Journal
SCIENCE OF THE TOTAL ENVIRONMENT
Volume 867, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.scitotenv.2023.161475
Keywords
HL-60 promyelocytic cell line; Black carbon; Electromagnetic fields; Gigahertz transverse electromagnetic cell; Specific absorption rate; Necrosis; apoptosis; BCL2a; FASR; CASP3 genes; Caspase-3; 8 proteins
Categories
Ask authors/readers for more resources
This study analyzed the effects of 2.45 GHz radio frequency radiation and black carbon particles on cell damage and pro-apoptotic response in the HL-60 promyelocytic cell line. The results showed that radiation and black carbon particles separately and jointly triggered cell necrosis and mitochondria-Caspase dependent apoptosis. These findings may have important implications for antimicrobial, inflammatory, and autoimmune responses in humans.
The cellular and molecular mechanisms by which atmospheric pollution from particulate matter and/or electromag-netic fields (EMFs) may prove harmful to human health have not been extensively researched. We analyzed whether the combined action of EMFs and black carbon (BC) particles induced cell damage and a pro-apoptotic response in the HL-60 promyelocytic cell line when exposed to 2.45 GHz radio frequency (RF) radiation in a gigahertz transverse elec-tromagnetic (GTEM) chamber at sub-thermal specific absorption rate (SAR) levels. RF and BC induced moderately sig-nificant levels of cell damage in the first 8 or 24 h for all exposure times/doses and much greater damage after 48 h irradiation and the higher dose of BC. We observed a clear antiproliferative effect that increased with RF exposure time and BC dose. Oxidative stress or ROS production increased with time (24 or 48 h of radiation), BC dose and the combination of both. Significant differences between the proportion of damaged and healthy cells were observed in all groups. Both radiation and BC participated separately and jointly in triggering necrosis and apoptosis in a pro-grammed way. Oxidative-antioxidant action activated mitochondrial anti-apoptotic BCL2a gene expression after 24 h irradiation and exposure to BC. After irradiation of the cells for 48 h, expression of FASR cell death receptors was activated, precipitating the onset of pro-apoptotic phenomena and expression and intracellular activity of caspase-3 in the mitochondrial pathways, all of which can lead to cell death. Our results indicate that the interaction between BC and RF modifies the immune response in the human promyelocytic cell line and that these cells had two fates mediated by different pathways: necrosis and mitochondria-caspase dependent apoptosis. The findings may be important in regard to antimicrobial, inflammatory and autoimmune responses in humans.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available