In a previous study, Qui et al. (2019) found that exposure to a 50 Hz magnetic field could induce cell proliferation and sphingosine kinase 1 activation, but the mechanism of action was unclear.
Cells were either exposed for 5-60 min or sham exposed and were partially treated with different inhibitors to examine underlying signal pathways: nifedipine (L-type calcium channel inhibitor), SKI II (inhibitor of sphingosine kinase 1), Gö6976 (protein kinase C-α inhibitor) or U0126 (inhibitor of ERK).
Exposure duration: 5 min, 10 min, 15 min, 30 min or 60 min
exposure system (sXc-ELF) consisted of two exposure chambers placed inside a CO2 incubator and a set of control devices outside the incubator; each chamber was composed of a set of square Helmholtz coils (20 x 20 cm2) which were double-wrapped with two lines of copper wire, and was encased by mu-metal which shielded the cells placed in the coils from stray magnetic field; a fan on the wall provided ventilation and maintained air and
temperature uniformity between inside the chamber and incubator; currents were fed into the Helmholtz coils with the same direction in the exposure chamber, whereas opposite direction currents were fed into the coils in the sham exposure chamber; during exposure, the atmosphere inside the incubator consisted of 95% humid air and 5% CO2; the temperature in the chambers was maintained at 37.0 ± 0.28°C throughout the exposure period; the difference in temperature between exposure and sham exposure conditions did not exceed 0.18°C; dishes containing cells were put in the center of the coils; the magnetic field was perpendicular to the dishes
|A sham exposure was conducted.
|magnetic flux density
Exposure to the magnetic field for 5 min or 10 min increased the intracellular calcium level significantly compared to the sham exposure. This effect was dependent on the L-type calcium channel. Exposure for 15 min or more did not show significant effects on the intracellular calcium level.
Western Blot showed, that the magnetic field exposure induced the calcium-dependent phosphorylation of ERK, sphingosine kinase 1 and protein kinase C-α. Inhibition of ERK, could block the magnetic field-induced sphingosine kinase 1 phosphorylation, but had no effect on protein kinase C-α phosphorylation. Inhibition of protein kinase C-α had no effect on sphingosine kinase 1 activation. Finally, the activation of ERK and protein kinase C-α could be blocked by inhibition of sphingosine kinase 1.
The authors conclude that 50 Hz magnetic field exposure could induce sphingosine kinase 1 activation via increase of intracellular calcium. There might also be a feedback mechanism between sphingosine kinase 1 and ERK activation.