The objective of this study was to investigate the effects of two sources of electromagnetic fields (EMFs) on the proteome of cerebellum, hippocampus, and frontal lobe in Balb/c mice following long-term whole body irradiation. Three equally divided groups of animals (6 animals/group) were used; the first group was exposed to a typical mobile phone, at a SAR level range of 0.17–0.37 W/kg for 3 h daily for 8 months, the second group was exposed to a wireless DECT base (Digital Enhanced Cordless Telecommunications/Telephone) at a SAR level range of 0.012–0.028 W/kg for 8 h/day also for 8 months and the third group comprised the sham-exposed animals. Comparative proteomics analysis revealed that long-term irradiation from both EMF sources altered significantly (p < 0.05) the expression of 143 proteins in total (as low as 0.003 fold downregulation up to 114 fold overexpression). Several neural function related proteins (i.e., Glial Fibrillary Acidic Protein (GFAP), Alpha-synuclein, Glia Maturation Factor beta (GMF), and apolipoprotein E (apoE)), heat shock proteins, and cytoskeletal proteins (i.e., Neurofilaments and tropomodulin) are included in this list as well as proteins of the brain metabolism (i.e., Aspartate aminotransferase, Glutamate dehydrogenase) to nearly all brain regions studied. Western blot analysis on selected proteins confirmed the proteomics data. The observed protein expression changes may be related to brain plasticity alterations, indicative of oxidative stress in the nervous system or involved in apoptosis and might potentially explain human health hazards reported so far, such as headaches, sleep disturbance, fatigue, memory deficits, and brain tumor long-term induction under similar exposure conditions.

Background: The widespread use of wireless devices during the last decades is raising concerns about adverse health effects of the radiofrequency electromagnetic radiation (RF‐EMR) emitted from these devices. Recent research is focusing on unraveling the underlying mechanisms of RF‐EMR and potential cellular targets. The “omics” high‐throughput approaches are powerful tools to investigate the global effects of RF‐EMR on cellular physiology.Methods: In this work, C57BL/6 adult male mice were whole‐body exposed (n_Exp = 8) for 2 hr to GSM 1800 MHz mobile phone radiation at an average electric field intensity range of 4.3–17.5 V/m or sham‐exposed (n_SE = 8), and the RF‐EMR effects on the hippocampal lipidome and transcriptome profiles were assessed 6 hr later.Results: The data analysis of the phospholipid fatty acid residues revealed that the levels of four fatty acids [16:0, 16:1 (6c + 7c), 18:1 9c, eicosapentaenoic acid omega‐3 (EPA, 20:5 ω3)] and the two fatty acid sums of saturated and monounsaturated fatty acids (SFA and MUFA) were significantly altered (p < 0.05) in the exposed group. The observed changes indicate a membrane remodeling response of the tissue phospholipids after nonionizing radiation exposure, reducing SFA and EPA, while increasing MUFA residues. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p < 0.05) between the two groups, revealing an impact on genes involved in critical biological processes, such as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis.Conclusions: This study provides preliminary evidence that mobile phone radiation induces hippocampal lipidome and transcriptome changes that may explain the brain proteome changes and memory deficits previously shown by our group.

Cerebral palsy (CP) is one of the most common childhood-onset motor disabilities, attributed to injuries of the immature brain in the foetal or early postnatal period. The underlying mechanisms are poorly understood, rendering prevention and treatment strategies challenging. The aim of the present study was to establish a mouse model of CP for preclinical assessment of new interventions. For this purpose, we explored the impact of a double neonatal insult (i.e. systemic inflammation combined with hypoxia) on behavioural and cellular outcomes relevant to CP during the prepubertal to adolescent period of mice. Pups were subjected to intraperitoneal lipopolysaccharide (LPS) injections from postnatal day (P) 3 to P6 followed by hypoxia at P7. Gene expression analysis at P6 revealed a strong inflammatory response in a brain region-dependent manner. A comprehensive battery of behavioural assessments performed between P24 and P47 showed impaired limb placement and coordination when walking on a horizontal ladder in both males and females. Exposed males also displayed impaired performance on a forelimb skilled reaching task, altered gait pattern and increased exploratory activity. Exposed females showed a reduction in grip strength and traits of anxiety-like behaviour. These behavioural alterations were not associated with gross morphological changes, white matter lesions or chronic inflammation in the brain. Our results indicate that the neonatal double-hit with LPS and hypoxia can induce subtle long-lasting deficits in motor learning and fine motor skills, which partly reflect the symptoms of children with CP who have mild gross and fine motor impairments.

The daily use by people of wireless communication devices has increased exponentially in the last decade, begetting concerns regarding its potential health hazards. Drosophila melanogaster four days-old adult female flies were exposed for 30 min to radiation emitted by a commercial mobile phone at a SAR of 0.15 W/kg and a SAE of 270 J/kg. ROS levels and apoptotic follicles were assayed in parallel with a genome-wide microarrays analysis. ROS cellular contents were found to increase by 1.6-fold (x), immediately after the end of exposure, in follicles of pre-choriogenic stages (germarium - stage 10), while sporadically generated apoptotic follicles (germarium 2b and stages 7–9) presented with an averaged 2x upregulation in their sub-population mass, 4 h after fly's irradiation with mobile device. Microarray analysis revealed 168 genes being differentially expressed, 2 h post-exposure, in response to radiofrequency (RF) electromagnetic field-radiation exposure (≥1.25x, P < 0.05) and associated with multiple and critical biological processes, such as basic metabolism and cellular subroutines related to stress response and apoptotic death. Exposure of adult flies to mobile-phone radiation for 30 min has an immediate impact on ROS production in animal's ovary, which seems to cause a global, systemic and non-targeted transcriptional reprogramming of gene expression, 2 h post-exposure, being finally followed by induction of apoptosis 4 h after the end of exposure. Conclusively, this unique type of pulsed radiation, mainly being derived from daily used mobile phones, seems capable of mobilizing critical cytopathic mechanisms, and altering fundamental genetic programs and networks in D. melanogaster.