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微波辐射对大鼠心肌细胞的凋亡作用及可能机制

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

作者信息

Zhu Wenhe, Cui Yan, Feng Xianmin, Li Yan, Zhang Wei, Xu Junjie, Wang Huiyan, Lv Shijie

机构信息

a Department of Biochemistry, Ji Lin Medical University, Ji Lin 132013, China.

b First Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Can J Physiol Pharmacol. 2016 Aug;94(8):849-57. doi: 10.1139/cjpp-2015-0537. Epub 2016 Mar 6.

DOI:10.1139/cjpp-2015-0537
PMID:27203380
Abstract

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.

摘要

微波可能在整合系统和细胞水平上对心血管系统产生不良生物学效应。然而,此类效应背后的机制仍知之甚少。在此,我们报告一种此前未被描述的微波损伤心肌细胞的机制。将大鼠用2450 MHz微波辐射,功率分别为50、100、150或200 mW/cm²,持续6分钟。微波处理显著提高了血清中各种酶的水平。此外,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的活性以及ATP水平。值得注意的是,受辐射的心肌细胞表现出结构损伤并发生凋亡。此外,蛋白质印迹分析显示参与氧化应激调节和凋亡信号通路的蛋白质表达水平有显著变化,表明微波辐射可通过干扰氧化应激和心脏能量代谢诱导心肌细胞凋亡。我们的研究结果为微波诱导心血管系统损伤的机制提供了有益的见解。

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