The study based on the results of a previous study by the authors (Luukkonen et al. 2014) and should enlarge the data. Menadione is a free radical-producing DNA damaging agent, and the antioxidant N-acetylcysteine were used in the tests to assess the influence of reactive oxygen species.
Cells were divided into the following groups: 1) exposure to the magnetic field, 2) co-exposure to the magnetic field and menadione, 3) co-exposure to the magnetic field and N-acetylcysteine, 4) co-exposure to the magnetic field, menadione and N-acetylcysteine. For each group, a respective control group with the same treatment but without exposure to the magnetic field was used. Cells were investigated 15, 30 and 45 days after exposure.
3 experiments with 2-3 samples per group, respectively, were performed. Positive controls were used.
Exposure duration: continuous for 24 hours
|Exposure duration||continuous for 24 hours|
|Chamber||cell culture dishes in temperature-controlled cell culture incubator with 5% CO2|
|Setup||a horizontal MF was generated by a pair of Helmholtz coils (340 mm Œ 460 mm, 220 mm distance between the coils) inside an incubator; all cell culture dishes were placed at the center of the coil system, where the magnetic field was homogenous|
|magnetic flux density||100 µT||-||measured||-||-|
The DNA damage was significantly elevated in groups exposed to the magnetic field (groups 1-4) compared to the respective control groups after 15 and 30 days, but not after 45 days.
Lipid peroxidation was significantly decreased in MF-exposed groups 1-4 compared to the respective control groups after 30 and 45 days.
The amount of reactive oxygen species was significantly increased in groups 3 and 4, which were exposed to the magnetic field and treated with N-acetylcysteine or menadione and N-acetylcysteine, compared to their respective control groups.
The authors conclude that exposure of human neuroblastoma cells to a 50 Hz magnetic field could induce DNA damage. Consistently with the previous study, this effect did not depend on co-exposure to menadione and was not blocked by simultaneous exposure to the antioxidant N-acetylcysteine, indicating that the increase in reactive oxygen species is no causal mechanism of action.