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Anti-Oxidative and Immune Regulatory Responses of THP-1 and PBMC to Pulsed EMF Are Field-Strength Dependent

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Authors not listed · 2021

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THP1 responded to weak EMF, while PBMC were primarily affected by strong EMF with severe cellular stress and enhanced apoptosis.

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Researchers compared the impact of different EMF flux densities in human leukemic THP1 cells and peripheral blood mononuclear cells (PBMC) of healthy donors. ROS levels increased in THP1 cells stimulated with LPS after one hour of EMF exposure, weak EMF mitigated NAD(P)H depletion in THP1, and neither effect occurred in PBMC. Transcriptional analysis revealed elevation of anti-oxidative enzymes PRDX6 (2-fold) and DHCR24 (6-fold) in THP1, and a 6-fold increase in IL10 expression indicating anti-inflammatory effects. THP1 responded to weak EMF, while PBMC were primarily affected by strong EMF with severe cellular stress and enhanced apoptosis indicated by HSP70 and caspase 3.

Cite This Study
Unknown (2021). Anti-Oxidative and Immune Regulatory Responses of THP-1 and PBMC to Pulsed EMF Are Field-Strength Dependent.
Show BibTeX
@article{anti_oxidative_and_immune_regulatory_responses_of_thp_1_and_pbmc_to_pulsed_emf_are_field_strength_dependent_ce3933,
  author = {Unknown},
  title = {Anti-Oxidative and Immune Regulatory Responses of THP-1 and PBMC to Pulsed EMF Are Field-Strength Dependent},
  year = {2021},
  doi = {10.3390/ijerph18189519},
  
}

Quick Questions About This Study

The study used human leukemic THP1 cells and peripheral blood mononuclear cells (PBMC) from healthy donors.
ROS levels increased in THP1 cells stimulated with LPS after one hour of EMF exposure.
Weak EMF mitigated the depletion of the reducing agent NAD(P)H in THP1.
PBMC were primarily affected by strong EMF, showing severe cellular stress and enhanced apoptosis indicated by HSP70 and caspase 3, while THP1 responded to weak EMF.
Transcriptional responses revealed elevation of anti-oxidative enzymes PRDX6 (2-fold) and DHCR24 (6-fold) in THP1, and a 6-fold increase in IL10 expression.