Fifty hertz extremely low-frequency electromagnetic field causes changes in redox and differentiative status in neuroblastoma cells

Int J Biochem Cell Biol. 2007;39(11):2093-106. doi: 10.1016/j.biocel.2007.06.001. Epub 2007 Jun 23.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antioxidants / metabolism
  • Apoptosis / drug effects
  • Biomarkers / metabolism
  • Cell Cycle / drug effects
  • Cell Differentiation* / drug effects
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • DNA Damage
  • Electromagnetic Fields*
  • GAP-43 Protein
  • Glutathione / metabolism
  • Humans
  • Neuroblastoma / pathology*
  • Neurofilament Proteins / metabolism
  • Oxidants / pharmacology
  • Oxidation-Reduction / drug effects
  • PPAR-beta / metabolism
  • Protein Transport / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Reactive Oxygen Species / metabolism
  • Transcription, Genetic / drug effects
  • Tumor Suppressor Protein p53

Substances

  • Antioxidants
  • Biomarkers
  • GAP-43 Protein
  • Neurofilament Proteins
  • Oxidants
  • PPAR-beta
  • Proto-Oncogene Proteins c-bcl-2
  • Reactive Oxygen Species
  • Tumor Suppressor Protein p53
  • neurofilament protein H
  • Glutathione