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.
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