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Kahya, M.C.; Nazıroğlu, M.; Çiğ, B. |
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Title |
Selenium reduces mobile phone (900 MHz)-induced oxidative stress, mitochondrial function, and apoptosis in breast cancer cells |
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Journal Article |
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Year |
2014 |
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Biological trace element research |
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160 |
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2 |
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285-293 |
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Keywords |
apoptosis; breast cancer; mitochondria; mobile phone; oxidative stress |
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Abstract |
Exposure to mobile phone-induced electromagnetic radiation (EMR) may affect biological systems by increasing free oxygen radicals, apoptosis, and mitochondrial depolarization levels although selenium may modulate the values in cancer. The present study was designed to investigate the effects of 900 MHz radiation on the antioxidant redox system, apoptosis, and mitochondrial depolarization levels in MDA-MB-231 breast cancer cell line. Cultures of the cancer cells were divided into four main groups as controls, selenium, EMR, and EMR + selenium. In EMR groups, the cells were exposed to 900 MHz EMR for 1 h (SAR value of the EMR was 0.36 ± 0.02 W/kg). In selenium groups, the cells were also incubated with sodium selenite for 1 h before EMR exposure. Then, the following values were analyzed: (a) cell viability, (b) intracellular ROS production, (c) mitochondrial membrane depolarization, (d) cell apoptosis, and (e) caspase-3 and caspase-9 values. Selenium suppressed EMR-induced oxidative cell damage and cell viability (MTT) through a reduction of oxidative stress and restoring mitochondrial membrane potential. Additionally, selenium indicated anti-apoptotic effects, as demonstrated by plate reader analyses of apoptosis levels and caspase-3 and caspase-9 values. In conclusion, 900 MHz EMR appears to induce apoptosis effects through oxidative stress and mitochondrial depolarization although incubation of selenium seems to counteract the effects on apoptosis and oxidative stress. |
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UNIBAS @ david.schuermann @ |
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621 |
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Kang, K.A.; Lee, H.C.; Lee, J.-J.; Hong, M.-N.; Park, M.-J.; Lee, Y.-S.; Choi, H.-D.; Kim, N.; Ko, Y.-G.; Lee, J.-S. |
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Title |
Effects of combined radiofrequency radiation exposure on levels of reactive oxygen species in neuronal cells |
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Journal Article |
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Year |
2014 |
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Journal of radiation research |
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55 |
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2 |
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265-276 |
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combined rf radiation; h 2 o 2; menadione; neuronal cells; reactive oxygen species |
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The objective of this study was to investigate the effects of the combined RF radiation (837 MHz CDMA plus 1950 MHz WCDMA) signal on levels of intracellular reactive oxygen species (ROS) in neuronal cells. Exposure of the combined RF signal was conducted at specific absorption rate values of 2 W/kg of CDMA plus 2 W/kg of WCDMA for 2 h. Co-exposure to combined RF radiation with either H2O2 or menadione was also performed. The experimental exposure groups were incubator control, sham-exposed, combined RF radiation-exposed with or without either H2O2 or menadione groups. The intracellular ROS level was measured by flow cytometry using the fluorescent probe dichlorofluorescein diacetate. Intracellular ROS levels were not consistently affected by combined RF radiation exposure alone in a time-dependent manner in U87, PC12 or SH-SY5Y cells. In neuronal cells exposed to combined RF radiation with either H2O2 or menadione, intracellular ROS levels showed no statically significant alteration compared with exposure to menadione or H2O2 alone. These findings indicate that neither combined RF radiation alone nor combined RF radiation with menadione or H2O2 influences the intracellular ROS level in neuronal cells such as U87, PC12 or SH-SY5Y. |
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UNIBAS @ david.schuermann @ |
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622 |
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Kantar Gok, D.; Akpinar, D.; Yargicoglu, P.; Ozen, S.; Aslan, M.; Demir, N.; Derin, N.; Agar, A. |
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Effects of extremely low-frequency electric fields at different intensities and exposure durations on mismatch negativity |
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Journal Article |
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2014 |
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Neuroscience |
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Neuroscience |
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272 |
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154-166 |
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4-hydroxy-2-nonenal; apoptosis; electric field; mismatch negativity; protein carbonyl |
