Fifty-hertz magnetic fields induce free radical formation in mouse bone marrow-derived promonocytes and macrophages
Fifty-hertz magnetic fields induce free radical formation in mouse bone marrow-derived promonocytes and macrophages
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DOI：
10.1016/j.bbagen.2004.06.024
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发表时间：
2004-11-01
影响因子：
3
通讯作者：
Simkó, M
中科院分区：
文献类型：
--
作者：
Rollwitz, J;Lupke, M;Simkó, M
我们的研究结果表明，小鼠骨髓源性 (MBM) 早单核细胞和巨噬细胞暴露于通量密度为 1 mT 的 50 Hz 电磁场后，自由基产生显着增加，表明极低频磁场 (ELF-MF) 的细胞激活能力。我们证明，暴露于 ELF-MF 后，主要在 MBM 巨噬细胞 (33%) 及其前体细胞 (24%) 中产生超氧阴离子自由基。为了阐明 NADPH 或 NADH 氧化酶功能是否是 MF 相互作用的靶蛋白，使用了黄素蛋白抑制剂氯化二苯碘铵 (DPI)。 DPI 不会抑制 MF 诱导的自由基产生，而十四烷酰佛波乙酸 (TPA) 诱导的自由基产生减少约 70%。 TPA 已知可通过 PKC 途径诱导 NADPH 氧化酶的直接激活。由于 DPI 对暴露于 MF 的 MBM 细胞缺乏抑制作用，因此我们认为 50 Hz MF 会刺激 NADH 氧化酶途径产生超氧阴离子自由基，但不会刺激 NADPH 途径。此外，我们发现小鼠巨噬细胞中超氧阴离子自由基释放存在振荡（1-10 天），表明 NADH 氧化酶活性的循环模式。 (C) 2004 Elsevier B.V. 保留所有权利。
Our findings show a significant increase of free radical production after exposure to 50 Hz electromagnetic fields at a flux density of 1 mT to mouse bone marrow-derived (MBM) promonocytes and macrophages, indicating the cell-activating capacity of extremely low frequency magnetic fields (ELF-MF). We demonstrate that after exposure to ELF-MF mainly superoxide anion radicals were produced, both in MBM macrophages (33%) and also in their precursor cells (24%). To elucidate whether NADPH- or NADH-oxidase functions are target proteins for MF interaction, the flavoprotein inhibitor diphenylenciodonium chloride (DPI) was used. MF-induced free radical production was not inhibited by DPI, whereas tetradecanoylphorbolacetate (TPA)-induced free radical production was diminished by about 70%. TPA is known to induce a direct activation of NADPH-oxidase through the PKC pathway. Since DPI lacks an inhibitory effect in MF-exposed MBM cells, we suggest that 50 Hz MF stimulates the NADH-oxidase pathway to produce superoxide anion radicals, but not the NADPH pathway. Furthermore, we showed an oscillation (1-10 days) in superoxide anion radical release in mouse macrophages, indicating a cyclic pattern of NADH-oxidase activity. (C) 2004 Elsevier B.V. All rights reserved.