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(Database last updated on Mar 27, 2024)
| ID Number | 2098 | |
| Study Type | In Vivo | |
| Model | 2450 MHz (CW) exposure to rats and analysis of oxidative stress in brain, blood, lens, testis and teeth. | |
| Details | Rats (n = 30) were exposed to 2450 MHz (CW) 60 min/day for 28 days and assessed for reactive oxygen and antioxidant enzyme expession in the brain as well as EEG recordings. The effects antioxidants selenium and L-carnitine in combination with exposure was also examined. The authors report decreases in cortex levels of vitamin A, vitamin C, vitamin E, and lipid peroxidation with exposure that was partially reversed with added selenium or L-carnitine in the diet. There was also an increase in the number of spikes in the alpha wave EEG pattern with exposure that was again reduced with antioxidant co-treatment. Earlier studies (2006) reported that in rats (n = 8 per group) exposed to 900 MHz (GSM) RF, melatonin administration resulted in a reversal of oxidative damage in cortical and hippocampal regions of the brain. AUTHORS' ABSTRACT: Cetin et al. 2014 (IEEE #5748): Objectives: The present study determined the effects of mobile phone (900 and 1800 MHz)-induced electromagnetic radiation (EMR) exposure on oxidative stress in the brain and liver as well as the element levels in growing rats from pregnancy to 6 weeks of age. Methods: Thirty-two rats and their offspring were equally divided into three different groups: the control, 900 MHz, and 1800 MHz groups. The 900 MHz and 1800 MHz groups were exposed to EMR for 60 min/d during pregnancy and neonatal development. At the 4th, 5th, and 6th weeks of the experiment, brain samples were obtained. Results: Brain and liver glutathione peroxidase activities, as well as liver vitamin A and ²-carotene concentrations decreased in the EMR groups, although brain iron, vitamin A, and ²-carotene concentrations increased in the EMR groups. In the 6th week, selenium concentrations in the brain decreased in the EMR groups. There were no statistically significant differences in glutathione, vitamin E, chromium, copper, magnesium, manganese, and zinc concentrations between the three groups. Conclusion: EMR-induced oxidative stress in the brain and liver was reduced during the development of offspring. Mobile phone-induced EMR could be considered as a cause of oxidative brain and liver injury in growing rats. AUTHORS' ABSTRACT: Oksay et al. 2012 (IEEE #5759): Wireless devices have become part of everyday life and mostly located near reproductive organs while they are in use. The present study was designed to determine the possible protective effects of melatonin on oxidative stress-dependent testis injury induced by 2.45-GHz electromagnetic radiation (EMR). Thirty-two rats were equally divided into four different groups, namely cage control (A1), sham control (A2), 2.45-GHz EMR (B) and 2.45-GHz EMR+melatonin (C). Group B and C were exposed to 2.45-GHz EMR during 60 min day(-1) for 30 days. Lipid peroxidation levels were higher in Group B than in Group A1 and A2. Melatonin treatment prevented the increase in the lipid peroxidation induced by EMR. Also reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) levels in Group D were higher than that of exposure group. Vitamin A and E concentrations decreased in exposure group, and melatonin prevented the decrease in vitamin E levels. In conclusion, wireless (2.45 GHz) EMR caused oxidative damage in testis by increasing the levels of lipid peroxidation and decreasing in vitamin A and E levels. Melatonin supplementation prevented oxidative damage induced by EMR and also supported the antioxidant redox system in the testis. AUTHORS' ABSTRACT: Tok et al. 2014 (IEEE #6172): INTRODUCTION: Melatonin has been considered a potent antioxidant that detoxifies a variety of reactive oxygen species in many pathophysiological states of eye. The present study was designed to determine the effects of Wi-Fi exposure on the lens oxidant, antioxidant redox systems, as well as the possible protective effects of melatonin on the lens injury induced by electromagnetic radiation (EMR). MATERIALS AND METHODS: Thirty-two rats were used in the current study and they were randomly divided into four equal groups as follows: First and second groups were