Role of NF-κB activation in mouse bone marrow stromal cells exposed to 900 MHz radiofrequency fields (RF). Issue 5 (4th March 2019)

• Record Type: Journal Article
• Authors: Zong, Lin; Gao, Zhen; Xie, Wen; Tong, Jian; Cao, Yi
• Is Part Of: Journal of toxicology and environmental health. Volume 82:Issue 5(2019)
• Page Start: 315
• Page End: 320
• Publication Date: 2019-03-04
• Subjects: Mouse bone marrow stromal cells -- radiofrequency fields -- NF-κB; Toxicology -- Periodicals; Environmental health -- Periodicals; 615.90205
• DOI: 10.1080/15287394.2018.1564196
• Languages: English
• ISSNs: 1528-7394

Abstract

ABSTRACT: Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a primary transcription factor which plays a key role in several cellular processes including proliferation and survival. It is well-known that exposure to non-ionizing radiofrequency fields (RF), which are ubiquitous, interact with cellular components. The aim of the study was thus to examine whether exposure of mouse bone marrow stromal cells (BMSC) to RF also resulted in cellular interactions. BMSC were exposed to 900 MHz RF at 120 μW/cm 2 power intensity for 4 hr/day for 5 consecutive days. The relative protein expression levels of NF-κB in the cytoplasm and nucleus of RF-exposed cells were compared to non-RF-exposed controls. At 30 min post-RF exposure a significant decrease in protein expression of NF-κB in the cytoplasm was accompanied by a concomitant increase in nuclear NF-κB protein expression levels. Similar responses were noted in the cytoplasm and nuclear NF-κB levels at 2 hr with a return to control concentrations in primary transcription factor at 24 hr post-RF treatment. Daily incubation of BAY 11–7082 an inhibitor of NF-κB for 90 min for 5 days followed by RF each day prevented the fall in cytoplasmic NF-κB and rise in nuclear primary transcription factor at 30 min and 2 hr. There were no marked alterations at 24 hr. Data showed that the effects of RF treatment on BMSC involved transient activation of NF-κB which may be attributed to RF-mediated cellular perturbation as evidenced by consequences of BAY 11–7082 inhibition.