To study the effects of radiofrequency in a mice strain characterized by age-determined carcinogenesis of lymphatic tissues (to investigate the biological modifications underlying carcinogenesis).
The evolution of carcinogenesis was followed up to 18 months. The maximal life span of control animals was about 24 months and the principal characteristic of the mice is to develop spontaneous lymphoid tumours in the course of ageing.
Exposure | Parameters |
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Exposure 1:
800 MHz
Exposure duration:
repeated exposure for 1 hour per week for 4 months
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Frequency | 800 MHz |
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Exposure duration | repeated exposure for 1 hour per week for 4 months |
Modulation type | unspecified |
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Exposure source | |
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Chamber | The RF exposure was carried out in a cylindrical polypropylene chamber, the exterior walls of which were covered with 10 mg/cm² aluminium foil, except for the top central area of 4 cm in diameter where the phone was positioned. |
Setup | The antenna of the cellular phone was located in the centre of the chamber. The animals were free to move in a circular corridor 5 cm wide and with a 2 cm separation from the antenna. |
Additional info | Two experiments were performed: In the first one, the 20 animals were divided equally into sham and exposure groups. The animals from both of these groups were injected intramuscularly with 10 µl isotonic calcium chloride 1 hour prior to their respective exposure or sham exposure treatments. In the second experiment, 24 animals were divided equally into sham and exposure groups. The animals from both these groups were injected intraperitionally with 30 µmol calcium 30 min prior to the their respective sham or exposure treatments. |
No parameters are specified for this exposure.
The data show that radiofrequency provoked an earlier general lymphocyte cell infiltration, formation of lymphoblastic ascites and extranodal tumours of different histological types, as well as an increased early mortality. The findings suggest that in exposed animals, carcinogenesis may be induced earlier and with different pathological forms than in control mice. The modifications in cellular calcium homeostasis and the age-determined thymus involution appear to be important factors involved in this carcinogenesis process.
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