title: Fifty hertz extremely low-frequency magnetic field exposure elicits redox and trophic response in rat-cortical neurons.
abstract: Large research activity has raised around the mechanisms of interaction between extremely low-frequency magnetic fields (ELF-MFs) and biological systems. ELF-MFs may interfere with chemical reactions involving reactive oxygen species (ROS), thus facilitating oxidative damages in living cells. Cortical neurons are particularly susceptible to oxidative stressors and are also highly dependent on the specific factors and proteins governing neuronal development, activity and survival. The aim of the present work was to investigate the effects of exposures to two different 50 Hz sinusoidal ELF-MFs intensities (0.1 and 1 mT) in maturing rat cortical neurons' major anti-oxidative enzymatic and non-enzymatic cellular protection systems, membrane peroxidative damage, as well as growth factor, and cytokine expression pattern. Briefly, our results showed that ELF-MFs affected positively the cell viability and concomitantly reduced the levels of apoptotic death in rat neuronal primary cultures, with no significant effects on the main anti-oxidative defences. Interestingly, linear regression analysis suggested a positive correlation between reduced glutathione (GSH) and ROS levels in 1 mT MF-exposed cells. On this basis, our hypothesis is that GSH could play an important role in the antioxidant defence towards the ELF-MF-induced redox challenge. Moreover, the GSH-based cellular response was achieved together with a brain-derived neurotrophic factor over-expression as well as with the interleukin 1beta-dependent regulation of pro-survival signaling pathways after ELF-MF exposure.
authors.affiliation: Institute for Organ Transplantation and Immunocytology (ITOI), CNR, L'Aquila, Italy.
authors.forename: Silvia
authors.initials: S
authors.lastname: Di Loreto
authors.forename: Stefano
authors.initials: S
authors.lastname: Falone
authors.forename: Valentina
authors.initials: V
authors.lastname: Caracciolo
authors.forename: Pierluigi
authors.initials: P
authors.lastname: Sebastiani
authors.forename: Antonella
authors.initials: A
authors.lastname: D'Alessandro
authors.forename: Alessandro
authors.initials: A
authors.lastname: Mirabilio
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Zimmitti
authors.forename: Fernanda
authors.initials: F
authors.lastname: Amicarelli
mesh_terms: D000328:Adult; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004574:Electromagnetic Fields; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D009414:Nerve Growth Factors / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism* / Q000528:radiation effects*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D016207:Cytokines; D053583:Interleukin-1beta; D009414:Nerve Growth Factors; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D005978:Glutathione