cage-control and sham-control rats. Rats in third group were exposed to Wi-Fi (2.45 GHz) for duration of 60 min/day for 30 days. As in the third group, the fourth group was treated with melatonin. The one-hour exposure to irradiation in second, third and fourth took place at noon each day. RESULTS: lipid peroxidation levels in the lens were slightly higher in third (Wi-Fi) group than in cage and sham control groups although their concentrations were significantly (P < 0.05) decreased by melatonin supplementation. Glutathione peroxidase (GSH-Px) activity was significantly (P < 0.05) lower in Wi-Fi group than in cage and sham control groups although GSH-Px (P < 0.01) and reduced glutathione (P < 0.05) values were significantly higher in Wi-Fi + melatonin group than in Wi-Fi group. CONCLUSIONS: There are poor oxidative toxic effects of one hour of Wi-Fi exposure on the lens in the animals. However, melatonin supplementation in the lens seems to have protective effects on the oxidant system by modulation of GSH-Px activity. AUTHORS' ABSTRACT: Naziroglu et al. 2012 (IEEE #6173): We aimed to investigate the protective effects of melatonin and 2.45 GHz electromagnetic radiation (EMR) on brain and dorsal root ganglion (DRG) neuron antioxidant redox system, Ca(2+) influx, cell viability and electroencephalography (EEG) records in the rat. Thirty two rats were equally divided into four different groups namely group A1: Cage control, group A2: Sham control, group B: 2.45 GHz EMR, group C: 2.45 GHz EMR+melatonin. Groups B and C were exposed to 2.45 GHz EMR during 60 min/day for 30 days. End of the experiments, EEG records and the brain cortex and DRG samples were taken. Lipid peroxidation (LP), cell viability and cytosolic Ca(2+) values in DRG neurons were higher in group B than in groups A1 and A2 although their concentrations were increased by melatonin, 2-aminoethyldiphenyl borinate (2-APB), diltiazem and verapamil supplementation. Spike numbers of EEG records in group C were lower than in group B. Brain cortex vitamin E concentration was higher in group C than in group B. In conclusion, Melatonin supplementation in DRG neurons and brain seems to have protective effects on the 2.45 GHz-induced increase Ca(2+) influx, EEG records and cell viability of the hormone through TRPM2 and voltage gated Ca(2+) channels. AUTHORS' ABSTRACT: Naziroglu et al. 2012 (IEEE #6184): AIMS: Exposure to electromagnetic radiation (EMR) may increase breast cancer risk by inducing oxidative stress and suppressing the production of melatonin. Aim of the present review is to discuss the mechanisms and risk factors of EMR and oxidative stress-induced breast cancer, to summarize the controlled studies evaluating measures for prevention, and to conclude with evidence-based strategies for prevention. MATERIALS: Review of the relevant literature and results from our recent basic studies, as well as critical analyses of published systematic reviews were obtained from the Pubmed and the Science Citation Index. RESULTS: It has been proposed that chronic exposure to EMR may increase the risk of breast cancer by suppressing the production of melatonin; this suppression may affect the development of breast cancer either by increasing levels of circulation of estrogen or through over production of free oxygen radicals. Most epidemiological studies have also indicated overall effect of EMR exposure in premenopausal women, particularly for estrogen receptor positive breast tumors. Enhanced voltage-dependent Ca(2+) current and impaired inhibitory G-protein function, and derangement of intracellular organelles with a Ca(2+) buffering effect, such as endoplasmic reticulum and mitochondria have been also shown to contribute to disturbed Ca(2+) signaling in breast cancer. CONCLUSION: Melatonin may modulate breast cancer through modulation of enhanced oxidative stress and Ca(2+) influx in cell lines. However, there is not enough evidence on increased risk of breast cancer related to EMR exposure. |
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| Findings | Effects | |
| Status | Completed With Publication | |
| Principal Investigator | Suleyman Demirel University, Isparta, Turkey - mnaziroglu@med.sdu.edu.tr | |
| Funding Agency | ????? | |
| Country | TURKEY | |
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