To determine whether sub-chronic radiofrequency exposure can cause constitutive induction of a stress response at a cellular and/or molecular level in hsp70.1-deficient mice due to repeated stimulation.
Previously the authors generated hsp70.1-deficient mice to elucidate the in vivo function of HSP70 (heat shock protein 70) in detail. The renal tissues and embryonic fibroblasts of these mice were shown to be more vulnerable to hyperosmotic stress.
Exposure | Parameters |
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Exposure 1:
849 MHz
Exposure duration:
twice daily for 45 min with a 15 min interval, 5 days a week for 4, 8 and 10 weeks
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Exposure 2:
849 MHz
Exposure duration:
one or two 45 min exposures
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Exposure 3:
1,763 MHz
Exposure duration:
twice daily for 45 min with a 15 min interval, 5 days a week for 4, 8 and 10 weeks
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Exposure 4:
1,763 MHz
Exposure duration:
one or two 45 min exposures
|
Frequency | 849 MHz |
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Type | |
Exposure duration | twice daily for 45 min with a 15 min interval, 5 days a week for 4, 8 and 10 weeks |
Exposure source |
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Chamber | Stainless steel reverberation chamber (2293 mm x 2296 mm x 1700 mm) fitted with mode stirrer for field uniformity |
Sham exposure | A sham exposure was conducted. |
Frequency | 1,763 MHz |
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Type | |
Exposure duration | twice daily for 45 min with a 15 min interval, 5 days a week for 4, 8 and 10 weeks |
Exposure source |
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No difference was revealed in the histopathological analysis between sham-exposed and radiofrequency exposed mice. There was no evidence of increased proliferative and apoptotic activities.
The levels of the heat shock proteins showed no obvious changes. Radiofrequency irradiation did not affect the phosphorylation status of stress-activated kinases.
The hsp70.1-deficient mice did not show any significant changes in terms of cell proliferation, apoptosis, or stress response due to exposure of 849 MHz or 1763 MHz radiofrequency fields.
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