Abstract
Abstract—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 Ca2+ chelators, such as 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl ester), on the intensity of the process. This decrease is hardly likely to be caused by effects of a hypomagnetic field on phosphorylation of NADPH-oxidase components, because addition of the protein kinase C inhibitor Ro 31-6233 decreases the fluorescence intensity of intracellular dichlorodihydrofluorescein little, if at all. Addition of phospholipase C inhibitor U73122 causes a negligible decrease in ROS production in the control and experiment, almost equally. Different concentrations of apocynin increase ROS production in nonactivated neutrophils and this effect is approximately two times lower under hypomagnetic conditions. The decrease in ROS production is more pronounced in cells treated with a hypomagnetic field with the presence of rotenone, indicating that the mitochondrial electron-transport chain is involved in the mechanism of the effect of hypomagnetism.
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