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Extremely low frequency electromagnetic fields exposure during the prenatal and postnatal periods alters pro-inflammatory cytokines levels by gender

Maternal exposure to the excessive electromagnetic fields is considered harmful to infants and associated with several health problems in life, such as neurological or immune diseases. In this present study we aimed to investigate the potential effects of extremely low-frequency electromagnetic fiel...

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Bibliographic Details
Published in:Electromagnetic biology and medicine 2022-04, Vol.41 (2), p.163-173
Main Authors: Ozturk, Hilal, Saribal, Devrim, Gelmez, Yusuf Metin, Deniz, Gunnur, Yilmaz, Abdullah, Kirectepe, Asli, Ercan, Alev Meltem
Format: Article
Language:English
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Summary:Maternal exposure to the excessive electromagnetic fields is considered harmful to infants and associated with several health problems in life, such as neurological or immune diseases. In this present study we aimed to investigate the potential effects of extremely low-frequency electromagnetic field (ELF-EMF) exposure during the gestational and lactational period of dams on immune system parameters. The development of white blood cells (WBC), lymphocyte subpopulations (CD4 + T cells, CD8 + T cells, Natural Killer (NK) cells, and B cells) and production of T cell related cytokines were explored in the offsprings. Significant changes were found in WBC and lymphocyte counts. Although no changes in lymphocyte subunits were observed among groups, CD4 + cells were significantly increased in the female group exposed to ELF-EMF. Also, IL-17A and IFN-γ levels increased in plasma and spleen. The mean IL-4 level and the expression level of the IL-4 gene were not changed, in the experimental groups. But the expression of the IL-17A gene was also upregulated, which supports cytokine quantification analyses. In conclusion, ELF-EMF exposure in the prenatal and postnatal period increases the level of IL-17A in the spleen and blood of young female rats, and it upregulates IL-17 gene expression in the spleen, resulting in CD4 + cell proliferation and inflammation.
ISSN:1536-8378
1536-8386
DOI:10.1080/15368378.2022.2046045