Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mechanism of short-term ERK activation by electromagnetic fields at mobile phone frequencies.

ABSTRACT: The exposure to non-thermal microwave electromagnetic fields generated by mobile phones affects the expression of many proteins. This effect on transcription and protein stability can be mediated by the MAPK (mitogen-activated protein kinase) cascades, which serve as central signalling pathways and govern essentially all stimulated cellular processes. Indeed, long-term exposure of cells to mobile phone irradiation results in the activation of p38 as well as the ERK (extracellular-signal-regulated kinase) MAPKs. In the present study, we have studied the immediate effect of irradiation on the MAPK cascades, and found that ERKs, but not stress-related MAPKs, are rapidly activated in response to various frequencies and intensities. Using signalling inhibitors, we delineated the mechanism that is involved in this activation. We found that the first step is mediated in the plasma membrane by NADH oxidase, which rapidly generates ROS (reactive oxygen species). These ROS then directly stimulate MMPs (matrix metalloproteinases) and allow them to cleave and release Hb-EGF [heparin-binding EGF (epidermal growth factor)]. This secreted factor activates the EGF receptor, which in turn further activates the ERK cascade. Thus this study demonstrates for the first time a detailed molecular mechanism by which electromagnetic irradiation from mobile phones induces the activation of the ERK cascade and thereby induces transcription and other cellular processes.

SUBMITTER: Friedman J

PROVIDER: S-EPMC2267306 | biostudies-other | 2007 Aug

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Time averaged transmitter power and exposure to electromagnetic fields from mobile phone base stations.

Project description:Models for exposure assessment of high frequency electromagnetic fields from mobile phone base stations need the technical data of the base stations as input. One of these parameters, the Equivalent Radiated Power (ERP), is a time-varying quantity, depending on communication traffic. In order to determine temporal averages of the exposure, corresponding averages of the ERP have to be available. These can be determined as duty factors, the ratios of the time-averaged power to the maximum output power according to the transmitter setting. We determine duty factors for UMTS from the data of 37 base stations in the Swisscom network. The UMTS base stations sample contains sites from different regions of Switzerland and also different site types (rural/suburban/urban/hotspot). Averaged over all regions and site types, a UMTS duty factor for the 24 h-average is obtained, i.e., the average output power corresponds to about a third of the maximum power. We also give duty factors for GSM based on simple approximations and a lower limit for LTE estimated from the base load on the signalling channels.

| S-EPMC4143847 | biostudies-literature

Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide excision repair in serum-deprived human glioblastoma cells.

Project description:Some epidemiological studies indicate that the use of mobile phones causes cancer in humans (in particular glioblastomas). It is known that DNA damage plays a key role in malignant transformation; therefore, we investigated the impact of the UMTS signal which is widely used in mobile telecommunications, on DNA stability in ten different human cell lines (six brain derived cell lines, lymphocytes, fibroblasts, liver and buccal tissue derived cells) under conditions relevant for users (SAR 0.25 to 1.00 W/kg). We found no evidence for induction of damage in single cell gel electrophoresis assays when the cells were cultivated with serum. However, clear positive effects were seen in a p53 proficient glioblastoma line (U87) when the cells were grown under serum free conditions, while no effects were found in p53 deficient glioblastoma cells (U251). Further experiments showed that the damage disappears rapidly in U87 and that exposure induced nucleotide excision repair (NER) and does not cause double strand breaks (DSBs). The observation of NER induction is supported by results of a proteome analysis indicating that several proteins involved in NER are up-regulated after exposure to UMTS; additionally, we found limited evidence for the activation of the ?-interferon pathway. The present findings show that the signal causes transient genetic instability in glioma derived cells and activates cellular defense systems.

| S-EPMC5896905 | biostudies-literature

Environmental Radiofrequency Electromagnetic Fields Exposure at Home, Mobile and Cordless Phone Use, and Sleep Problems in 7-Year-Old Children.

