To study a time-course description of effects after acute microwave exposure in the rat brain by measuring 1) the neuronal activation using the c-fos expression and 2) glial reactivity as an indicator of parallel neuronal damage in seizure-related rat model.
Rats were made seizure-prone by injection of a subconvulsive dose of the GABA antagonist picrotoxin.
72 adult male rats were divided into 12 groups: 1) picrotoxin treated (to induce seizure proneness), exposed for 2 h and investigated after 90 min., 2) picrotoxin treated, sham-exposed for 2 h and investigated after 90 min., 3) no picrotoxin administration, exposed for 2 h and investigated after 90 min., 4) no picrotoxin administration, sham-exposed for 2 h and investigated after 90 min., 5) picrotoxin treated, exposed for 2 h and investigated after 24 h, 6) picrotoxin treated, sham-exposed for 2 h and investigated after 24 h, 7) no picrotoxin administration, exposed for 2 h and investigated after 24 h, 8) no picrotoxin administration, sham-exposed for 2 h and investigated after 24 h, 9) picrotoxin treated, exposed for 2 h and investigated after three days, 10) picrotoxin treated, sham-exposed for 2 h and investigated after three days, 11) no picrotoxin administration, exposed for 2h and investigated after three days, 12) no picrotoxin administration, sham-exposed for 2 h and investigated after three days.
| Exposure | Parameters |
|---|---|
|
Exposure 1:
900 MHz
Modulation type:
pulsed
Exposure duration:
continuous for 2 h
|
|
rats were treated in 12 groups: i) rats injected with picrotoxin (PT) 5 min before the experiment and immobilized in methacrylate tubes with exposure to GSM for 2 h; rats studied 90 min after end of immobilization ii) rats injected with picrotoxin (PT) 5 min before the experiment and immobilized in methacrylate tubes without GSM exposure for 2 h; rats studied 90 min after end of immobilization ii) rats injected with vehicle (no PT) 5 min before the experiment and immobilized in methacrylate tubes with exposure to GSM for 2 h; rats studied 90 min after end of immobilization iv) rats injected with vehicle (no PT) 5 min before the experiment and immobilized in methacrylate tubes without GSM exposure for 2 h; rats studied 90 min after end of immobilization v) as i) but rats studied 24 h after end of immobilization vi) as ii) but rats studied 24 h after end of immobilization vii) as iii) but rats studied 24 h after end of immobilization viii) as iv) but rats studied 24 h after end of immobilization ix) as i) but rats studied 3 days after end of immobilization x) as ii) but rats studied 3 days after end of immobilization xi) as iii) but rats studied 3 days after end of immobilization xii) as iv) but rats studied 3 days after end of immobilization
| Frequency | 900 MHz |
|---|---|
| Type | |
| Exposure duration | continuous for 2 h |
| Exposure source | |
|---|---|
| Setup | methacrylate tubes with immobilized rats placed in a 150 cm x 46 cm x 70 cm radiation cage with an incorporated transmission antenna |
| Sham exposure | A sham exposure was conducted. |
| Measurand | Value | Type | Method | Mass | Remarks |
|---|---|---|---|---|---|
| power | 1 W | - | - | - | output power |
| power | 192.67 mW | maximum | - | - | 178.37 - 192.67 mW mean absorbed power with PT |
| power | 202.33 mW | maximum | - | - | 189.41 - 202.33 mW mean absorbed power without PT |
| SAR | 1.44 W/kg | mean | estimated | brain | 1.32 - 1.44 W/kg with PT |
| SAR | 1.38 W/kg | mean | estimated | brain | 1.35 - 1.38 W/kg without PT |
| SAR | 1.62 W/kg | peak value | estimated | 1 g | 1.48 - 1.62 W/kg in the brain with PT |
| SAR | 1.55 W/kg | peak value | estimated | 1 g | 1.52 - 1.55 W/kg in the brain without PT |
| SAR | 0.81 W/kg | mean | estimated | whole body | 0.74 - 0.81 W/kg with PT |
| SAR | 0.78 W/kg | mean | estimated | whole body | 0.76 - 0.78 W/kg without PT |
| SAR | 4.47 W/kg | peak value | estimated | 1 g | 4.09 - 4.47 W/kg in the body with PT |
| SAR | 4.28 W/kg | peak value | estimated | 1 g | 4.19 - 4.28 W/kg in the body without PT |
The data revealed that c-fos expression and glial markers were triggered by the combined stress of non-thermal mobile phone exposure and the toxic effect of picrotoxin on cerebral tissues:
90 minutes after exposure high levels of c-fos expression were recorded in the neocortex and paleocortex along with low hippocampus activation in picrotoxin treated animals. Most brain areas, except the piriform cortex, showed important increases in neuronal activation 24 h after exposure and picrotoxin administration. Three days after picrotoxin treatment, exposure effects were still apparent in the neocortex, and the hippocampal sturctures (dentate gyrus and CA3), but a significant decrease in activity was found in the palaeocortex structures (piriform cortex and entorhinal cortex). During this time, glial reactivity increased in brain regions of irradiated, picrotoxin-treated animals.
The findings suggest the need for further examination of the effects of mobile telephone exposure on epileptic patients.
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