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The effect of a hypomagnetic field on dichlorofluorescein fluorescence in neutrophil suspensions with and without the presence of phospholipase C inhibitor U73122. Y-axis: the maximum fluorescence intensity as percentage of the basal control (mean values and standard deviations, n = 10). X-axis: 1, control group; 2, experiment. Open bars: no additives; gray bars: 2 μM U73122. * Differences between groups significant at p < 0.05. ** Differences within a group significant at p < 0.05.
Source publication
It is shown that the lower intensity of 2,7-dichlorodihydrofluorescein oxidation processes in inactivated neutrophils exposed to hypomagnetic field (the residual static magnetic field 20 nT) is not related to calcium-mediated mechanisms as shown by the absence of the effect of cell-permeant Ca 2+ chelators, such as 1,2-bis(2-aminophenoxy)ethane-N,N...
Citations
... HMF (<0.2 µT) reduced H 2 O 2 levels in human neuroblastoma cells by inhibiting the activity of CuZn-SOD, and the enhanced cell proliferation caused by HMF can be remedied by additional H 2 O 2 supplementation [40]. HMF (20 nT) also reduced ROS production in mice peritoneal neutrophils by affecting NOX activity and mitochondrial ETC [41,42]. However, an in vitro study of mouse skeletal muscle cells showed that HMF (<3 µT) could cause an increase in its ROS levels, leading to a decrease in cell function [43]. ...
... The different results of HMF affecting ROS levels may be related to the differences in magnetic strength, duration of exposure, cell type, or method of HMF generation. [41,42] DG: Dentate Gyrus, CA: Cornu Ammonis, aNSCs: adult neural stem/progenitor cell. ...
The geomagnetic field (GMF) is crucial for the survival and evolution of life on Earth. The weakening of the GMF, known as the hypomagnetic field (HMF), significantly affects various aspects of life on Earth. HMF has become a potential health risk for future deep space exploration. Oxidative stress is directly involved in the biological effects of HMF on animals or cells. Oxidative stress occurs when there is an imbalance favoring oxidants over antioxidants, resulting in cellular damage. Oxidative stress is a double-edged sword, depending on the degree of deviation from homeostasis. In this review, we summarize the important experimental findings from animal and cell studies on HMF exposure affecting intracellular reactive oxygen species (ROS), as well as the accompanying many physiological abnormalities, such as cognitive dysfunction, the imbalance of gut microbiota homeostasis, mood disorders, and osteoporosis. We discuss new insights into the molecular mechanisms underlying these HMF effects in the context of the signaling pathways related to ROS. Among them, mitochondria are considered to be the main organelles that respond to HMF-induced stress by regulating metabolism and ROS production in cells. In order to unravel the molecular mechanisms of HMF action, future studies need to consider the upstream and downstream pathways associated with ROS.
It has been shown that pulsed magnetic fields (the first mode: pulse duration of 2 ms, frequency repetitions of 6.25 Hz, the pulse was bell-shaped; and the second mode: pulse duration of 1 ms, repetition frequency of 100 Hz, the pulse was bell-shaped) affected the intensity of luminol-dependent chemiluminescence of neutrophils in a wide range of pulsed magnetic fields (0.0004–10 mT). For the detection of the effects of pulsed magnetic fields by this method, it was necessary to add forbol-12-meristat-13-acetate, an activator of the production of reactive oxygen species, to the suspension of neutrophils. However, this mechanism of action of pulsed magnetic fields on the production of reactive oxygen species in neutrophils was not the only one, since lucigenin-dependent chemiluminescence also reacted to their action in a system without activators.
It has been shown that 30-min incubation of neutrophils in the presence of a near null magnetic field produced with the use of permalloy for magnetic shielding (a residual static magnetic field not greater than 20 nT) leads to a significant decrease (by 48%) in the intensity of lucigenin-dependent chemiluminescence measured directly after removal of the hypomagnetic field. At 20 min after being in hypomagnetic conditions (followed by a 20 min of incubation of neutrophils in the geomagnetic field), the degree of the differences between the control and experimental samples is completely preserved. When the time periods of incubation of experimental samples in the geomagnetic field (static magnetic field 44 μT) were extended (40 min and 60 min) after exposure to a near-null magnetic field, the differences between experimental and appropriate control groups of samples were smaller, by up to 32 and 22%.
This paper reports that pre-incubation of a neutrophil suspension in the presence of a near-null magnetic field produced using a system of magnetic shields (a residual constant magnetic field not greater than 20 nT) results in a considerable decrease in the intensity of neutrophil lucigenin-dependent chemiluminescence. The addition of the NADPH oxidase inhibitor diphenyliodonium to the incubation medium reduced the chemiluminescence intensity in both the experimental and the control samples (geomagnetic field). It should be noted that the differences observed between the groups, which were caused by the exposure to a near-null magnetic field, are almost the same both at lower (2.5, 5, and 10 μM) and higher (50 and 100 μM) diphenyliodonium concentrations. In contrast, the addition of 2,4-dinitrophenol, an uncoupler of oxidative phosphorylation in mitochondria, in concentrations starting from 5 μM and up to 200 μM almost completely eliminated the difference between the control and experimental samples, which was observed at low inhibitor concentrations, or in its absence.
It was shown that 40-min exposure of peritoneal neutrophils to hypomagnetic conditions (with a residual field of 0.01 μT) caused a significant (25%) decrease in the intensity of intracellular dichlorofluorescein fluorescence. This effect of the weak magnetic field persisted if the constant magnetic field was increased to 1 μT. Upon further increase of the field to 2.5 μT, the effect of the field disappeared and reappeared at 5 μT in a reduced form, reaching a maximum at 7 μT. There was an equally pronounced and stable inhibitory effect under a sequential increase in the induction of a constant magnetic field (9, 15, and 19.5 μT), the degree of manifestation of which was significantly reduced only at 30 μT. Fluorescence intensity of the 2,7-dichlorodydrofluorescein oxidation products did not differ from the control values at a constant magnetic field of 45 μT. There was no observed effect on these processes under further increase of the field to 74 μT and 100 μT.
We propose that biological systems may detect static and slowly varying magnetic fields by the modification of the timing of firing of adjacent nerve cells through the local influence of the magnetic field generated by current from one cell's firing on its nearest neighbors. The time delay of an adjacent nerve cell pulse with respect to the initial clock nerve cell pulse could serve as a signal for sensing the magnitude and direction of the magnetic field in a direction perpendicular to the current flows in the cells. It has been shown that changes in static magnetic fields modify concentrations of reactive oxygen species, calcium, pH, the growth rates of fibrosarcoma cells, and membrane potentials. These are linked to changes in membrane potentials that can either inhibit or accelerate the firing rate of pacemaker or clock cells. This mechanism may have applications to animals' use of magnetic fields for navigation or other purposes, possibly in conjunction with other mechanisms. Bioelectromagnetics.