Project description:We evaluated if exposure to RF-EMF was associated with reported quality of sleep in 2,361 children, aged 7 years.This study was embedded in the Amsterdam Born Children and their Development (ABCD) birth cohort study. When children were about five years old, school and residential exposure to RF-EMF from base stations was assessed with a geospatial model (NISMap) and from indoor sources (cordless phone/WiFi) using parental self-reports. Parents also reported their children's use of mobile or cordless phones. When children were seven years old, we evaluated sleep quality as measured with the Child Sleep Habits Questionnaire (CSHQ) filled in by parents. Of eight CSHQ subscales, we evaluated sleep onset delay, sleep duration, night wakenings, parasomnias and daytime sleepiness with logistic or negative binomial regression models, adjusting for child's age and sex and indicators of socio-economic position of the parents. We evaluated the remaining three subscales (bedtime resistance, sleep anxiety, sleep disordered breathing) as unrelated outcomes (negative control) because these were a priori hypothesised not to be associated with RF-EMF.Sleep onset delay, night wakenings, parasomnias and daytime sleepiness were not associated with residential exposure to RF-EMF from base stations. Sleep duration scores were associated with RF-EMF levels from base stations. Higher use mobile phones was associated with less favourable sleep duration, night wakenings and parasomnias, and also with bedtime resistance. Cordless phone use was not related to any of the sleeping scores.Given the different results across the evaluated RF-EMF exposure sources and the observed association between mobile phone use and the negative control sleep scale, our study does not support the hypothesis that it is the exposure to RF-EMF that is detrimental to sleep quality in 7-year old children, but potentially other factors that are related to mobile phone usage.

| S-EPMC4625083 | biostudies-literature

Enhancement of mesenchymal stem cell chondrogenesis with short-term low intensity pulsed electromagnetic fields.

Project description:Pulse electromagnetic fields (PEMFs) have been shown to recruit calcium-signaling cascades common to chondrogenesis. Here we document the effects of specified PEMF parameters over mesenchymal stem cells (MSC) chondrogenic differentiation. MSCs undergoing chondrogenesis are preferentially responsive to an electromagnetic efficacy window defined by field amplitude, duration and frequency of exposure. Contrary to conventional practice of administering prolonged and repetitive exposures to PEMFs, optimal chondrogenic outcome is achieved in response to brief (10 minutes), low intensity (2 mT) exposure to 6 ms bursts of magnetic pulses, at 15 Hz, administered only once at the onset of chondrogenic induction. By contrast, repeated exposures diminished chondrogenic outcome and could be attributed to calcium entry after the initial induction. Transient receptor potential (TRP) channels appear to mediate these aspects of PEMF stimulation, serving as a conduit for extracellular calcium. Preventing calcium entry during the repeated PEMF exposure with the co-administration of EGTA or TRP channel antagonists precluded the inhibition of differentiation. This study highlights the intricacies of calcium homeostasis during early chondrogenesis and the constraints that are placed on PEMF-based therapeutic strategies aimed at promoting MSC chondrogenesis. The demonstrated efficacy of our optimized PEMF regimens has clear clinical implications for future regenerative strategies for cartilage.

| S-EPMC5572790 | biostudies-literature

Semi-quantitative proteomics of mammalian cells upon short-term exposure to non-ionizing electromagnetic fields.

Project description:The potential effects of non-ionizing electromagnetic fields (EMFs), such as those emitted by power-lines (in extremely low frequency range), mobile cellular systems and wireless networking devices (in radio frequency range) on human health have been intensively researched and debated. However, how exposure to these EMFs may lead to biological changes underlying possible health effects is still unclear. To reveal EMF-induced molecular changes, unbiased experiments (without a priori focusing on specific biological processes) with sensitive readouts are required. We present the first proteome-wide semi-quantitative mass spectrometry analysis of human fibroblasts, osteosarcomas and mouse embryonic stem cells exposed to three types of non-ionizing EMFs (ELF 50 Hz, UMTS 2.1 GHz and WiFi 5.8 GHz). We performed controlled in vitro EMF exposures of metabolically labeled mammalian cells followed by reliable statistical analyses of differential protein- and pathway-level regulations using an array of established bioinformatics methods. Our results indicate that less than 1% of the quantitated human or mouse proteome responds to the EMFs by small changes in protein abundance. Further network-based analysis of the differentially regulated proteins did not detect significantly perturbed cellular processes or pathways in human and mouse cells in response to ELF, UMTS or WiFi exposure. In conclusion, our extensive bioinformatics analyses of semi-quantitative mass spectrometry data do not support the notion that the short-time exposures to non-ionizing EMFs have a consistent biologically significant bearing on mammalian cells in culture.

| S-EPMC5325209 | biostudies-literature

Targeted treatment of cancer with radiofrequency electromagnetic fields amplitude-modulated at tumor-specific frequencies.

