Fifty hertz extremely low-frequency electromagnetic field causes changes in redox and differentiative status in neuroblastoma cells.
The current study was designed to establish whether extremely low-frequency electromagnetic fields might affect neuronal homeostasis through redox-sensitive mechanisms. To this end, intracellular reactive oxygen species production, antioxidant and glutathione-based detoxifying capability and genomic integrity after extremely low-frequency electromagnetic fields exposure were investigated. Moreover, we also studied potential extremely low-frequency electromagnetic fields-dependent changes in the proliferative and differentiative cellular status. Results seem to support redox-mediated extremely low-frequency electromagnetic fields effects on biological models as, although no major oxidative damage was detected, after exposure we observed a positive modulation of antioxidant enzymatic expression, as well as a significant increase in reduced glutathione level, indicating a shift of cellular environment towards a more reduced state. In addition, extremely low-frequency electromagnetic fields treatment induced a more differentiated phenotype as well as an increased expression in peroxisome proliferators-activated receptor isotype beta, a class of transcription factors related to neuronal differentiation and cellular stress response. As second point, to deepen how extremely low-frequency electromagnetic fields treatment could affect neuroblastoma cell antioxidant capacity, we examined the extremely low-frequency electromagnetic fields-dependent modifications of cell susceptibility to pro-oxidants. Results clearly showed that 50 Hz extremely low-frequency electromagnetic fields exposure reduces cell tolerance towards oxidative attacks.
Falone
Stefano
S
Department of Biomedical Sciences, Excellent Center on Aging Studies, Faculty of Medicine G. d'Annunzio, Via dei Vestini, 66013 Chieti, Italy.
Grossi
Maria R
MR
Cinque
Benedetta
B
D'Angelo
Barbara
B
Tettamanti
Enzo
E
Cimini
Annamaria
A
Di Ilio
Carmine
C
Amicarelli
Fernanda
F
D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D015415:Biomarkers / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004249:DNA Damage; D004574:Electromagnetic Fields; D019922:GAP-43 Protein; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D009447:Neuroblastoma / Q000473:pathology*; D016900:Neurofilament Proteins / Q000378:metabolism; D016877:Oxidants / Q000494:pharmacology; D010084:Oxidation-Reduction / Q000187:drug effects; D048068:PPAR-beta / Q000378:metabolism; D021381:Protein Transport / Q000187:drug effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects; D016159:Tumor Suppressor Protein p53
D000975:Antioxidants; D015415:Biomarkers; D019922:GAP-43 Protein; D016900:Neurofilament Proteins; D016877:Oxidants; D048068:PPAR-beta; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; C051774:neurofilament protein H; D005978:Glutathione