ID Number		1566
Study Type		In Vitro
Model		1.8, 2.4 GHz (CW, GSM) exposure to human lymphocytes +/- chemical mutagens and analysis of DNA breaks and protein expression.
Details		Human lymphocytes (n = 4 donors) exposed to 1800 MHz (CW) RF for 2 hours at 3 W/kg with or without mitomycin C (crosslinker) bleomycin (radiomimetic), ethyl methane sulfonate (alkylator), or 4-nitroquinoline-1-oxide (UV mimetic). The authors report no effects of RF exposure alone, but in combination with MMC and 4-NQO there was an increase in DNA breaks (i.e., synergistic effect) as measured by comet assay. There was no effect on DNA damage when RF was used in combination with BLM or MMS. In subsequent studies, the authors exposed as above for 1.5 or 4 hours either with or without UV-C radiation or the DNA damaging agend doxorubicin (Adriamycin). The authors again report no effect of RF exposure alone, but decreased DNA damage when exposed in combination with UV-C for 1.5 hours, and increased DNA damage when exposed in combination with UV-C for 4 hours. With doxorubicin, co-exposure increased DNA damage with a classic dose response. In a study of 1800 MHz (GSM) exposure at 2 W/kg for 24 hours to primary human lymphocytes followed by X-ray exposure, the authors report no effect on subsequent DNA repair. AUTHORS' ABSTRACT: Zhijian et al. 2013 (IEEE 5365): In the present study, the protein microarray was used to investigate the protein expression in human B-cell lymphoblastoid cells intermittently exposed to 1.8-GHz GSM radiofrequency radiation (RFR) at the specific absorption rate (SAR) of 2.0 W/kg for 24 h. The differential expression of 27 proteins was found, which were related to DNA damage repair, apoptosis, oncogenesis, cell cycle and proliferation (ratio >1.5-fold, P<0.05). The results validated with Western blot assay indicated that the expression of RPA32 was significantly down-regulated (P<0.05) while the expression of p73 was significantly up-regulated in RFR exposure group (P<0.05). Because of the crucial roles of those proteins in DNA repair and cell apoptosis, the results of present investigation may explain the biological effects of RFR on DNA damage/repair and cell apoptosis.
Findings		Effects
Status		Completed With Publication
Principal Investigator		Zhejiang University, Hangzhou, Zhejiang, China
Funding Agency		CDC / NIEHS, China
Country		CHINA
References		Zhijian, C et al. Mutat Res., (2010) 695:16-21 Zhijian, C et al. Mutat Res, (2009) 677:100-104 Baohong, W et al. Toxicology, (2007) 232:311-316 Baohong, W et al. Mutation Research, (2005) 578:149-157 Zhijian, C et al. Biochem Biophys Res Commun., (2013) 433:36-39
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