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The effects of extremely low-frequency electric fields (ELF-EFs, 3-300Hz) on lipid peroxidation levels and antioxidant enzyme activities have been shown in many tissues and plasma after exposure to 50-Hz alternating current (AC) electric fields. However, similar studies investigating brain lipid peroxidation status are limited. Moreover and as far as we know, no study has been conducted to examine mismatch negativity (MMN) response in rats following exposure to a 50-Hz AC electric field. Therefore, the purpose of the study was to investigate different intensities and exposure durations of ELF-EFs on MMN component of event-related potentials (ERPs) as well as apoptosis and oxidative brain damage in rats. Ninety male rats, aged 3months were used in our study. A total of six groups, composed of 15 animals each, was formed as follows: sham-exposed rats for 2weeks (C2), sham-exposed rats for 4weeks (C4), rats exposed to 12-kV/m and 18-kV/m electric fields for 2weeks (E12-2 and E18-2), rats exposed to 12- and 18-kV/m electric fields for 4weeks (E12-4 and E18-4). At the end of the experimental period, MMN responses were recorded in urethane-anesthetized rats by electrodes positioned stereotaxically to the surface of the dura. After MMN recordings, animals were killed by exsanguination and their brain tissues were removed for 4-hydroxy-2-nonenal (4-HNE), protein carbonyl and TUNEL analysis. In the current study, different change patterns in ERP parameters were observed dependent on the intensity and exposure duration of ELF-EFs. There were differences in the amplitudes of ERP between the responses to the standard and the deviant tones in all groups. When peak-to-peak amplitude of the difference curves was evaluated, MMN amplitude was significantly decreased in the E18-4 group compared with the C4 group. Additionally, the amount of 4-HNE was increased in all experimental groups compared with the control group. Consequently, it could be concluded that electric field decreased MMN amplitudes possibly induced by lipid peroxidation. |
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Department of Physiology, Faculty of Medicine, Akdeniz University, Arapsuyu, 07070 Antalya, Turkey |
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0306-4522 |
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PMID:24811084 |
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CBM.UAM @ ccobaleda @ |
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592 |
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Khushi, M.; Liddle, C.; Clarke, C.L.; Graham, J.D. |
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Binding sites analyser (BiSA): software for genomic binding sites archiving and overlap analysis |
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Journal Article |
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2014 |
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PloS one |
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PLoS One |
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9 |
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2 |
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e87301 |
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Genome-wide mapping of transcription factor binding and histone modification reveals complex patterns of interactions. Identifying overlaps in binding patterns by different factors is a major objective of genomic studies, but existing methods to archive large numbers of datasets in a personalised database lack sophistication and utility. Therefore we have developed transcription factor DNA binding site analyser software (BiSA), for archiving of binding regions and easy identification of overlap with or proximity to other regions of interest. Analysis results can be restricted by chromosome or base pair overlap between regions or maximum distance between binding peaks. BiSA is capable of reporting overlapping regions that share common base pairs; regions that are nearby; regions that are not overlapping; and average region sizes. BiSA can identify genes located near binding regions of interest, genomic features near a gene or locus of interest and statistical significance of overlapping regions can also be reported. Overlapping results can be visualized as Venn diagrams. A major strength of BiSA is that it is supported by a comprehensive database of publicly available transcription factor binding sites and histone modifications, which can be directly compared to user data. The documentation and source code are available on http://bisa.sourceforge.net. |
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Westmead Institute for Cancer Research, Sydney Medical School, University of Sydney and the Westmead Millennium Institute, Westmead, New South Wales, Australia |
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1932-6203 |
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PMID:24533055 |
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CBM.UAM @ ccobaleda @ |
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535 |
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Kirschvink, J.L. |
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Title |
Sensory biology: Radio waves zap the biomagnetic compass |
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Journal Article |
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2014 |
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Nature |
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Nature |
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Division of Geological and Planetary Sciences, California Institute of Technology, Pasadena, California 91125, USA, and at the Earth-Life Science Institute, Tokyo Institute of Technology, Japan |
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0028-0836 |
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PMID:24805230 |
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CBM.UAM @ ccobaleda @ |
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463 |
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