ID Number		1119
Study Type		In Vivo
Model		Analysis of gene expression and oxidative stress in laboratory animals exposed to RF signals.
Details		Sprague Dawley rats were exposed to 900 MHz (GSM) for 20 min/day, 30 days using mobile phone handsets as exposure systems (hooked to the network and placed beneath Plexiglas cages). Max transmitting power (250 mW) was assumed, and SAR was calculated using FDTD as 0.52 W/kg (whole body average) with a peak 1 gram SAR of 3.13 W/kg. Analysis of bcl-2 (anti-apoptotic) gene expression in the brain and testes following exposure revealed no change as compared to control animals. In a subsequent study, Wistar rats (n = 31) were exposed to 900 MHz (GSM) for 2 hr/day, 7 days/wk, for 10 months in a carousel exposure chamber and brains analyzed for indicators of oxidative stress. Immunohistochemical analysis showed decreased expression of the active (cleaved) form of caspase-3 (apoptosis marker) and decreased overall apoptosis with no change in p53 expression. The authors also report an increase in catalase and other anti-oxidant proteins and no increase in measures of oxidative stress. AUTHORS' ABSTRACT: Dasdag and Akdag 2016 (IEEEE #6507): Wireless communication such as cellular telephones and other types of handheld phones working with frequencies of 900 MHz, 1800 MHz, 2100 MHz, 2450 MHz have been increasing rapidly. Therefore, public opinion concern about the potential human health hazards of short and long-term effect of exposure to radiofrequency (RF) radiation. Oxidative stress is a biochemical condition, which is defined by the imbalance between reactive oxygen species (ROS) and the anti-oxidative defense. In this review, we evaluated available in vitro and in vivo studies carried out on the relation between RF emitted from mobile phones and oxidative stress. The results of the studies we reviewed here indicated that mobile phones and similar equipment or radars can be thought as a factor, which cause oxidative stress. Even some of them claimed that oxidative stress originated from radiofrequencies can be resulted with DNA damage. For this reason one of the points to think on is relation between mobile phones and oxidative stress. However, more performance is necessary especially on human exposure studies. AUTHORS' ABSTRACT: Bilgin EEE #7205): Ubiquitous and ever increasing use of mobile phones led to the growing concern about the effects of radiofrequency radiation (RFR) emitted by cell phones on biological systems. The aim of this study is to explore whether long-term RFR exposure at different frequencies affects DNA damage and oxidant-antioxidant parameters in the blood and brain tissue of rats. 28 male Sprague Dawley rats were randomly divided into four equal groups (n = 7). They were identified as Group 1: sham-control, Group 2: 900 MHz, Group 3: 1800 MHz, and Group 4: 2100 MHz. Experimental groups of rats were exposed to RFR 2 h/day for 6 months. The sham-control group of rats was subjected to the same experimental condition but generator was turned off. Specific absorption rates (SARs) at brain with 1 g average were calculated as 0.0845 W/kg, 0.04563 W/kg, and 0.03957, at 900 MHz, 1800 MHz, and 2100 MHz, respectively. Additionally, malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), total antioxidant status (TAS), and total oxidant status (TOS) analyses were conducted in the brain tissue samples. Results of the study showed that DNA damage and oxidative stress indicators were found higher in the RFR exposure groups than in the sham-control group. In conclusion, 900-, 1800-, and 2100-MHz RFR emitted from mobile phones may cause oxidative damage, induce increase in lipid peroxidation, and increase oxidative DNA damage formation in the frontal lobe of the rat brain tissues. Furthermore, 2100-MHz RFR may cause formation of DNA single-strand breaks.
Findings		No Effects
Status		Completed With Publication
Principal Investigator		Dicle University, Turkey - dasdag@dicle.edu.tr
Funding Agency		Private/Instit.
Country		TURKEY
References		Dasdag, S et al. Electromagn Biol Med, (2009) 28:342-354 Yilmaz, F et al. Electromagn Biol Med, (2008) 27:65-72 Dasdag, S et al. Journal of Chemical Neuroanatomy., (2016) 75 (Part B):85-93 Alkis, ME et al. Electromagn Biol Med., (2019) 38:32-47 Delen, K et al. Bioelectromagnetics., (2021) 42:159-172 Yavas, MC et al. Electromagn Biol Med., (2021) 40:84-91 Alkis, ME et al. Bioelectromagnetics., (2021) 42:76-85
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