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叙利亚仓鼠胚胎细胞在体外暴露于50Hz磁场、苯并(a)芘和佛波酯后的微核诱导情况。

Micronucleus induction in Syrian hamster embryo cells following exposure to 50 Hz magnetic fields, benzo(a)pyrene, and TPA in vitro.

作者信息

Simkó M, Richard D, Kriehuber R, Weiss D G

机构信息

Division of Environmental Physiology, Institute of Cell Biology and Biosystems Technology, University of Rostock, Universitätsplatz 2, D-18051 Rostock, Germany.

出版信息

Mutat Res. 2001 Aug 22;495(1-2):43-50. doi: 10.1016/s1383-5718(01)00192-9.

Abstract

Electromagnetic fields (EMFs) have been associated with increased incidence of cancer suggested by epidemiological studies. To test the carcinogenic potency of EMF, the in vitro micronucleus assay with SHE cells has been used as a screening method for genotoxicity. A 50Hz magnetic field (MF) of 1mT field strength was applied either alone or with the tumour initiator benzo(a)pyrene (BP) or the tumour promoter 12-O-tetradecanoylphorbol-13-acetate (TPA). All three treatments were applied in single, double or triple treatment regimes. MF or TPA (1nM) alone did not affect the number of micronuclei (MN) in initiated and non-initiated SHE cells. Changing the schedule of the typical initiation protocol, namely applying the initiator (BP) during exposure to MF, results in an 1.8-fold increased MN formation compared to BP treatment alone. Combined experiment with BP, TPA and MF did not cause further MN formation. Since initiation during MF exposure caused a significant increased MN formation, our findings suggest that MFs enhance the initiation process of BP. We think that this MF-enhanced co-carcinogenic effect is caused by an indirect "cell activation" process. The resulting genomic instability is proposed to be due to free radicals and/or to the unscheduled "switching-on" of signal transduction pathways.

摘要

流行病学研究表明,电磁场(EMF)与癌症发病率的增加有关。为了测试EMF的致癌潜力,采用SHE细胞体外微核试验作为遗传毒性的筛选方法。单独或与肿瘤引发剂苯并(a)芘(BP)或肿瘤促进剂12-O-十四酰佛波醇-13-乙酸酯(TPA)一起施加1mT场强的50Hz磁场(MF)。所有三种处理均采用单次、两次或三次处理方案。单独的MF或TPA(1nM)不影响起始和未起始的SHE细胞中的微核(MN)数量。改变典型起始方案的时间表,即在暴露于MF期间施加引发剂(BP),与单独的BP处理相比,MN形成增加了1.8倍。BP、TPA和MF的联合实验未导致进一步的MN形成。由于在MF暴露期间起始导致MN形成显著增加,我们的研究结果表明MF增强了BP的起始过程。我们认为这种MF增强的协同致癌作用是由间接的“细胞激活”过程引起的。由此产生的基因组不稳定性被认为是由于自由基和/或信号转导途径的意外“开启”。

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