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Static, Low-Frequency, and Pulsed Magnetic Fields
In nature, biological systems are considered to be one of the nonlinear systems
most sensitive to various external magnetic fields, including SMFs and EMFs (Zhadin
2001), and it has been estimated that some of these responses are mediated through
free radical reactions. In particular, millitesla-level SMFs have field strengths that
must be subjected to increased investigation because SMF therapy could be useful
in treating vascular and circulatory diseases, including ischemic pain and hypertension, primarily due to the modulation of blood flow or blood pressure or both partly
through free radical reactions such as an NO-mediated pathway (Okano 2008a,b).
However, recent studies have implicated ROS/RNS in the pathogenesis of vascular
dysfunction and hypertension and the activation of the sympathetic nervous system
(SNS) (Campese et al. 2004; Zhao et al. 2006), although the lifetimes of ROS and RNS
in biological systems are extremely short, for example, nanoseconds to microseconds
for ROS (Gorman and Rodgers 1992) and a few seconds for NO (one RNS) (Blanchard
et al. 1997). Since NO exerts a tonic inhibition of central SNS activity (Ye, Nosrati,
and Campese 1997), increased production of ROS could inactivate the neuronal isoform of nitric oxide synthase (nNOS) and subsequently result in activation of the SNS
(Campese et al. 2004). In addition, ROS/RNS are generated after ischemia/reperfusion
from intracellular oxidases present in the myocardium and in infiltrating leukocytes
(Becker 2004). Karogodina, Sergeeva, and Stass (2009) suggest that SMF effect due
to a radical pair involving NO in a biological system requires either a rather strong
SMF in the tesla range or an internal enhancer of SMF. Although oxidative stress may
be important in hypertension as well as in other cardiovascular disorders (Hirooka,
2011), the underlying mechanisms of SMF-induced ROS/RNS generation have not
been clarified.
There is no established effect of repetitive exposures to SMF on a cumulative disorder
(Schenck 2005). Nonetheless, there are safety concerns regarding MRI for diagnostic
imaging and magnetic levitation for transportation using high-intensity SMF in the tesla
range (Prato et al. 2010). Based on advanced studies of SMF effects on oxidative stress
reactions, the potentially hazardous effect of SMF on living organisms is that exposure
to SMF can increase the activity, concentration, and lifetime of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis (Mohtat
et al. 1998; Zhang et al. 2003; Okano 2008a; Dini 2010). In particular, SMF exposure
initiates an iron-mediated process that increases free radical formation in brain cells,
leading to the breaking of DNA strands and cell death.
Although iron ions are important components of normally functioning organisms,
in some cases iron ions can be toxic to organisms (Dobson 2007). Because of its redox
potential, Fe (II) generally has the potential to do more damage than oxidized Fe (III).
For this reason, iron ions are primarily stored as Fe (III) within ferritin in organisms.
The association of abnormal accumulation of metal ions with specific neurodegenerative
disorders, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, has been known
for over 50 years (Goodman 1953). Various forms of metal ions may play a significant
role in the biochemical processes that lead to the progression of neurodegenerative diseases (Dobson 2007). Although there is much speculation about this role, the primary
mechanism is thought to be the result of oxidative stress, that is, free radical generation
Static, Low-Frequency, and Pulsed Magnetic Fields
In nature, biological systems are considered to be one of the nonlinear systems
most sensitive to various external magnetic fields, including SMFs and EMFs (Zhadin
2001), and it has been estimated that some of these responses are mediated through
free radical reactions. In particular, millitesla-level SMFs have field strengths that
must be subjected to increased investigation because SMF therapy could be useful
in treating vascular and circulatory diseases, including ischemic pain and hypertension, primarily due to the modulation of blood flow or blood pressure or both partly
through free radical reactions such as an NO-mediated pathway (Okano 2008a,b).
However, recent studies have implicated ROS/RNS in the pathogenesis of vascular
dysfunction and hypertension and the activation of the sympathetic nervous system
(SNS) (Campese et al. 2004; Zhao et al. 2006), although the lifetimes of ROS and RNS
in biological systems are extremely short, for example, nanoseconds to microseconds
for ROS (Gorman and Rodgers 1992) and a few seconds for NO (one RNS) (Blanchard
et al. 1997). Since NO exerts a tonic inhibition of central SNS activity (Ye, Nosrati,
and Campese 1997), increased production of ROS could inactivate the neuronal isoform of nitric oxide synthase (nNOS) and subsequently result in activation of the SNS
(Campese et al. 2004). In addition, ROS/RNS are generated after ischemia/reperfusion
from intracellular oxidases present in the myocardium and in infiltrating leukocytes
(Becker 2004). Karogodina, Sergeeva, and Stass (2009) suggest that SMF effect due
to a radical pair involving NO in a biological system requires either a rather strong
SMF in the tesla range or an internal enhancer of SMF. Although oxidative stress may
be important in hypertension as well as in other cardiovascular disorders (Hirooka,
2011), the underlying mechanisms of SMF-induced ROS/RNS generation have not
been clarified.
There is no established effect of repetitive exposures to SMF on a cumulative disorder
(Schenck 2005). Nonetheless, there are safety concerns regarding MRI for diagnostic
imaging and magnetic levitation for transportation using high-intensity SMF in the tesla
range (Prato et al. 2010). Based on advanced studies of SMF effects on oxidative stress
reactions, the potentially hazardous effect of SMF on living organisms is that exposure
to SMF can increase the activity, concentration, and lifetime of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis (Mohtat
et al. 1998; Zhang et al. 2003; Okano 2008a; Dini 2010). In particular, SMF exposure
initiates an iron-mediated process that increases free radical formation in brain cells,
leading to the breaking of DNA strands and cell death.
Although iron ions are important components of normally functioning organisms,
in some cases iron ions can be toxic to organisms (Dobson 2007). Because of its redox
potential, Fe (II) generally has the potential to do more damage than oxidized Fe (III).
For this reason, iron ions are primarily stored as Fe (III) within ferritin in organisms.
The association of abnormal accumulation of metal ions with specific neurodegenerative
disorders, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, has been known
for over 50 years (Goodman 1953). Various forms of metal ions may play a significant
role in the biochemical processes that lead to the progression of neurodegenerative diseases (Dobson 2007). Although there is much speculation about this role, the primary
mechanism is thought to be the result of oxidative stress, that is, free radical generation