Abstract
Magnetic field as ecological factor has influence on all living beings. The aim of this study was to determine if extremely low frequency magnetic field (ELF-MF, 50 Hz, 0.5 mT) affects oxidative stress in the brain of gerbils submitted to 10-min global cerebral ischemia. After occlusion of both carotid arteries, 3-month-old gerbils were continuously exposed to ELF-MF for 7 days. Nitric oxide and superoxide anion production, superoxide dismutase activity and index of lipid peroxidation were examined in the forebrain cortex, striatum and hippocampus on the 7th (immediate effect of ELF-MF) and 14th day after reperfusion (delayed effect of ELF-MF). Ischemia per se increased oxidative stress in the brain on the 7th and 14th day after reperfusion. ELF-MF also increased oxidative stress, but to a greater extent than ischemia, only immediately after cessation of exposure. Ischemic gerbils exposed to ELF-MF had increased oxidative stress parameters on the 7th day after reperfusion, but to a lesser extent than ischemic or ELF-MF-exposed animals. On the 14th day after reperfusion, oxidative stress parameters in the brain of these gerbils were mostly at the control levels. Applied ELF-MF decreases oxidative stress induced by global cerebral ischemia and thereby reduces possible negative consequences which free radical species could have in the brain. The results presented here indicate a beneficial effect of ELF-MF (50 Hz, 0.5 mT) in the model of global cerebral ischemia.
Highlights
Cerebral ischemia as a consequence of restricted blood flow, implicating insufficient glucose and oxygen supply, leads to increased production of free radical species [1]
Upon one-way analysis of variance, it was obvious that exposure to extremely low frequency magnetic field (ELF-MF) significantly affects production of nitric oxide (NO) and O22, superoxide dismutase (SOD) activity and Index of Lipid Peroxidation (ILP) in the brain of gerbils submitted to 10-min global cerebral ischemia (Table 1)
Our results showed that ischemia per se increased oxidative stress in all examined brain structures
Summary
Cerebral ischemia as a consequence of restricted blood flow, implicating insufficient glucose and oxygen supply, leads to increased production of free radical species [1]. Enormous production of reactive oxygen and nitrogen species (ROS and RNS, respectively) has deleterious effects during pathogenesis of ischemic insult [2,3]. Production of free radicals overwhelm possibility of detoxification and capacity for its removal by enzymes of antioxidative protection like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and nonenzymatic antioxidants (vitamin C and E, glutathione) resulting in fast and severe damage of cellular proteins, lipids and DNA [3,5]. Production of ROS in mitochondria from molecular oxygen presents normal physiological reaction, enormous activation of N-methyl-D-aspartate (NMDA) receptors during cerebral ischemia results in higher production of ROS and nitric oxide (NO). Peroxidation of lipid membranes produces toxic aldehydes like 4-hydroxynonenal (4-HNE) which damage ion channels, transporters and cytoskeletal proteins. Free radicals activate specific signal pathways like mitogen-activated protein kinase which further contribute to ischemic damage [9]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