Project description:In the past century, there have been many attempts to treat cancer with low levels of electric and magnetic fields. We have developed noninvasive biofeedback examination devices and techniques and discovered that patients with the same tumor type exhibit biofeedback responses to the same, precise frequencies. Intrabuccal administration of 27.12 MHz radiofrequency (RF) electromagnetic fields (EMF), which are amplitude-modulated at tumor-specific frequencies, results in long-term objective responses in patients with cancer and is not associated with any significant adverse effects. Intrabuccal administration allows for therapeutic delivery of very low and safe levels of EMF throughout the body as exemplified by responses observed in the femur, liver, adrenal glands, and lungs. In vitro studies have demonstrated that tumor-specific frequencies identified in patients with various forms of cancer are capable of blocking the growth of tumor cells in a tissue- and tumor-specific fashion. Current experimental evidence suggests that tumor-specific modulation frequencies regulate the expression of genes involved in migration and invasion and disrupt the mitotic spindle. This novel targeted treatment approach is emerging as an appealing therapeutic option for patients with advanced cancer given its excellent tolerability. Dissection of the molecular mechanisms accounting for the anti-cancer effects of tumor-specific modulation frequencies is likely to lead to the discovery of novel pathways in cancer.

| S-EPMC3845545 | biostudies-literature

Effects of global system for mobile communications 1800 MHz radiofrequency electromagnetic fields on gene expression in MCF-7 cells

2010-07-20 | GSE22991 | GEO

Effects of global system for mobile communications 1800 MHz radiofrequency electromagnetic fields on gene expression in MCF-7 cells

Project description:Despite many studies over a decade, it still remains ambiguous as to the real biological effects induced by radiofrequency electromagnetic fields (RF EMF). Epidemiological studies indicates that long-term exposure to EMF could increase the risk of breast cancer. Some reports have showed that in vitro EMF exposures change cellular gene expression. In this study, we investigated global gene expression responses to RF EMF simulating the Global System for Mobile Communications (GSM) 1800 MHz signal in human breast cancer cell line MCF-7 using transcriptomic approaches. MCF-7 cells were intermittently (5 min fields on/10 min fields off) exposed to RF EMF at an average specific absorption rate (SAR) of 2.0 W/kg (2 W/kg exposure group) or sham-exposed (2 W/kg control group) for 24 h, or exposed to RF EMF at a higher level of 3.5 W/kg (3.5 W/kg exposure group) or sham-exposed (3.5 W/kg control group).

2010-07-20 | E-GEOD-22991 | biostudies-arrayexpress

Mobile phone use, exposure to radiofrequency electromagnetic field, and brain tumour: a case-control study.

Project description:In a case-control study in Japan of brain tumours in relation to mobile phone use, we used a novel approach for estimating the specific absorption rate (SAR) inside the tumour, taking account of spatial relationships between tumour localisation and intracranial radiofrequency distribution. Personal interviews were carried out with 88 patients with glioma, 132 with meningioma, and 102 with pituitary adenoma (322 cases in total), and with 683 individually matched controls. All maximal SAR values were below 0.1 W kg(-1), far lower than the level at which thermal effects may occur, the adjusted odds ratios (ORs) for regular mobile phone users being 1.22 (95% confidence interval (CI): 0.63-2.37) for glioma and 0.70 (0.42-1.16) for meningioma. When the maximal SAR value inside the tumour tissue was accounted for in the exposure indices, the overall OR was again not increased and there was no significant trend towards an increasing OR in relation to SAR-derived exposure indices. A non-significant increase in OR among glioma patients in the heavily exposed group may reflect recall bias.

| S-EPMC2243154 | biostudies-other

Effects of mobile phone electromagnetic radiation on rat hippocampus proteome.

Project description:Worldwide, number of mobile phone users have increased from 5.57 billion in 2011 to 6.8 billion in 2019. However short and long term impacts of the electromagnetic radiations emitting of mobile phone on tissue homeostasis with particular to brain proteome composition needs further investigation. In this study, we attempted a global proteome profiling study of rat hippocampus exposed to mobile phone radiation for 20 weeks (for 3 hrs/day for 5 days/week) to identify deregulated proteins and western blot analysis for validation. As a result, we identified 358 hippocampus proteins, of which 16 showed deregulation (log2 (exposed/control)>±1.0, p-value<0.05). Majority of these deregulated proteins grouped to three clusters sharing similar molecular functions/pathways. A set of four proteins (Aldehyde dehydrogenase:Aldh5a1, Na+ K+ transporting ATPase:Atp1b2, plasma membrane calcium transporting ATPase:PMCA and protein S100b) presenting each functional pathways were selected as important molecules. Western blot analysis of this protein set, expect Atp1b2, in independent samples corroborated the mass spectrometry findings. Aldh5a1 involve in cellular energy metabolism, both Atp1b2 and PMCA responsible for membrane transport and protein S100b has neuroprotective role. In conclusion, we present deregulated hippocampus proteome upon mobile phone radiation which might impact healthy functioning of brain.

2019-11-08 | MSV000084559 | MassIVE

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data