Effect of static magnetic fields and phloretin on antioxidant defense system of human fibroblasts

Environ Sci Pollut Res Int. 2016 Aug;23(15):14989-96. doi: 10.1007/s11356-016-6653-x. Epub 2016 Apr 15.

Abstract

The available evidence from in vitro and in vivo studies is deemed not sufficient to draw conclusions about the potential health effects of static magnetic field (SMF) exposure. Therefore, the aim of the present study was to determine the influence of static magnetic fields and phloretin on the redox homeostasis of human dermal fibroblasts. Control fibroblasts and fibroblasts treated with phloretin were subjected to the influence of static magnetic fields. Three chambers with static magnetic fields of different intensities (0.4, 0.55, and 0.7 T) were used in the study. Quantification of superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPX1), microsomal glutathione S-transferase 1 (MGST1), glutathione reductase (GSR), and catalase (CAT) messenger RNAs (mRNAs) was performed by means of real-time reverse transcription PCR (QRT-PCR) technique. Superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities were measured using a commercially available kit. No significant differences were found in SOD1, SOD2, GPX1, MGST1, GSR, and CAT mRNA levels among the studied groups in comparison to the control culture without phloretin and without the magnet. There were also no changes in SOD, GPx, and CAT activities. In conclusion, our study indicated that static magnetic fields generated by permanent magnets do not exert a negative influence on the oxidative status of human dermal fibroblasts. Based on these studies, it may also be concluded that phloretin does not increase its antioxidant properties under the influence of static magnetic fields. However, SMF-induced modifications at the cellular and molecular level require further clarification.

Keywords: Antioxidant defense system; Fibroblasts; Phloretin; QRT-PCR; Redox homeostasis; Static magnetic field.

MeSH terms

  • Antioxidants / metabolism*
  • Catalase / genetics
  • Catalase / metabolism
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibroblasts / radiation effects*
  • Glutathione Peroxidase / genetics
  • Glutathione Peroxidase / metabolism
  • Glutathione Peroxidase GPX1
  • Glutathione Transferase / genetics
  • Glutathione Transferase / metabolism
  • Humans
  • Magnetic Fields / adverse effects*
  • Oxidative Stress / drug effects
  • Phloretin / pharmacology*
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Superoxide Dismutase-1 / genetics
  • Superoxide Dismutase-1 / metabolism

Substances

  • Antioxidants
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Superoxide Dismutase-1
  • superoxide dismutase 2
  • microsomal glutathione S-transferase-I
  • Glutathione Transferase
  • Phloretin
  • Glutathione Peroxidase GPX1
  • GPX1 protein, human