Study type: Medical/biological study (experimental study)

Exposure to 1800 MHz radiofrequency radiation induces oxidative damage to mitochondrial DNA in primary cultured neurons. med./bio.

Published in: Brain Res 2010; 1311: 189-196

Aim of study (acc. to author)

To study whether radiofrequency irradiation can cause oxidative damage to mitochondrial DNA (mtDNA) in primary cultured cortical neurons of rats.

Background/further details

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.

Endpoint

Exposure

Exposure Parameters
Exposure 1: 1,800 MHz
Modulation type: pulsed
Exposure duration: 5 min on - 10 min off - for 24 hr
  • SAR: 2 W/kg average over mass

General information

cells were treated in five groups: i) sham exposure ii) Melatonin iii) RF exposure iv) RF exposure + Melatonin (4 hr prior to exposure) v) H2O2 exposure for 24 hr

Exposure 1

Main characteristics
Frequency 1,800 MHz
Type
Exposure duration 5 min on - 10 min off - for 24 hr
Modulation
Modulation type pulsed
Duty cycle 12.5 %
Repetition frequency 217 Hz
Exposure setup
Exposure source
Sham exposure A sham exposure was conducted.
Parameters
Measurand Value Type Method Mass Remarks
SAR 2 W/kg average over mass - - -

Reference articles

  • Zhao R et al. (2007): Studying gene expression profile of rat neuron exposed to 1800 MHz radiofrequency electromagnetic fields with cDNA microassay.
  • Diem E et al. (2005): Non-thermal DNA breakage by mobile-phone radiation (1800 MHz) in human fibroblasts and in transformed GFSH-R17 rat granulosa cells in vitro.

Exposed system:

Methods Endpoint/measurement parameters/methodology

Investigated system:
Time of investigation:
  • after exposure

Main outcome of study (acc. to author)

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.

Study character:

Study funded by

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