Abstract

Electromagnetic pulse (EMP) causes central nervous system damage and neurobehavioral disorders, and sevoflurane protects the brain from ischemic injury. We investigated the effects of sevoflurane on EMP-induced brain injury. Rats were exposed to EMP and immediately treated with sevoflurane. The protective effects of sevoflurane were assessed by Nissl staining, Fluoro-Jade C staining and electron microscopy. The neurobehavioral effects were assessed using the open-field test and the Morris water maze. Finally, primary cerebral cortical neurons were exposed to EMP and incubated with different concentration of sevoflurane. The cellular viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assayed. TUNEL staining was performed, and the expression of apoptotic markers was determined. The cerebral cortexes of EMP-exposed rats presented neuronal abnormalities. Sevoflurane alleviated these effects, as well as the learning and memory deficits caused by EMP exposure. In vitro, cell viability was reduced and LDH release was increased after EMP exposure; treatment with sevoflurane ameliorated these effects. Additionally, sevoflurane increased SOD activity, decreased MDA levels and alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, Bax and Bcl-2. These findings demonstrate that Sevoflurane conferred neuroprotective effects against EMP radiation-induced brain damage by inhibiting neuronal oxidative stress and apoptosis.

Highlights

  • Most electrical equipment and wireless communication devices produce electromagnetic radiation

  • The central nervous system (CNS) is sensitive to electromagnetic radiation, and pathological damage and neurobehavioral disorders have been observed after Electromagnetic pulse (EMP) exposure [30]

  • It is of great importance to investigate the biological effects of electromagnetic fields on the CNS and to develop potential preventive strategies

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Summary

Introduction

Most electrical equipment and wireless communication devices produce electromagnetic radiation. There is widespread concern regarding the adverse effects on human health caused by exposure to many types of electromagnetic fields (EMFs) [1,2]. Previous studies indicate that the non-thermal effects of EMF exposure can lead to cellular changes [3,4,5]. EMF can increase reactive oxygen species (ROS) and reactive nitrogen species (RNS) in organs and cause histopathological damage and oxidative stress [6,7,8,9]; for example, under particular circumstances, exposure to a GSMmodulated, 900-MHz signal acts as a co-stressor for oxidative damage of neural cells [10]. Several studies suggest that occupational exposure to electromagnetic fields may be associated with increased risk of neurodegenerative diseases [11,12]

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