Xu S, Zhong M, Zhang L, Zhou Z, Zhang W, Wang Y, Wang X, Li M, Chen Y, Chen C, He M, Zhang G, Yu Z. Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial DNA in primary cultured neurons. Brain Res. Oct 30 2009. Ahead of print.

Scientific evidence suggests that oxidative stress may contribute to the adverse effects of radiofrequency (RF) radiation on the nervous system. Mitochondrial DNA (mtDNA) is particularly susceptible to oxidative stress. Oxidative damage to mtDNA contributes to mitochondrial dysfunction in various mitochondrial-related diseases. MtDNA damage is characterized by mtDNA mutations, by a decline in mtDNA copy number and by a reduced number of mitochondrial RNA (mtRNA) transcripts.

The objective of this study was to address whether RF radiation can cause oxidative damage to mtDNA in nerve cells.

Primary cultured cortical neurons of SD rats were intermittently exposed to 1800 MHz RF electromagnetic fields (5 min fields on/10 min fields off) at an average SAR of 2 W/kg for 24 hours, or sham-exposed. The temperature difference between sham- and RF-exposed cultures did not exceed 0.05°C. The cultured cells were assigned to one of five exposure groups: 1) sham; 2) melatonin, 3) RF-radiation, 4) RF-radiation + melatonin, 5) hydrogen peroxide (H2O2) – positive control. After the exposures, the following analyses were conducted: assay of intracellular reactive oxygen species (ROS) based on the oxidation of DCFH-DA; determination of 8-hydroxyguanine (8-OHdG) levels in mitochondria to assess DNA oxidative damage, real time PCR to detect mtDNA copy number and mtRNA transcript levels.

RF exposure resulted in a significant increase in ROS production and mitochondrial 8-OhdG levels (as a marker of DNA oxidative damage), and a reduction in the mtDNA copy number and in mtRNA transcript levels. These changes were attenuated by pre-treatment of the cells with melatonin.

Interpretation and Conclusion
The findings of this study indicate that 1800 MHz RF radiation induced oxidative damage to mtDNA and that melatonin prevented this damage. Evidence from previous studies on whether or not RF radiation can cause oxidative stress is conflicting. The discrepancies may be related to differences in the RF signals and cell types used in different experiments. The authors have concluded that oxidative damage to mtDNA may be an important mechanism of adverse effects of RF radiation. However, they caution against direct extrapolation of their results obtained using rodent cultured cells to human exposure conditions.

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