Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation will increase in lipopolysaccharide-induced inflammation in vitro model.

Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation will increase in lipopolysaccharide-induced inflammation in vitro model.
复制标题

脂多糖诱导炎症体外模型中螺旋神经节神经元对手机电磁辐射损伤的敏感性增加

DOI:
10.1186/s12974-015-0300-1
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发表时间:
2015-05-29
影响因子:
9.3
通讯作者:
Kong WJ
Kong WJ
中科院分区:
医学1区
文献类型:
--
作者:
Zuo WQ;Hu YJ;Yang Y;Zhao XY;Zhang YY;Kong W;Kong WJ

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背景随着移动的手机的日益普及,射频电磁辐射(RF-EMR)对听觉系统的潜在危害仍不清楚。除了RF-EMR,人类还暴露于各种物理和化学因素。我们建立了一个脂多糖(LPS)诱导的炎症在体外模型,以探讨是否可能的敏感性螺旋神经节神经元所造成的损害由移动的手机电磁辐射(在特定的吸收率:2,4 W/kg)将increased.MethodsSpiral神经节神经元(SGN)获得新生儿(1- 3-d)的SD大鼠道利。用不同浓度(0、20、40、50、100、200和400 μg/ml)的LPS处理SGN后,分别用CCK-8试剂盒和碱性彗星试验检测SGN细胞活性和DNA损伤。在RF-EMR暴露前,用中等浓度的LPS处理SGN。以2和4 W/kg的吸收率间歇暴露24 h后,采用碱性彗星试验检测DNA损伤,透射电镜观察超微结构变化,免疫荧光和激光共聚焦扫描显微镜观察自噬标志物LC 3-II和Beclin 1的表达。结果LPS(100 μg/ml)可诱导细胞DNA损伤,抑制细胞活性(P0.05)。LPS(40 μg/ml)未表现出细胞活性变化或DNA损伤(P0.05);因此,在暴露于RF-EMR之前,使用40 μg/ml作为预处理浓度。RF-EMR不能直接引起DNA损伤。而4 W/kg + LPS(40 μg/ml)组则出现线粒体空泡、核固缩、溶酶体和自噬体的存在以及LC 3-II和Beclin 1表达增加。4 W/kg组、4 W/kg + LPS(40 μg/ml)组和H2 O2组的ROS值均显著升高(P0.05,0.01)。结论射频电磁辐射短期暴露对正常螺旋神经节细胞DNA无直接损伤作用,但在特定SAR 4.0W/kg时,细胞处于脆性或微损伤状态时,可引起细胞超微结构的改变。在脂多糖诱导的体外炎症模型中,SGN对移动的手机电磁辐射引起的损伤的敏感性似乎会增加。
BackgroundWith the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase.MethodsSpiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley® (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 μg/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay.ResultsLPS (100 μg/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 μg/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 μg/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 μg/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 μg/ml) exposure, and H2O2 groups (P < 0.05, 0.01).ConclusionsShort-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model.
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