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The apoptotic effect and the plausible mechanism of microwave radiation on rat myocardial cells

机译:微波辐射对大鼠心肌细胞的凋亡作用及其可能机制

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摘要

Microwaves may exert adverse biological effects on the cardiovascular system at the integrated system and cellular levels. However, the mechanism underlying such effects remains poorly understood. Here, we report a previously uncharacterized mechanism through which microwaves damage myocardial cells. Rats were treated with 2450 MHz microwave radiation at 50, 100, 150, or 200 mW/cm(2) for 6 min. Microwave treatment significantly enhanced the levels of various enzymes in serum. In addition, it increased the malondialdehyde content while decreasing the levels of antioxidative stress enzymes, activities of enzyme complexes I-IV, and ATP in myocardial tissues. Notably, irradiated myocardial cells exhibited structural damage and underwent apoptosis. Furthermore, Western blot analysis revealed significant changes in expression levels of proteins involved in oxidative stress regulation and apoptotic signaling pathways, indicating that microwave irradiation could induce myocardial cell apoptosis by interfering with oxidative stress and cardiac energy metabolism. Our findings provide useful insights into the mechanism of microwave-induced damage to the cardiovascular system.
机译:微波可能在集成系统和细胞水平上对心血管系统产生不利的生物学影响。但是,这种作用的机理尚不清楚。在这里,我们报道了微波破坏心肌细胞的先前未知的机制。用2450 MHz微波辐射以50、100、150或200 mW / cm(2)处理大鼠6分钟。微波处理显着提高了血清中各种酶的水平。另外,它增加了丙二醛含量,同时降低了心肌组织中抗氧化应激酶的水平,酶复合物I-IV和ATP的活性。值得注意的是,受辐照的心肌细胞表现出结构损伤并发生凋亡。此外,蛋白质印迹分析揭示了参与氧化应激调节和凋亡信号通路的蛋白质表达水平的显着变化,表明微波辐射可通过干扰氧化应激和心脏能量代谢来诱导心肌细胞凋亡。我们的发现为微波诱导的心血管系统损害机理提供了有用的见识。

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