT) induces a slight but significant increase in DNA
fragmentation in the comet assay. The results showed that EMF-induced responses are
dependent on cell proliferation, suggesting that processes of DNA replication rather
than the DNA itself may be affected. Consistently, the effects correlated with a reduction
in actively replicating cells and a concomitant increase in apoptotic cells in exposed cultures, whereas a combined formamidopyrimidine glycosylase (Fpg)–Comet test failed
to produce evidence for oxidative DNA base damage. Hence, ELF-EMF-induced effects
are reproducible under specific conditions and can be explained by minor disturbances
Static, Low-Frequency, and Pulsed Magnetic Fields
the alternative pathway, whereas the delayed gene expression of FOS, IL2RA, and the
melatonin-synthesizing enzyme HIOMT suggested the suppression of inflammatory
processes. Accordingly, the authors suggested that ELF-EMF activates human monocytes via the alternative pathway. The same research group further demonstrated that
ELF-EMFs (50 Hz, 0.05–1.0 mT, for 48 hours) significantly elevated phagocytic activity,
free radical release, and IL-1β production and concluded that ELF-EMFs did not induce
any genotoxic effect (Frahm et al. 2006).
Simkó (2007) hypothesized that ELF-EMFs can modify the activity of an organism by
changing ROS levels leading to oxidative stress, because free radicals can interact with
DNA resulting in single-strand breaks. The author reviewed several studies on oxidative
stress, as well as the changes in oxidant and antioxidant content after ELF-EMF exposure. Finally, the author concluded that modulations of the oxidant and antioxidant levels through ELF-EMF exposure can play a causal role in cancer development. However,
the mechanisms of ELF-EMF-induced genotoxicity are not yet clear.
Koyama et al. (2008) investigated the effects of an ELF-EMF (60 Hz, 5 mT, for
24 hours) on cell functions. The number of apurinic/apyrimidinic (AP) sites in human
glioma A172 cells was measured following ELF-EMF exposure. The cells were exposed
to an ELF-EMF, to genotoxic agents, to methyl methane sulfonate (MMS), and to hydrogen peroxide (H 2 O 2 ) alone, or to an ELF-EMF with the genotoxic agents. There was no
difference in the number of AP sites between ELF-EMF-exposed cells and sham controls. With MMS or H 2 O 2 alone, the number of AP sites increased with longer treatment times. The exposure to ELF-EMF in combination with genotoxic agents increased
AP-site levels compared with exposure to genotoxic agents alone. These results suggested that the number of AP sites induced by MMS or H 2 O 2 is enhanced by exposure to
ELF-EMFs. The authors postulated that ELF-EMFs can enhance the activity or lengthen
the lifetime of radical pairs.
Di Loreto et al. (2009) investigated the effects of ELF-EMF (50 Hz, 0.1 and 1 mT)
on oxidative damage. The authors showed that ELF-EMFs increased cell viability and
reduced the levels of apoptotic death in rat neuronal primary cultures, with no significant effects on the main antioxidative defenses. Linear regression analysis suggested
a positive correlation between reduced GSH and ROS levels in 1-mT EMF-exposed
cells. They assumed that GSH plays an important role in antioxidant defense toward
the ELF-EMF-induced redox challenge. Moreover, the GSH-based cellular response was
achieved together with an overexpression of a brain-derived neurotrophic factor as well
as with the IL-1β-dependent regulation of prosurvival signaling pathways after ELFEMF exposure.
Focke et al. (2010) confirmed that intermittent exposure of human primary fibroblasts to an ELF-EMF (50 Hz, 1 mT) induces a slight but significant increase in DNA
fragmentation in the comet assay. The results showed that EMF-induced responses are
dependent on cell proliferation, suggesting that processes of DNA replication rather
than the DNA itself may be affected. Consistently, the effects correlated with a reduction
in actively replicating cells and a concomitant increase in apoptotic cells in exposed cultures, whereas a combined formamidopyrimidine glycosylase (Fpg)–Comet test failed
to produce evidence for oxidative DNA base damage. Hence, ELF-EMF-induced effects
are reproducible under specific conditions and can be explained by minor disturbances