Biophysics Department, Cerrahpasa Medical Faculty, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Biophysics Department, Faculty of Medicine, Istanbul Aydın University, Istanbul, Turkey.
Biol Trace Elem Res. 2020 Apr;194(2):368-378. doi: 10.1007/s12011-019-01811-6. Epub 2019 Jul 17.
Several epidemiological studies have shown that exposure to electromagnetic radiation (EMR) can be harmful to human health. The purpose of this study was to examine oxidative parameters and apoptosis induced by EMR in human kidney embryonic cells (HEK293) and to investigate whether zinc (Zn) has protective effect on EMR-induced apoptosis in HEK293 cells. For our experiment, HEK293 cells were divided into four main groups, control, EMR, 50 μM Zn + EMR, and 100 μM Zn + EMR. HEK293 cells of EMR groups were exposed to 2.45 GHz EMR for 1 h. In Zn groups, HEK293 cells were incubated with different concentrations of Zn for 48 h before EMR exposure. Oxidative stress parameters were determined by spectrophotometric method; bcl-2 and caspase-3 were assessed immunohistochemically and TUNEL method was performed for apoptotic activity. EMR group had higher malondialdehyde (MDA) level and lower superoxide dismutase (SOD) activity compared with control group. In Zn-applied groups, MDA was decreased and SOD activity was increased compared with EMR group. The number of the apoptotic cells and caspase-3 immunopositive cells at EMR group was increased significantly compared with the control group, whereas bcl-2 was decreased. Besides, Zn-treated groups showed a significant reduction in the number of apoptotic cells and caspase-3 from that of EMR group, whereas there was an increase in bcl-2 immunopositivity. Our findings show that EMR caused oxidative stress and apoptotic activation in HEK293 cells. Zn seems to have protective effects on the EMR by increasing SOD activity and bcl-2 immunopositivity, decreasing lipid peroxidation and caspas-3 immunopositivity.
几项流行病学研究表明,电磁辐射(EMR)暴露可能对人类健康有害。本研究旨在研究 EMR 对人肾胚胎细胞(HEK293)的氧化参数和凋亡的诱导作用,并探讨锌(Zn)是否对 EMR 诱导的 HEK293 细胞凋亡具有保护作用。在我们的实验中,将 HEK293 细胞分为四个主要组,对照组、EMR 组、50μM Zn+EMR 组和 100μM Zn+EMR 组。EMR 组的 HEK293 细胞接受 2.45GHz EMR 照射 1 小时。在 Zn 组中,在暴露于 EMR 之前,HEK293 细胞用不同浓度的 Zn 孵育 48 小时。通过分光光度法测定氧化应激参数;用免疫组织化学法评估 bcl-2 和 caspase-3,并用 TUNEL 法检测细胞凋亡活性。与对照组相比,EMR 组的丙二醛(MDA)水平升高,超氧化物歧化酶(SOD)活性降低。与 EMR 组相比,Zn 处理组 MDA 降低,SOD 活性升高。与对照组相比,EMR 组的凋亡细胞数和 caspase-3 免疫阳性细胞数明显增加,而 bcl-2 减少。此外,Zn 处理组的凋亡细胞数和 caspase-3 阳性细胞数比 EMR 组明显减少,而 bcl-2 免疫阳性细胞数增加。我们的研究结果表明,EMR 导致 HEK293 细胞氧化应激和凋亡激活。Zn 通过增加 SOD 活性和 bcl-2 免疫阳性率、降低脂质过氧化和 caspase-3 免疫阳性率,对 EMR 具有保护作用。