50 Hz magnetic fields activate mussel immunocyte p38 MAP kinase and induce HSP70 and 90

Davide Malagoli1, Mauro Lusvardi, Fabriziomaria Gobba

  • 1Department of Animal Biology, University of Modena and Reggio Emilia, via Campi 213/D, 41100 Modena, Italy.

Insights

Fifty hertz magnetic fields (MFs) can alter heat shock protein (HSP) expression in mussels. Higher intensity MFs, specifically at 400 microT and above, induced a notable increase in HSPs, suggesting a potential for controlled biological responses.

Area of Science:

  • Environmental Science
  • Molecular Biology
  • Marine Biology

Background:

  • Heat shock proteins (HSPs) are crucial cellular protectants.
  • Magnetic fields (MFs) are environmental factors with potential biological effects.
  • Mussels (Mytilus galloprovincialis) are sensitive marine bioindicators.

Purpose of the Study:

  • To investigate the effect of 50 Hz magnetic fields (MFs) on HSP70 and HSP90 expression in mussel immunocytes.
  • To determine the relationship between MF intensity, exposure duration, and HSP induction.
  • To explore the involvement of the p38 MAP kinase pathway in MF-induced HSP expression.

Main Methods:

  • Exposure of Mytilus galloprovincialis to 50 Hz MFs at varying intensities (300, 400, 600 microT) and durations.
  • Quantification of HSP70 and HSP90 expression using Western blot analysis.
  • Assessment of p38 MAP kinase pathway activation.

Main Results:

  • No significant changes in HSP expression were observed at 300 microT.
  • A time-dependent increase in HSP expression was noted at 400 microT.
  • Significant HSP induction occurred at 600 microT, independent of exposure duration.
  • HSP induction was accompanied by p38 MAP kinase pathway activation.

Conclusions:

  • Fifty hertz MFs can modulate HSP expression in mussel immunocytes.
  • MF intensity is a critical factor in inducing HSPs, with higher intensities showing a stronger effect.
  • The findings suggest that controlled MF exposure could be used to modulate cellular stress responses, potentially via the p38 MAP kinase pathway.