TY - JOUR
T1 - Cell physiological responses of RAW264 macrophage cells to a 50-Hz magnetic field
AU - Nishigaki, Chihiro
AU - Nakayama, Maresuke
AU - Miyata, Hidetake
N1 - Funding Information:
This work was supported by MEXT, Japan [a Grant-in-Aid number 426610128] and by Tohoku University Scholarship (Weaving Science Web beyond Particle-Matter Hierarchy).
Publisher Copyright:
© Copyright © 2020 Taylor & Francis Group LLC.
PY - 2020
Y1 - 2020
N2 - Purpose: We previously showed that a 0.5-mT, 50-Hz sinusoidal magnetic field (LFMF) enhanced DNA single-strand breaks (SSB) and necrosis in RAW264 macrophages that had been stimulated by bacterial endotoxin (lipopolysaccharide; LPS). LPS enhances production of nitric oxide (NO) and superoxide anion (O2−) that react with each other to generate peroxynitrite (ONOO−). ONOO− causes DNA strand breaks. Hence, we anticipated that 0.5-mT, 50-Hz sinusoidal magnetic field increased production of NO, thereby increasing intracellular ONOO− concentration and promoted DNA strand breaks. However, the NO production was not increased. In this study, we examined if the exposure of the cell to 0.5-mT, 50-Hz magnetic field for 24 h (1) promotes O2− production, (2) elevated the degree of apoptosis, because apoptosis is an upstream event of necrosis, (3) lowers mitochondrial membrane potential (ΔΦm), because it would also promote necrosis. Materials and methods: O2−, was measured with nitroblue tetrazolium and water-soluble tetrazolium salt. Necrosis and apoptosis were quantified with propidium iodide and fluorescence labelling of caspases, respectively. The ΔΦm was measured with a fluorescent probe (JC-1) that reflects ΔΦm. Results and conclusions: In the LPS-stimulated macrophage, the LFMF did not promote O2− production. Thus, the LFMF-promoted DNA strand breaks did not result from the increase in the O2− production. The LFMF did not promote apoptosis, whereas it tended to increase the degree of necrosis, as we showed previously. The ΔΦm slightly declined in the LFMF-exposed cell without statistical significance.
AB - Purpose: We previously showed that a 0.5-mT, 50-Hz sinusoidal magnetic field (LFMF) enhanced DNA single-strand breaks (SSB) and necrosis in RAW264 macrophages that had been stimulated by bacterial endotoxin (lipopolysaccharide; LPS). LPS enhances production of nitric oxide (NO) and superoxide anion (O2−) that react with each other to generate peroxynitrite (ONOO−). ONOO− causes DNA strand breaks. Hence, we anticipated that 0.5-mT, 50-Hz sinusoidal magnetic field increased production of NO, thereby increasing intracellular ONOO− concentration and promoted DNA strand breaks. However, the NO production was not increased. In this study, we examined if the exposure of the cell to 0.5-mT, 50-Hz magnetic field for 24 h (1) promotes O2− production, (2) elevated the degree of apoptosis, because apoptosis is an upstream event of necrosis, (3) lowers mitochondrial membrane potential (ΔΦm), because it would also promote necrosis. Materials and methods: O2−, was measured with nitroblue tetrazolium and water-soluble tetrazolium salt. Necrosis and apoptosis were quantified with propidium iodide and fluorescence labelling of caspases, respectively. The ΔΦm was measured with a fluorescent probe (JC-1) that reflects ΔΦm. Results and conclusions: In the LPS-stimulated macrophage, the LFMF did not promote O2− production. Thus, the LFMF-promoted DNA strand breaks did not result from the increase in the O2− production. The LFMF did not promote apoptosis, whereas it tended to increase the degree of necrosis, as we showed previously. The ΔΦm slightly declined in the LFMF-exposed cell without statistical significance.
KW - Low frequency magnetic field
KW - mitochondria
KW - peroxynitrite
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U2 - 10.1080/09553002.2020.1837983
DO - 10.1080/09553002.2020.1837983
M3 - Article
C2 - 33052723
AN - SCOPUS:85094877248
VL - 96
SP - 1628
EP - 1632
JO - International Journal of Radiation Biology
JF - International Journal of Radiation Biology
SN - 0955-3002
IS - 12
ER -