Evaluation of HSP70 Expression and DNA Damage in Cells of a Human Trophoblast Cell Line Exposed to 1.8 GHz Amplitude-Modulated Radiofrequency Fields

Interdepartment Centre for Environmental Science Research, University of Bologna, 48100 Ravenna, Italy.
Radiation Research (Impact Factor: 2.91). 04/2008; 169(3):270-9. DOI: 10.1667/RR1061.1
Source: PubMed


The aim of this study was to determine whether high-frequency electromagnetic fields (EMFs) could induce cellular effects. The human trophoblast cell line HTR-8/SVneo was used as a model to evaluate the expression of proteins (HSP70 and HSC70) and genes (HSP70A, B, C and HSC70) of the HSP70 family and the primary DNA damage response after nonthermal exposure to pulse-modulated 1817 MHz sinusoidal waves (GSM-217 Hz; 1 h; SAR of 2 W/kg). HSP70 expression was significantly enhanced by heat, which was applied as the prototypical stimulus. The HSP70A, B and C transcripts were differentially expressed under basal conditions, and they were all significantly induced above basal levels by thermal stress. Conversely, HSC70 protein and gene expression was not influenced by heat. Exposing HTR-8/SVneo cells to high-frequency EMFs did not change either HSP70 or HSC70 protein or gene expression. A significant increase in DNA strand breaks was caused by exposure to H(2)O(2), which was used as a positive stimulus; however, no effect was observed after exposure of cells to high-frequency EMFs. Overall, no evidence was found that a 1-h exposure to GSM-217 Hz induced a HSP70-mediated stress response or primary DNA damage in HTR-8/SVneo cells. Nevertheless, further investigations on trophoblast cell responses after exposure to GSM signals of different types and durations are needed.

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    • "Cells were exposed for 1 h to a 1.8 GHz sinusoidal wave, whose amplitude was modulated by rectangular pulses with a repetition frequency of 217 Hz [36] applied at timeaveraged SAR values of 2 W/Kg.s, the safety limit for mobile phone emission according to INCIRP (International Commission on Non-Ionizing Radiation Protection). The exposure system was developed and built by the Foundation for Research and Information Technologies in Society (IT'IS Foundation, Zurich, Switzerland) following the specifications outlined in 5 [36] and extensively described in [37]. The system consisted of two 128.5 × 65 × 424 mm 3 brass singlemode waveguide resonators operated inside the Forma thermostat . "
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    ABSTRACT: We investigated the effect of high-frequency electromagnetic fields (HF-EMFs) and 17- β -estradiol on connexins (Cxs), integrins (Ints), and estrogen receptor (ER) expression, as well as on ultrastructure of trophoblast-derived HTR-8/SVneo cells. HF-EMF, 17- β -estradiol, and their combination induced an increase of Cx40 and Cx43 mRNA expression. HF-EMF decreased Int alpha1 and β 1 mRNA levels but enhanced Int alpha5 mRNA expression. All the Ints mRNA expressions were increased by 17- β -estradiol and exposure to both stimuli. ER- β mRNA was reduced by HF-EMF but augmented by 17- β -estradiol alone or with HF-EMF. ER- β immunofluorescence showed a cytoplasmic localization in sham and HF-EMF exposed cells which became nuclear after treatment with hormone or both stimuli. Electron microscopy evidenced a loss of cellular contact in exposed cells which appeared counteracted by 17- β -estradiol. We demonstrate that 17- β -estradiol modulates Cxs and Ints as well as ER- β expression induced by HF-EMF, suggesting an influence of both stimuli on trophoblast differentiation and migration.
    Oxidative Medicine and Cellular Longevity 05/2013; 2013(7):280850. DOI:10.1155/2013/280850 · 3.36 Impact Factor
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    • "Evidence has been found for changes in the expression of HSPs in various models of human cell lines (Lee et al., 2005; Caraglia et al., 2005; Alfieri et al., 2006) or in vivo rat tissue (Jorge-Mora et al., 2010) after exposure to experimental radio frequency systems. Other studies report no apparent changes in these biological markers after applying other experimental models in the laboratory (Wang et al., 2006; Chauhan et al., 2006; Valbonesi et al., 2008). "
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    ABSTRACT: Non-ionizing radiation at 2.45 GHz may modify the expression of genes that codify heat shock proteins (HSP) in the thyroid gland. Using the enzyme-linked immunosorbent assay (ELISA) technique, we studied levels of HSP-90 and HSP-70. We also used hematoxilin eosin to look for evidence of lesions in the gland and applied the DAPI technique of fluorescence to search for evidence of chromatin condensation and nuclear fragmentation in the thyroid cells of adult female Sprague-Dawley rats. Fifty-four rats were individually exposed for 30 min to 2.45 GHz radiation in a Gigahertz transverse electromagnetic (GTEM) cell at different levels of non-thermal specific absorption rate (SAR), which was calculated using the finite difference time domain (FDTD) technique. Ninety minutes after radiation, HSP-90 and HSP-70 had decreased significantly (P<0.01) after applying a SAR of 0.046±1.10 W/Kg or 0.104±5.10(-3) W/Kg. Twenty-four hours after radiation, HSP-90 had partially recovered and HSP-70 had recovered completely. There were few indications of lesions in the glandular structure and signs of apoptosis were negative in all radiated animals. The results suggest that acute sub-thermal radiation at 2.45 GHz may alter levels of cellular stress in rat thyroid gland without initially altering their anti-apoptotic capacity.
    Biology Open 09/2012; 1(9):831-8. DOI:10.1242/bio.20121297 · 2.42 Impact Factor
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    • "Concerning the expression of HSC70, our data are not in agreement with previously published results showing that neither short term (1 h) (Valbonesi et al., 2008) nor long term (24 h) (Franzellitti et al., 2008) exposure to GSM-1800 MHz at SAR 2 W/kg was able to alter HSC70 expression (mRNA and protein). However, an increase in the mRNA level of the HSP70C isoform was observed. "
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    ABSTRACT: The expanding use of GSM devices has resulted in public concern. Chaperone-mediated autophagy (CMA) is a way for protein degradation in the lysosomes and increases under stress conditions as a cell defense response. α-synuclein, a CMA substrate, is a component of Parkinson disease. Since GSM might constitute a stress signal, we raised the possibility that GSM could alter the CMA process. Here, we analyzed the effects of chronic exposure to a low GSM-900MHz dose on apoptosis and CMA. Cultured cerebral cortical cells were sham-exposed or exposed to GSM-900MHz at specific absorption rate (SAR): 0.25W/kg for 24 h using a wire-patch cell. Apoptosis was analyzed by DAPI stain of the nuclei and western blot of cleaved caspase-3. The expression of proteins involved in CMA (HSC70, HSP40, HSP90 and LAMP-2A) and α-synuclein were analyzed by western blot. CMA was also quantified in situ by analyzing the cell localization of active lysosomes. 24 h exposure to GSM-900MHz resulted in ∼0.5°C temperature rise. It did not induce apoptosis but increased HSC70 by 26% and slightly decreased HSP90 (<10%). It also decreased α-synuclein by 24% independently of CMA, since the localization of active lysosomes was not altered. Comparable effects were observed in cells incubated at 37.5°C, a condition that mimics the GSM-generated temperature rise. The GSM-induced changes in HSC70, HSP90 and α-synuclein are most likely linked to temperature rise. We did not observe any immediate effect on cell viability. However, the delayed and long term consequences (protective or deleterious) of these changes on cell fate should be examined.
    Toxicology 12/2011; 292(2-3):136-44. DOI:10.1016/j.tox.2011.12.003 · 3.62 Impact Factor
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