Extra-low-frequency magnetic fields alter cancer cells through metabolic restriction med./bio.

To investigate the effects of exposure to extremely low frequency magnetic fields on karyotype changes in five different cancer cell lines.

Nine experiments were conducted (see "field characteristics" for additional information):
1.) Five different cell lines were exposed to different magnetic flux densities for six days and examined afterwards.
2.) To test whether the effects were due to the magnetic field itself or due to the induced currents in the culture media, an experiment with horizontal and vertical magnetic fields was performed with K562 cells. The horizontal coil induced electric currents six times higher than the vertical one whereas the magnetic flux density stayed the same (due to geometry of the culture dish).
3.) K562 cells were exposed to the extremely low frequency magnetic field (ELF-MF) for 3 weeks and examined weekly. After the 3 weeks, the ELF-MF was increased or decreased and cells were examined after further 6 days.
4.) K562 cells were exposed for 6 days to magnetic fields with different frequencies.
5.) K562 cells were incubated while a) ELF-MF was shielded to < 5 nT and static magnetic field was 74 µT or b) ELF-MF was shielded to < 5 nT and static magnetic field to < 3 µT.
6.) To test the hypothesis that ELF-MF and oligomycin (adenosine triphosphate synthetase (ATPS) inhibitor) share a common mode of action, K562 cells were grown under ELF-MF exposure or with oligomycin.
7.) To test if the ELF-MF inhibits ATPS and therefore activates adenosine monophosphate-activated protein kinase (AMPK), ELF-MF exposed K562 cells were grown in the presence of metformin (activates AMPK) or resistin (inhibits AMPK).
8.) Culture media were exposed at 3 different conditions and given to incubated K562 cells (cells incubated for 7 h, 2-2.7 µT, (due to 60 Hz background field in the incubator)).
9.) Cell proliferation and cell morphology was investigated in NCI-H460 cells or MCF-7 cells.
As a control group, unexposed cells were kept in culture flasks under anoxia and MFs below 4 nT (60 Hz).

• intact cell/cell culture
• culture medium
• K562 and HEL 92.1.7 cells (human erythroleukemic cell lines), MCF-7 cells (human breast cancer cell line), NCI-H460 cells (human lung cancer cell line), Colo 320 DM cells (human colon carcinoma cell line)

Remark EMF-Portal: If not stated otherwise, significance of the results is not noted in the article.
All exposed cell lines showed magnetic field induced losses in the karyotype with a mostly flat dose response (exp. 1), also when different frequencies were used (exp. 4).
Similar numbers of chromosomes were observed between cell cultures with a horizontal and vertical alignment of the magnetic field. Therefore, the authors conclude that the magnetic field itself was responsible for the observed changes (exp. 2). After 3 weeks of exposure, the karyotype values returned to the baseline (number of chromosomes without exposure). An increase or decrease of the magnetic field after these 3 weeks induced again karyotype reductions (exp. 3). Cell cultures which were shielded against ELF-MF and static magnetic field (exp. 5b) showed a small drift downward in karyotyping but an obvious increase in the proliferation rate.
Magnetic field exposure, as well as oligomycin had similar effects, i.e. the cell size was smaller compared to the baseline (exp. 6). The amplification of the observed effects by metformin and the attenuation by resistin, indicated an involvement of the ATPS-AMPK pathway (exp. 7). Cells were significantly smaller when incubated in medium exposed to "very small magnetic field" compared to medium exposed to condition 3 (exp. 8). In magnetic field exposed MCF-7 cells (5 µT), remarkable morphological changes appeared when compared to the cells incubated at 4 nT. Furthermore, the cell proliferation was increased in magnetic field exposed NCI-H460 cells in comparison to the 4 nT exposed group (exp. 9).
The authors conclude that magnetic field exposure could induce karyotype changes in different cancer cell lines, and that these changes are possibly due to alterations in the ATPS-AMPK pathway.