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      Effects of radiofrequency electromagnetic waves (RF-EMW) from cellular phones on human ejaculated semen: an in vitro pilot study

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      Fertility and Sterility
      Elsevier BV

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          Abstract

          To evaluate effects of cellular phone radiofrequency electromagnetic waves (RF-EMW) during talk mode on unprocessed (neat) ejaculated human semen. Prospective pilot study. Center for reproductive medicine laboratory in tertiary hospital setting. Neat semen samples from normal healthy donors (n = 23) and infertile patients (n = 9). After liquefaction, neat semen samples were divided into two aliquots. One aliquot (experimental) from each patient was exposed to cellular phone radiation (in talk mode) for 1 h, and the second aliquot (unexposed) served as the control sample under identical conditions. Evaluation of sperm parameters (motility, viability), reactive oxygen species (ROS), total antioxidant capacity (TAC) of semen, ROS-TAC score, and sperm DNA damage. Samples exposed to RF-EMW showed a significant decrease in sperm motility and viability, increase in ROS level, and decrease in ROS-TAC score. Levels of TAC and DNA damage showed no significant differences from the unexposed group. Radiofrequency electromagnetic waves emitted from cell phones may lead to oxidative stress in human semen. We speculate that keeping the cell phone in a trouser pocket in talk mode may negatively affect spermatozoa and impair male fertility.

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          [241 Total antioxidant status in plasma and body fluids

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            Mechanism of short-term ERK activation by electromagnetic fields at mobile phone frequencies.

            The exposure to non-thermal microwave electromagnetic fields generated by mobile phones affects the expression of many proteins. This effect on transcription and protein stability can be mediated by the MAPK (mitogen-activated protein kinase) cascades, which serve as central signalling pathways and govern essentially all stimulated cellular processes. Indeed, long-term exposure of cells to mobile phone irradiation results in the activation of p38 as well as the ERK (extracellular-signal-regulated kinase) MAPKs. In the present study, we have studied the immediate effect of irradiation on the MAPK cascades, and found that ERKs, but not stress-related MAPKs, are rapidly activated in response to various frequencies and intensities. Using signalling inhibitors, we delineated the mechanism that is involved in this activation. We found that the first step is mediated in the plasma membrane by NADH oxidase, which rapidly generates ROS (reactive oxygen species). These ROS then directly stimulate MMPs (matrix metalloproteinases) and allow them to cleave and release Hb-EGF [heparin-binding EGF (epidermal growth factor)]. This secreted factor activates the EGF receptor, which in turn further activates the ERK cascade. Thus this study demonstrates for the first time a detailed molecular mechanism by which electromagnetic irradiation from mobile phones induces the activation of the ERK cascade and thereby induces transcription and other cellular processes.
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              Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: molecular mechanism for cancer- and blood-brain barrier-related effects.

              We have examined whether non-thermal exposures of cultures of the human endothelial cell line EA.hy926 to 900 MHz GSM mobile phone microwave radiation could activate stress response. Results obtained demonstrate that 1-hour non-thermal exposure of EA.hy926 cells changes the phosphorylation status of numerous, yet largely unidentified, proteins. One of the affected proteins was identified as heat shock protein-27 (hsp27). Mobile phone exposure caused a transient increase in phosphorylation of hsp27, an effect which was prevented by SB203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38MAPK). Also, mobile phone exposure caused transient changes in the protein expression levels of hsp27 and p38MAPK. All these changes were non-thermal effects because, as determined using temperature probes, irradiation did not alter the temperature of cell cultures, which remained throughout the irradiation period at 37 +/- 0.3 degrees C. Changes in the overall pattern of protein phosphorylation suggest that mobile phone radiation activates a variety of cellular signal transduction pathways, among them the hsp27/p38MAPK stress response pathway. Based on the known functions of hsp27, we put forward the hypothesis that mobile phone radiation-induced activation of hsp27 may (i) facilitate the development of brain cancer by inhibiting the cytochrome c/caspase-3 apoptotic pathway and (ii) cause an increase in blood-brain barrier permeability through stabilization of endothelial cell stress fibers. We postulate that these events, when occurring repeatedly over a long period of time, might become a health hazard because of the possible accumulation of brain tissue damage. Furthermore, our hypothesis suggests that other brain damaging factors may co-participate in mobile phone radiation-induced effects.
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                Author and article information

                Journal
                Fertility and Sterility
                Fertility and Sterility
                Elsevier BV
                00150282
                October 2009
                October 2009
                : 92
                : 4
                : 1318-1325
                Article
                10.1016/j.fertnstert.2008.08.022
                18804757
                aea3aa12-255d-49e0-b56a-b6df8dfedd5c
                © 2009

                https://www.elsevier.com/tdm/userlicense/1.0/

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