Pushchino, Moscow, Russian Federation
It has been shown that the decrease in intensity of 2,7-dichlorodihydrofluorescein oxidation processes in neurophils under hypomagnetic field exposure is not related to the calcium-mediated mechanisms as evidenced by the absence of the effect of cell-permeant Ca2+ chelators such as 1,2-bis-(2-amino-phenoxy)ethane- N,N,N',N'-tetraacetic acid acetoxymethyl ester on the intensity of the process alluded. This decrease is hardly caused by effects of exposure to hypomagnetic field on phosphorylation of NADPH-oxidase components because addition of a protein kinase C inhibitor, Ro 31-6233, did not virtually decrease the fluorescence intensity of intracellular dichlorodihydrofluorescein. Addition of a phospholipase C inhibitor, U73122, led to a negligible decrease in ROS production in control (almost same extent as in the experiment). In the presence of apocynin at different concentrations ROS production in unactivated neutrophils increased and it was 2 time lower under hypomagnetic field conditions. A decrease in ROS production which was more apparent during the experiment after addition of rotenone is indicative of the fact that the mitochondrial electron-transport chain is involved in the mechanism of the effect of a “zero” magnetic field. All this sharply distinguishes the effect of the “zero” field from the effects of combined magnetic fields, which are based on the effect on the calcium-dependent regulatory mechanisms that control the respiratory burst in neutrophils.
hypomagnetic conditions, combined magnetic fields, fluorescence, chemiluminescence, reactive oxygen species, neutrophils
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