Mus musculus
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ABSTRACT:
PROVIDER: PRJNA360284 | ENA |
REPOSITORIES: ENA
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Project description:The widespread use of wireless devices during the last decades is rising the concern about the adverse health effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted from these devices. Studies are targeting on unrevealing the underlying mechanisms of RF-EMR action. The contribution of the “omics” high throughput approaches is a prerequisite towards this direction. In the present work, C57BL/6 adult male mice were sham-exposed (nSE=8) or whole-body exposed (nExp=8) for 2h to GSM 1800 MHz mobile phone radiation at 11 V/m average electric field intensity, and the RF-EMR effects on the hippocampal lipidome and transcriptome profile were evaluated. The data analysis of the phospholipids’ fatty acid residues revealed that the levels of six fatty acids (16:0, 16:1 6+7c, 18:1 9c, 20:5 w3, SFA, MUFA) were significantly altered (p<0.05) in the exposed group. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p<0.05) between the two groups with a fold change cut off of 1.5. In general, the observed changes point out the attention to a membrane remodeling response of the tissue phospholipids after non-ionizing radiation exposure, reducing the Saturated Fatty Acids (SFA) and EPA omega-3 (20:5 w3) and increasing Monounsaturated Fatty Acids (MUFA) residues and in parallel reflect an impact to genes implicated in critical biological processes, as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism and cancer
2017-07-10 | GSE93199 | GEO
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 vs control). 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.
2019-12-20 | MSV000084732 | MassIVE
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), 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.
2019-12-20 | MSV000084731 | MassIVE
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 vs control). 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.
2020-01-03 | MSV000084746 | MassIVE
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
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.
2010-07-20 | GSE22991 | GEO
Project description:Protocol describing step-by-step of an in-gel digestion to analyze Medaka proteome after acute exposure to ionizing radiation as alternative to epidemiological studies.
2020-06-28 | PXD014206 | JPOST Repository
Project description:Background: The brain undergoes ionizing radiation exposure in many clinical situations, particularly during radiotherapy for brain tumors. The critical role of hippocampus in the pathogenesis of radiation-induced neurocognitive dysfunction is well recognized. Aim: The goal of this study is to test the potential contribution of non-targeted effects in the detrimental response of hippocampus to irradiation and to elucidate the mechanisms involved. Material and Methods: C57Bl/6 mice were whole body (WBI) or partial body (PBI) irradiated with 0.1 or 2.0 Gy of X-rays or sham irradiated. PBI consisted in the exposure of the lower third of the mouse body, whilst the upper two thirds were shielded. Hippocampi were collected 15 days or 6 months post-irradiation and a multi-omics approach was adopted to assess the molecular changes in non-coding RNAs, proteins and metabolic levels, as well as histological changes in the rate of hippocampal neurogenesis. Results: Notably, at 2.0 Gy the pattern of early molecular and histopathological changes induced in the hippocampus at 15 days following PBI was similar in quality and quantity to the effects induced by WBI, thus providing a proof of principle of the existence of out-of-target radiation response in the hippocampus of conventional mice. We detected major alterations in DAG/IP3 and TGF- signaling pathways as well as in the expression of proteins involved in the regulation of long-term neuronal synaptic plasticity and synapse organization, coupled with defects in NSCs self-renewal in the hippocampal dentate gyrus. However, compared to the persistence of the WBI effects, most of the PBI effects were only transient and tended to decrease at 6 months post-irradiation, indicating important mechanistic difference. On the contrary, at low dose we identified a progressive accumulation of molecular defects that tended to manifest at later post-irradiation times. These data, indicating that both targeted and non-targeted radiation effects might contribute to the pathogenesis of hippocampal radiation-damage, have general implications for human health
2021-09-10 | PXD024975 | Pride
Project description:Accidents with ionizing radiation (IR) often involve acute high dose exposures that can lead to acute radiation syndrome and late effects. IR can induce genomic lesions, cell death or carcinogenesis. Here, we investigated acute IR-induced cellular genomic signatures at the genome wide level. After exposing the adenocarcinoma cell line A549 to an acute 6 Gy 240 kV X-Ray dose, four surviving clonogenic cells were recovered by minimal dilution and further expanded and analyzed by cytogenetics, chromosome painting and tiling-path array CGH, with the non-irradiated clone0 serving as control. It was found that acute X-ray exposure induced changes in modal chromosome number and specific translocations in the four irradiation surviving clones. Furthermore, clone4 displayed an increased radiosensitivity at D > 5 Gy. Array CGH disclosed unique and recurrent genomic changes, predominantly gains, and disclosed fragile sites FRA3B and FRA16D as preferential regions of genomic alterations in all irradiated clones, which likely relates to irradiation-induced genomic stress. Gene expression analysis revealed a specific profile of 364 genes in clone4, of which p53 pathway genes may contribute to its increased radiosensitivity. IR-induced genomic changes AND fragile site expression highlight the capacity of a single acute radiation exposure to resculpture the genome of tumor cells by inflicting genomic stress. Gene expression in A549 cell line was analysed after exposure to 6Gy X-rays at a dose rate of 1Gy/min.
2011-02-04 | E-GEOD-24876 | biostudies-arrayexpress