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Finse studie: DNA schade en straling van mobiele telefonie    
Ga naar overzicht berichten in: Onderzoeken

Finse studie: DNA schade en straling van mobiele telefonie
woensdag, 14 januari 2009 - Dossier: Algemeen


Bron: Mutation Research 24 december 2008

Enhancement of chemically induced reactive oxygen species production and DNA damage in human SH-SY5Y neuroblastoma cells by 872MHz radiofrequency radiation.

Luukkonen J, Hakulinen P, Mäki-Paakkanen J, Juutilainen J, Naarala J.

Department of Environmental Science, University of Kuopio, Bioteknia 2, P.O. Box 1627, FI-70211 Kuopio, Finland.

The objective of the study was to investigate effects of 872MHz radiofrequency (RF) radiation on intracellular reactive oxygen species (ROS) production and DNA damage at a relatively high SAR value (5W/kg). The experiments also involved combined exposure to RF radiation and menadione, a chemical inducing intracellular ROS production and DNA damage. The production of ROS was measured using the fluorescent probe dichlorofluorescein and DNA damage was evaluated by the Comet assay. Human SH-SY5Y neuroblastoma cells were exposed to RF radiation for 1h with or without menadione. Control cultures were sham exposed. Both continuous waves (CW) and a pulsed signal similar to that used in global system for mobile communications (GSM) mobile phones were used. Exposure to the CW RF radiation increased DNA breakage (p<0.01) in comparison to the cells exposed only to menadione. Comparison of the same groups also showed that ROS level was higher in cells exposed to CW RF radiation at 30 and 60min after the end of exposure (p<0.05 and p<0.01, respectively). No effects of the GSM signal were seen on either ROS production or DNA damage. The results of the present study suggest that 872MHz CW RF radiation at 5W/kg might enhance chemically induced ROS production and thus cause secondary DNA damage. However, there is no known mechanism that would explain such effects from CW RF radiation but not from GSM modulated RF radiation at identical SAR.

PMID: 19135463

Voor het originele abstract zie:
www.ncbi.nlm.nih.gov/pubmed/19135463?dopt=Abstract .


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