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目的：观察高功率微波辐照后人T淋巴细胞活性氧和线粒体跨膜电位的变化,并探索某些干预措施对其损伤后的影响。方法：采用DCFH-DA分子探针和荧光染料罗丹明-123结合流式细胞仪分别检测人T细胞经0、10、30、50mW/cm~2微波辐照及给予某些干预措施后细胞内活性氧和线粒体跨膜电位的变化。结果：(1)经10mW辐照后即可见T细胞内活性氧水平的升高,于30mW辐照后达到峰值；而10mW辐照后T细胞线粒体跨膜电位出现明显降低,于30mW辐照后降至最低。(2)于照前给予活性氧抑制剂能有效抑制T细胞内活性氧水平的升高；T细胞转入bcl-X_L基因后也能明显抑制细胞内活性氧水平的升高和线粒体跨膜电位的下降,高剂量组更为明显。结论：一定强度的高功率微波能引起T细胞活性氧和线粒体跨膜电位变化等早期凋亡事件的发生,活性氧抑制剂和bcl-X_L基因过表达能有效抑制这些早期事件的发生。
Objective: To observe the changes of reactive oxygen species (ROS) and mitochondrial transmembrane potential of human T lymphocytes after high power microwave irradiation and to explore the effects of some interventions on their injury. Methods: Human T cells were irradiated with 0, 10, 30 and 50 mW / cm ~ 2 microwaves respectively by DCFH-DA molecular probe and fluorescent dye rhodamine-123 combined with flow cytometry Changes of reactive oxygen species and mitochondrial transmembrane potential. Results: (1) The level of reactive oxygen species (ROS) in T cells increased after irradiation with 10 mW and peaked at 30 mW after irradiation. The mitochondrial transmembrane potential of T cells decreased significantly after irradiation with 10 mW. After irradiation at 30 mW Minimize. (2) Pretreatment with ROS inhibitor can effectively inhibit the increase of reactive oxygen species in T cells; T cells transfected with bcl-X_L gene also markedly inhibited the increase of reactive oxygen species level and mitochondrial transmembrane potential Decline, high-dose group is more obvious. CONCLUSION: A certain intensity of high power microwave can induce the occurrence of early apoptotic events such as reactive oxygen species (ROS) and mitochondrial transmembrane potential. Oxygenase inhibitor and bcl-X_L gene overexpression can effectively inhibit the occurrence of these early events.