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Electromagnetic Fields in Biological Systems
the incidence of micronuclei (MN) and percent polychromatic erythrocytes (PCEs) in
the blood and bone marrow, respectively. The data indicated that values of both indices
in PEMF-exposed mice were not significantly different from those observed in shamexposed animals. In contrast, positive control mice exhibited significantly increased
MN levels and decreased PCEs in both tissues. The results suggested that PEMF did not
induce significantly increased genotoxicity and cytotoxicity in experimental mice.
3.3.2 Tissue, Molecular, and Cellular Studies
These so-called “in-vitro” studies on magnetic field effects, designed primarily to explore
the underlying mechanisms, are reviewed in the following sections: Cell Growth,
Proliferation, and Differentiation (3.3.2.1); Cell Membrane and Metabolic Activity
(3.3.2.2); In Vitro Genotoxicity (3.3.2.3).
3.3.2.1 Cell Growth, Proliferation, and Differentiation
Regarding the effect of SMF on angiogenesis, Wang et al. (2009) investigated the effects
of gradient SMF (B max of 400 mT, 2.09 T/m, for 11 days) on angiogenesis both in vitro
and in vivo and suggested that gradient SMF might inhibit or prevent the formation of
new blood vessels and could be helpful for the treatment of some diseases relevant to
tumor angiogenesis (see also Section 3.5.5). In contrast to the inhibition angiogenesis by
gradient SMF, Okano et al. (2006) and Okano, Tomita, and Ikada (2007, 2008) reported
that gradient SMF promoted angiogenesis (B max of 120 mT, 28 T/m, for 10 days) in vitro.
Therefore, the effects and mechanisms of gradient SMF on angiogenesis have not yet
been determined.
Dini et al. (2009) investigated the morphofunctional influence of an SMF (6 mT, for
72 hours) during differentiation induced by 12-O-tetradecanoyl-13-phorbol acetate
(TPA, 50 ng/ml) in human leukaemia U937 cells. The cell morphology of U937 cells
was investigated by optic and electron microscopy. Specific antibodies or molecules or
both were used to label CD11c, CD14, phosphatidylserine, and F-actin and to investigate the distribution and activity of lysosomes, mitochondria, and smooth endoplasmic
reticulum (SER). The ion [Ca 2+ ] i was evaluated with a spectrophotometer. The degree of
differentiation in SMF-exposed cells was lower than that of nonexposed cells in a timedependent manner. The SMF-exposed cells showed cell shape and F-actin modification,
inhibition of cell attachment, appearance of membrane roughness and large blebs, and
impaired expression of specific macrophagic markers on the cell surface. The intracellular localization of SER and lysosomes was only partially affected by exposure. A significant localization of mitochondria with an intact membrane potential at the cell
periphery in nonexposed, TPA-stimulated cells was observed; conversely, in the presence of SMF mitochondria were mainly localized near the nucleus. In no case did SMF
exposure affect cell viability. The authors suggested that the sharp intracellular increase
of [Ca 2+ ] i could be one of the causes of the aforementioned changes.
The Dini research group (Dini and Panzarini 2010) further reported that an exposure
to 6-mT SMF affects fluid-phase endocytosis and phagocytosis in monocyte/macrophages in a differentiation degree–dependent manner. The phagocytosis index and rate
of phagocytosis decreased under SMF exposure, whereas the number of latex particles
Electromagnetic Fields in Biological Systems
the incidence of micronuclei (MN) and percent polychromatic erythrocytes (PCEs) in
the blood and bone marrow, respectively. The data indicated that values of both indices
in PEMF-exposed mice were not significantly different from those observed in shamexposed animals. In contrast, positive control mice exhibited significantly increased
MN levels and decreased PCEs in both tissues. The results suggested that PEMF did not
induce significantly increased genotoxicity and cytotoxicity in experimental mice.
3.3.2 Tissue, Molecular, and Cellular Studies
These so-called “in-vitro” studies on magnetic field effects, designed primarily to explore
the underlying mechanisms, are reviewed in the following sections: Cell Growth,
Proliferation, and Differentiation (3.3.2.1); Cell Membrane and Metabolic Activity
(3.3.2.2); In Vitro Genotoxicity (3.3.2.3).
3.3.2.1 Cell Growth, Proliferation, and Differentiation
Regarding the effect of SMF on angiogenesis, Wang et al. (2009) investigated the effects
of gradient SMF (B max of 400 mT, 2.09 T/m, for 11 days) on angiogenesis both in vitro
and in vivo and suggested that gradient SMF might inhibit or prevent the formation of
new blood vessels and could be helpful for the treatment of some diseases relevant to
tumor angiogenesis (see also Section 3.5.5). In contrast to the inhibition angiogenesis by
gradient SMF, Okano et al. (2006) and Okano, Tomita, and Ikada (2007, 2008) reported
that gradient SMF promoted angiogenesis (B max of 120 mT, 28 T/m, for 10 days) in vitro.
Therefore, the effects and mechanisms of gradient SMF on angiogenesis have not yet
been determined.
Dini et al. (2009) investigated the morphofunctional influence of an SMF (6 mT, for
72 hours) during differentiation induced by 12-O-tetradecanoyl-13-phorbol acetate
(TPA, 50 ng/ml) in human leukaemia U937 cells. The cell morphology of U937 cells
was investigated by optic and electron microscopy. Specific antibodies or molecules or
both were used to label CD11c, CD14, phosphatidylserine, and F-actin and to investigate the distribution and activity of lysosomes, mitochondria, and smooth endoplasmic
reticulum (SER). The ion [Ca 2+ ] i was evaluated with a spectrophotometer. The degree of
differentiation in SMF-exposed cells was lower than that of nonexposed cells in a timedependent manner. The SMF-exposed cells showed cell shape and F-actin modification,
inhibition of cell attachment, appearance of membrane roughness and large blebs, and
impaired expression of specific macrophagic markers on the cell surface. The intracellular localization of SER and lysosomes was only partially affected by exposure. A significant localization of mitochondria with an intact membrane potential at the cell
periphery in nonexposed, TPA-stimulated cells was observed; conversely, in the presence of SMF mitochondria were mainly localized near the nucleus. In no case did SMF
exposure affect cell viability. The authors suggested that the sharp intracellular increase
of [Ca 2+ ] i could be one of the causes of the aforementioned changes.
The Dini research group (Dini and Panzarini 2010) further reported that an exposure
to 6-mT SMF affects fluid-phase endocytosis and phagocytosis in monocyte/macrophages in a differentiation degree–dependent manner. The phagocytosis index and rate
of phagocytosis decreased under SMF exposure, whereas the number of latex particles