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The effects of exposure of human neuroblastoma cells to a 50 Hz magnetic field on oxidative stress and DNA damage should be investigated.
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.
ばく露時間: continuous for 24 hours
|continuous for 24 hours
|cell culture dishes in temperature-controlled cell culture incubator with 5% CO2
|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
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.