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在45摄氏度或41摄氏度热休克后,热休克蛋白27(HSP27)的磷酸化增加,但在非热时分多址(TDMA)或全球移动通信系统(GSM)暴露后则不会增加。

HSP27 phosphorylation increases after 45 degrees C or 41 degrees C heat shocks but not after non-thermal TDMA or GSM exposures.

作者信息

Vanderwaal Robert P, Cha Bibianna, Moros Eduardo G, Roti Roti Joseph L

机构信息

Department of Radiation Oncology, Washington University School of Medicine, St Louis, MO 63108, USA.

出版信息

Int J Hyperthermia. 2006 Sep;22(6):507-19. doi: 10.1080/02656730600924406.

Abstract

PURPOSE

Experiments with cultured HeLa, S3 and E.A. Hy296 cells were performed to determine if exposure to acute (30 min at 45 degrees C) or chronic (2 h at 41 degrees C) heat shocks or to non-thermal exposures of radiofrequency radiation (RF) induce changes in HSP27 phosphorylation.

MATERIALS AND METHODS

The radiofrequency (RF) exposures used in this study were 847 MHz time division multiple access modulated (TDMA) at a specific absorption rate (SAR) of 5 W kg-1 for 1, 2 or 24 h or 900 MHz GSM modulated (GSM) at a SAR of 3.7 W kg-1 for 1, 2 or 5 h. HSP27 phosphorylation was evaluated by resolving the various phosphorylation forms using two-dimensional gel electrophoresis measuring the relative amount of each by densitometry. Alternatively, an antibody specific for phosphorylated HSP27 was used to detect changes in HSP27 phosphorylation levels. All heat shock and RF exposure conditions were analysed simultaneously along with a matched incubator control sample. Each experiment was repeated three times.

RESULTS

Following heat shock, the degree of phosphorylation of HSP27 varied with the heat dose, with acute hyperthermia (45 degrees C) having an increased proportion of higher phosphorylated forms. Exposure of HeLa S3 cells to 5 W kg-1 TDMA for 1, 2 or 24 h did not induce significant differences in the levels of HSP27 phosphorylation compared to incubator control or sham. Exposure of E.A. Hy926 cells to 3.7 W kg-1 900 MHz GSM for 1, 2 or 5 h did not induce significant differences in the levels of HSP27 phosphorylation compared to sham exposed.

CONCLUSIONS

Acute and moderate hyperthermia significantly increase HSP27 phosphorylation, but there was no significant change in the levels of HSP27 following non-thermal exposure to TDMA and GSM modulated RF radiations.

摘要

目的

进行了对培养的HeLa、S3和E.A. Hy296细胞的实验,以确定暴露于急性(45摄氏度30分钟)或慢性(41摄氏度2小时)热休克或射频辐射(RF)的非热暴露是否会诱导热休克蛋白27(HSP27)磷酸化的变化。

材料与方法

本研究中使用的射频(RF)暴露为847兆赫兹时分多址调制(TDMA),比吸收率(SAR)为5瓦/千克,持续1、2或24小时,或900兆赫兹全球移动通信系统调制(GSM),SAR为3.7瓦/千克,持续1、2或5小时。通过二维凝胶电泳解析各种磷酸化形式并通过光密度测定法测量每种形式的相对量来评估HSP27磷酸化。或者,使用针对磷酸化HSP27的特异性抗体来检测HSP27磷酸化水平的变化。所有热休克和RF暴露条件均与匹配的培养箱对照样品同时进行分析。每个实验重复三次。

结果

热休克后,HSP27的磷酸化程度随热剂量而变化,急性高热(45摄氏度)时较高磷酸化形式的比例增加。与培养箱对照或假处理相比,HeLa S3细胞暴露于5瓦/千克TDMA 1、2或24小时并未诱导HSP27磷酸化水平的显著差异。与假暴露相比,E.A. Hy926细胞暴露于3.7瓦/千克900兆赫兹GSM 1、2或5小时并未诱导HSP27磷酸化水平的显著差异。

结论

急性和中度高热显著增加HSP27磷酸化,但在非热暴露于TDMA和GSM调制的RF辐射后,HSP27水平没有显著变化。

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