ID Number		1707
Study Type		In Vivo
Model		900 MHz (GSM) exposure to rats and analysis of oxidative stress endpoints.
Details		Wistar rats (n = 10) were exposed to 900 MHz (GSM) RF (+/- vitamin C) while free roaming in cages for 4 weeks, with an estimated SAR of 1.2 W/kg (whole body). Exposure used an actual mobile phone handset suspended above the cage and hooked up to the local network. Following exposure, cornea and lens tissue was isolated and homogenized, and analyzed for free radicals using oxidative stress markers (MDA, SOD, GSH-Px, and CAT). The authors report significant increases in MDA and CAT in lens and cornea tissue, and a significant decrease in SOD activity. No effect on GSH-Px activity was reported. Vitamin C helped reverse the RF effects. The authors conclude (nonthermal) mobile phone exposure can induce degenerative changes in the cornea via an unknown mechanism, with protection provided by antioxidants. AUTHORS' ABSTRACT: Imge et al. 2010 (IEEE #6260): PURPOSE: To evaluate effects of mobile phone use on brain tissue and a possible protective role of vitamin C. MATERIALS AND METHODS: Forty female rats were divided into four groups randomly (Control, mobile phone, mobile phone plus vitamin C and, vitamin C alone). The mobile phone group was exposed to a mobile phone signal (900 MHz), the mobile phone plus vitamin C group was exposed to a mobile phone signal (900 MHz) and treated with vitamin C administered orally (per os). The vitamin C group was also treated with vitamin C per os for four weeks. Then, the animals were sacrificed and brain tissues were dissected to be used in the analyses of malondialdehyde (MDA), antioxidant potential (AOP), superoxide dismutase, catalase (CAT), glutathione peroxidase (GSH-Px), xanthine oxidase, adenosine deaminase (ADA) and 5'nucleotidase (5'-NT). RESULTS: Mobile phone use caused an inhibition in 5'-NT and CAT activities as compared to the control group. GSH-Px activity and the MDA level were also found to be reduced in the mobile phone group but not significantly. Vitamin C caused a significant increase in the activity of GSH-Px and non-significant increase in the activities of 5'-NT, ADA and CAT enzymes. CONCLUSION: Our results suggest that vitamin C may play a protective role against detrimental effects of mobile phone radiation in brain tissue. AUTHORS' ABSTRACT: Balci et al. 2009 (IEEE #6266): PURPOSE: This study aims to investigate the possible effects of computer monitor-emitted radiation on the oxidant/antioxidant balance in corneal and lens tissues and to observe any protective effects of vitamin C (vit C). METHODS: Four groups (PC monitor, PC monitor plus vitamin C, vitamin C, and control) each consisting of ten Wistar rats were studied. The study lasted for three weeks. Vitamin C was administered in oral doses of 250 mg/kg/day. The computer and computer plus vitamin C groups were exposed to computer monitors while the other groups were not. Malondialdehyde (MDA) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities were measured in corneal and lens tissues of the rats. RESULTS: In corneal tissue, MDA levels and CAT activity were found to increase in the computer group compared with the control group. In the computer plus vitamin C group, MDA level, SOD, and GSH-Px activities were higher and CAT activity lower than those in the computer and control groups. Regarding lens tissue, in the computer group, MDA levels and GSH-Px activity were found to increase, as compared to the control and computer plus vitamin C groups, and SOD activity was higher than that of the control group. In the computer plus vitamin C group, SOD activity was found to be higher and CAT activity to be lower than those in the control group. CONCLUSION: The results of this study suggest that computer-monitor radiation leads to oxidative stress in the corneal and lens tissues, and that vitamin C may prevent oxidative effects in the lens.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Ankara Hospital, Turkey
Funding Agency		Private/Instit.
Country		TURKEY
References		Balci, M et al. Curr Eye Res, (2007) 32:21-25 Imge, EB et al. Int J Radiat Biol., (2010) 86:1044-1049 Balci, M et al. Mol Vis., (2009) 15:2521-2525
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