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Ratten ontwikkelen eerder kanker bij blootstelling aan HF straling Speciale ratten die een genetische afwijking hebben waardoor ze snel kanker aan de lymfenklieren ontwikkelen zijn in dit onderzoek gebruikt. Een groep werd 1 uur per week blootgesteld aan HF straling op 800 MHz gedurende 4 maanden. De andere groep werd niet blootgesteld. De blootgestelde groep ratten ontwikkelde sneller kanker en overleed eerder dan de niet-blootgestelde groep ratten. Int J Radiat Biol. 2005 Mar;81(3):205-9. Related Articles, Links Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering factor. www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16019929&dopt=Abstract www.emf-portal.de/viewer.php?l=g&aid=12248 Anghileri LJ, Mayayo E, Domingo JL, Thouvenot P. Biophysics Laboratory, Faculty of Medicine, University of Nancy, France. leopoldo.anghileri@wanadoo.fr The aim was to study the effects of radiofrequency (Rf) in a mice strain characterized by age-determined carcinogenesis of lymphatic tissues. Mice were treated with a 1?h/week Rf exposure for 4 months. A group submitted to sham exposure was used as control animals. The evolution of carcinogenesis was followed up to 18 months. The maximal life span of control mice was about 24 months. All dead animals were clinically and histologically examined to give an age-determined comparative quantification of the evolving carcinogenesis. A radiocalcium tracer method permitted the evaluation of Rf effects on transmembrane transport of extracellular calcium at 1 and 24 h after exposure. The determination of induced lipid peroxidation completed this second study. The findings show that Rf 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 results suggest that in Rf-exposed mice, carcinogenesis may be induced earlier and with different pathological forms than in control animals. 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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