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Background Electromagnetic radiation (EMR) exposure has been linked to oxidative stress and neurochemical imbalances, potentially compromising cellular integrity. By increasing free radical production, EMR disrupts the antioxidant defense system, including glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT); which may contribute to neuronal damage and cognitive impairment. Method This study examines the impact of intrauterine mobile phone radiation (MPR) exposure on hippocampal neurotransmitters and oxidative stress markers in albino mice and their offspring. Thirty-five healthy mice, obtained from pregnant females aged 10–14 weeks (weighing 18–20 g), were randomly divided into seven groups (n = 5 per group), Group I (control, no MPR exposure); Groups II–IV (exposed to 2G 0.9 GHz, 3G 1.5 GHz, and 4G 1.95 GHz MPR until parturition, respectively); and Groups V–VII (exposed to the same frequencies until weaning). Results After eight weeks of exposure, hippocampal tissues were analyzed for neurochemical markers (acetylcholinesterase (AChE) and glutamate (GLU)) as well as oxidative stress biomarkers (malondialdehyde (MDA), SOD, and GSH) and their histological structure. MPR exposure resulted in a significant reduction ( p  < 0.05) in AChE levels in groups III–VII, except for group II ( p  > 0.05), while GLU levels significantly increased ( p  < 0.05) in group VII. Oxidative stress analysis revealed significantly elevated MDA and SOD levels ( p  < 0.05) and a marked reduction in GSH levels across all exposed groups ( p  < 0.05). Conclusion Intrauterine exposure to MPR induces oxidative stress and neurochemical imbalances in albino mice, which is characterized by decreased AChE and GSH levels and increased MDA, SOD, and GLU concentrations. These findings suggest that prolonged MPR exposure may disrupt hippocampal function, potentially affecting cognitive and neurodevelopmental processes.

In an era where electronic advancements surge forward at an unprecedented pace, public apprehension surrounding the health ramifications of radio-frequency (RF) radiation intensifies. This study looked into the impact of chronic exposure to mobile phone radiation, coupled with glutathione supplementation, on serum lipid profiles and body weight in mice—a subject vital for understanding potential health risks in humans and animals respectively. Thirty-five male mice were divided into seven groups, each subjected to various mobile phone modes and glutathione treatments. Over five weeks, these mice were exposed to 300 missed calls daily, simulating real-world exposure scenarios. Different serum lipid parameters—triglycerides, cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL)—were monitored and observed throughout the study period. Remarkably, triglycerides, cholesterol, and LDL levels exhibited no noteworthy statistical variances compared to the control group or among experimental cohorts exposed to diverse range of mobile phone radiation modes or glutathione supplements. However, we noted some little deviations in HDL levels, particularly in the silent and silent+glutathione groups. Moreover, we also noted an unexpected result in weight loss across all groups by week three, which was pronounced by week five, and notably pronounced in the glutathione-administered cohorts. This outcome hints at glutathione’s complex role in mitigating some complications of mobile phone radiation exposure. In conclusion, the study suggests a potential interplay between glutathione supplementation, mobile phone radiation exposure, and HDL levels in mice—an avenue ripe for further exploration into the understanding of cellular response to modern technological exposures.

The widespread presence of electromagnetic fields (EMF) produced by modern technologies may pose a significant threat to animal health. Ionizing radiation, a byproduct of EMF exposure, has the potential to contribute to serious diseases, including cancer. This study examines the impact of chronic exposure to 900-1800 MHz GSM-EMF-induced electromagnetic radiation on liver enzymes and serum electrolytes in mice, and the potential mitigating effects of exogenous glutathione (GSH) administration. Thirty-five adult male mice were randomly divided into seven groups and exposed to various modes of mobile phone radiation for five weeks, with or without GSH administration. Liver enzymes, Alkaline phosphates (ALP), Alanine transaminase (ALT) , Aspartate aminotransferase (AST) and, serum electrolytes, sodium, potassium and bicarbonate were analyzed. Results showed significant increases in ALP levels in the Silent, Ringtone + GSH, and Silent + GSH groups compared to control group, while ALT and AST levels remained largely unchanged with the exception of some groups across the experimental cohorts. Serum electrolyte concentrations did not significantly differ across the control group. Our study found that chronic mobile phone radiation exposure in mice generally does not significantly affect liver enzyme levels or serum electrolyte concentrations. However, certain combinations with GSH administration notably increased some biochemical markers like ALP, ALT, and AST levels. Our study concluded that chronic mobile phone radiation had no significant impact on liver enzymes or serum electrolytes in mice. However, glutathione administration in combination with radiation increased liver enzyme levels, suggesting a potential role in oxidative stress mitigation. Further research is needed to explore these findings.Competing Interest StatementThe authors have declared no competing interest.Footnotes* This version has been revised to capture more details on Methodology and discussion as well as Authors affiliations