Histological and biochemical assessment of hippocampal structure, neurotransmitters, and oxidative stress markers in mice following mobile phone radiation exposure

Abstract 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.