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Extremely Low Frequency Magnetic Field (ELF-MF) Exposure Sensitizes SH-SY5Y Cells to the Pro-Parkinson's Disease Toxin MPP(.).

TitleExtremely Low Frequency Magnetic Field (ELF-MF) Exposure Sensitizes SH-SY5Y Cells to the Pro-Parkinson's Disease Toxin MPP(.).
Publication TypeArticolo su Rivista peer-reviewed
Year of Publication2016
AuthorsBenassi, Barbara, Filomeni Giuseppe, Montagna Costanza, Merla Caterina, Lopresto Vanni, Pinto Rosanna, Marino Carmela, and Consales Claudia
JournalMol Neurobiol
Volume53
Issue6
Pagination4247-4260
Date Published2016 08
ISSN15591182
Keywords1-Methyl-4-phenylpyridinium, Cell Line, Tumor, cell proliferation, cell shape, Cell Survival, homeostasis, Humans, Magnetic fields, Oxidation-Reduction, Oxidative stress, Parkinson disease, protein carbonylation, Sulfhydryl Compounds
Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by dopaminergic neuron loss, with an etiopathogenesis involving both genetic and environmental factors. The occupational/residential exposure to the electromagnetic fields has been recently associated with an increased risk of neurodegenerative diseases; it has been thus proposed that the extremely low frequency magnetic field (ELF-MF) may contribute to neurodegenerative etiopathogenesis, as its interaction with biological systems directly impairs redox homeostasis in specific areas of the brain. The molecular mechanisms elicited by ELF-MF, and their potential involvement in PD onset, still remain unclear. To this end, we set up a generator of ELF-MF able to stably and homogeneously reproduce environmental prolonged exposure to ELF-MF (50 Hz, 1 mT). Results obtained indicate that ELF-MF exposure alters cell response of SH-SY5Y cells to MPP(+). We demonstrate that ELF-MF does not affect per se survival, shape, and morphology of both proliferating and differentiated SH-SY5Y cells but significantly impairs redox homeostasis and thiol content, triggering an increase in protein carbonylation. As a result, toxicity of MPP(+), even at low doses, is highly enhanced in ELF-MF-exposed cells due to a significant increase in ROS levels, potentiation of oxidative damage, and induction of a caspase-dependent apoptosis. Pre-incubation with the thiol antioxidants N-acetyl-L-cysteine and GSH ethyl-ester significantly reduces the extent of oxidative damage and protects cells from death induced by the combined treatment ELF-MF/MPP(+). Taken overall, our results demonstrate the redox-based molecular interaction between ELF-MF and PD neurotoxins in vitro, and open a new scenario for defining the synergy of environmental factors in PD onset.

DOI10.1007/s12035-015-9354-4
Alternate JournalMol. Neurobiol.
Citation Key6755
PubMed ID26223801