Bio-effects Induced By1800MHz Electromagnetic Radiation In NIH/3T3Cells

With the rapid development of wireless communication technology, the healtheffects of electromagnetic radiation (EMR) from mobile phones gain more and morepublic attention. By far, the results of the studies on health effects induced by mobilephone EMR were inconsistent. In May2011, the International Agency for Researchon Cancer (IARC) classified EMR including mobile phone radiation as classified2BCarcinogen which means suspected human carcinogen.1800MHz is the mainelectromagnetic wave frequency of Global System for Mobile communication, it isthe most occupied frequency of CDMA, GSM and3G mobile phones. The maximumSAR limit for a mobile phone used against the head or body in accordance with theInternational Commission on Non-Ionizing Radiation Protection (ICNIRP)guidelines is2W/kg.In this study, a NIH/3T3cell strain was used to observe the short and long termbio-effects induced by1800MHz EMR at a SAR of2W/kg for its sensitivity toenvironmental factors. Further more, the influences on expression of oncogens andtumor suppressor genes were detected by qPCR array.In short-term exposure, cells were intermittently exposed (5min on/10min off)to electromagnetic field at a SAR of2W/kg. They were respectively exposed for0.5h,1h,2h,4h,6h and8h. After exposure, we detected intracellular ROS, DNAdouble strand breaks (DSBs) and apoptosis. Results showed that intracellular ROSlevel in1h,4h,8h exposure groups significantly increased compared with theircorresponding sham groups and reached the peak in1h exposure group, andapoptosis increased significantly in1h,4h and8h exposure groups compared withtheir corresponding sham groups. But the number of DSBs didn’t show significantlydifference with corresponding sham groups.In long-term exposure, cells were intermittently exposed (5min on/10min off)to electromagnetic field at a SAR of2W/kg, which were exposed for5h each day.After exposure, cell viability, cell cycle, apoptosis, and the activity of Caspase3weredetected. To observe the effect of EMR on ability of clone forming, we conductedplate clone forming experiment and soft agar cloning formation experiment, and thendetected the expression profiling of84oncogenes and tumor suppressor genes byqPCR arrays. After60days’ exposure, compared with sham group, cell viabilitydecreased, cell cycle was blocked in S phase and G2/M phase, apoptosis increased,and the activity of Caspase3increased obviously in exposure group. qPCR assayshowed that2genes changed more than5folds. They were p53(up-regulated19.63folds) and serpinb5(up-regulated8.57folds). After138days’ exposure, cell viabilitydecreased obviously when exposed cells were cultured for24h and48h, and cell viability increased when exposed cells cultured for96h,120h,144h but which wasnot obviously compared with the sham groups. Cell cycle was blocked in G0/G1phaseand G2/M phase, and the activity of Caspase3and number of apoptosis cells bothincreased obviously in exposure group compared with the sham group. Cells both inexposure group and sham group didn’t form soft agar clone, but the number of formedclones in plates of the exposure group increased significantly compared with shamgroup.2genes changed more than5folds were respectively cdkn2b (down-regulated13.6folds) and tnf (up regulation5.46folds). However, the p53and serpinb5up-regulated before were down-regulated after138days’ exposure.In summary, the short-term radiation could induce an increase in intracellularROS level and cell apoptosis in exposed NIH/3T3cells. After60days’ exposure, theexpression of p53and serpinb5in exposed NIH/3T3cells were up-regulatedsignificantly and promoted apoptosis. After138days’ exposure, the expression ofcdkn2b gene was down-regulated and implied that cell proliferation accelerated.However, the expression of tnf gene was up-regulated, suggesting that the exposedNIH/3T3cells might have been malignant transformation and some of them beinginduced apoptosis.