mtDNA defects are closely associated with various nervous system diseases and mtDNA is particularly susceptible to oxidative stress.
The cells were assigned to one of five groups: (1) sham exposure group, (2) melatonin group, (3) radiofrequency exposure group, (4) radiofrequency exposure+melatonin group, (5) hydrogen peroxide exposure (100 µM for 24 h, as a positive control of oxidative stress). In groups (2) and (4), melatonin was freshly diluted with cell medium before application (4 h prior to radiofrequency exposure, at a concentration of 200 nM). Groups (2) and (5) were put into the incubator for sham exposure.
|Exposure duration||5 min on - 10 min off - for 24 hr|
|Duty cycle||12.5 %|
|Repetition frequency||217 Hz|
|Sham exposure||A sham exposure was conducted.|
|SAR||2 W/kg||average over mass||-||-||-|
Exposure to radiofrequency irradiation for a period of 24 h significantly increased the production of reactive oxygen species compared with sham exposure group. Thus, radiofrequency exposure induced oxidative stress in the neurons, and this effect could be reversed by melatonin pretreatment.
At 24 h after exposure, radiofrequency exposure induced a significant increase in the levels of 8-hydroxy-2-deoxyguanosine in the mitochondria of neurons. Concomitant with this finding, the copy number of mitochondrial DNA and the levels of mitochondrial RNA transcripts showed an obvious reduction after radiofrequency exposure. These findings further proved that radiofrequency exposure damaged mitochondrial DNA in neurons. Each of these mitochondrial DNA disturbances could be reversed by pretreatment with the antioxidant melatonin.
The authors conclude that these results suggested that 1800 MHz radiofrequency exposure could cause oxidative damage to mitochondrial DNA in primary cultured neurons.