In previous studies by the authors (Martinez et al. 2012, Martinez et al. 2016 and Martinez et al. 2019), it was found that proliferation of NB69 cells was increased by magnetic field exposure and that it was mediated by activation of signal pathways MAPK-ERK1/2 and p38. In the present study, it should be investigated whether NADPH could be involved in the activation of the aforementioned signal pathways. As NADPH oxidase is the main source of ROS in cells, tests were conducted with and without Diphenyleneiodonium (DPI), used to inhibit NADPH oxidase, and N-acetyl-L-cysteine, used as a ROS scavenger.
Cells were exposed for 5-30 minutes. For each exposure group, a respective sham exposure was conducted.
|Setup||one Helmholtz pair was placed inside each of two magnetically shielded chambers located within two identical CO2 incubators; in each experimental run Petri dishes or well plates, containing the cell samples, were stacked in the central region of the Helmholtz coil gap to ensure uniformity of MF exposure; in each experimental run only one set of coils was energized, the samples in the unenergized set being considered sham-exposed controls; following a random sequence, both coil sets and incubators were alternatively used for MF- or sham-exposure|
|Sham exposure||A sham exposure was conducted.|
Exposure to the magnetic field for 10 minutes significantly increased the level of ROS in NB69 cells compared to the sham exposure and induced transient significanty increased expression of p67phox after 10-15 minutes of exposure. The MF-induced activation of the MAPK-JNK pathway, but not that of -ERK1/2 or -p38 pathways, was prevented in the presence of DPI.
The authors concluded that exposure of NB69 cells to a 50 Hz magnetic field might increase ROS production via NADPH oxidase activity. However, taken together with the results of the previous studies, there seem to be further mechanisms of MF-induced proliferative response mediated by MAPK signaling activation.