Pathophysiology of cell phone radiation: Oxidative stress and carcinogenesis with focus on male reproductive system

Center for Reproductive Medicine, Glickman Urological and Kidney Institute and Obstetrics and Gynecology and Women's Health Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Reproductive Biology and Endocrinology (Impact Factor: 2.23). 10/2009; 7(1):114. DOI: 10.1186/1477-7827-7-114
Source: PubMed


Hazardous health effects stemming from exposure to radiofrequency electromagnetic waves (RF-EMW) emitted from cell phones have been reported in the literature. However, the cellular target of RF-EMW is still controversial. This review identifies the plasma membrane as a target of RF-EMW. In addition, the effects of RF-EMW on plasma membrane structures (i.e. NADH oxidase, phosphatidylserine, ornithine decarboxylase) and voltage-gated calcium channels are discussed. We explore the disturbance in reactive oxygen species (ROS) metabolism caused by RF-EMW and delineate NADH oxidase mediated ROS formation as playing a central role in oxidative stress (OS) due to cell phone radiation (with a focus on the male reproductive system). This review also addresses: 1) the controversial effects of RF-EMW on mammalian cells and sperm DNA as well as its effect on apoptosis, 2) epidemiological, in vivo animal and in vitro studies on the effect of RF-EMW on male reproductive system, and 3) finally, exposure assessment and dosimetry by computational biomodeling.

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Available from: Ashok Agarwal,
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    • "Microwave radiation is responsible for the generation of free radicals and reactive oxygen species, which might be a possible link between male reproductive impairments and microwave exposure. Nonthermal effects of cell phones lead to oxidative stress on the male reproductive system through increased generation of seminal reactive oxygen species and reduction in antioxidant enzymes [37]. The extract of Morinda officinalis has shown antioxidant properties [38] [39]. "
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    ABSTRACT: The present study aimed to assess the protective effects of aqueous extract from Morinda officinalis F. C. How on microwave-induced reproductive impairment in male rats. Microwave exposure injury was induced by exposure of 900 MHz microwaves at 218 μm/cm(2)radiation densities, 24 hours/day for 10 days. Male Sprague-Dawley rats were randomized to: normal control, microwave exposure model, or water layer or ethyl acetate layer of aqueous extract 40 g/kg treatment groups. After 2 weeks of treatment, sexual performance, serum levels of gonadotrophin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) or testosterone, morphological analysis of testis and epididymis, and GnRH protein expression in the hypothalamus were measured. Pretreatment with water layer of aqueous extract 40 g/kg significantly improved sexual performance, increased serum testosterone level, and decreased LH and GnRH level compared with microwave exposed model rats (all P < 0.05). Water layer of aqueous extract treatment significantly increased seminiferous cell or sperm number in testis and epididymis. Protein expression of GnRH in the hypothalamus significantly decreased in the water layer of aqueous extract treated group (P < 0.05). Ethyl acetate layer of aqueous extract did not show obvious effects on the measured parameters. These findings suggest that water layer of aqueous extract 40 g/kg ameliorates microwave-reduced reproductive impairment.
    Evidence-based Complementary and Alternative Medicine 10/2015; 2015(4):360730. DOI:10.1155/2015/360730 · 1.88 Impact Factor
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    • "This means that the intensity of radiation was far below observable thermal effects in biological tissues, and far below safety limits of the International Commissions on Non-Ionizing Radiation Protection (ICNIRP) (ICNIRP, 1998). To date, molecular mechanisms of non-thermal effects of RFR are still a bottleneck in the research on the biological/ health effects of low-intensity RFR, although recently many studies have been carried out on metabolic changes in living cells under low-intensity RFR, and comprehensive reviews were published (Belyaev, 2010; Consales et al., 2012; Desai et al., 2009; Yakymenko et al., 2011). In the present work, we analyze the results of molecular effects of low-intensity RFR in living cells and model systems, with a special emphasis on oxidative effects and free radical mechanisms. "
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    ABSTRACT: This review aims to cover experimental data on oxidative effects of low-intensity radiofrequency radiation (RFR) in living cells. Analysis of the currently available peer-reviewed scientific literature reveals molecular effects induced by low-intensity RFR in living cells; this includes significant activation of key pathways generating reactive oxygen species (ROS), activation of peroxidation, oxidative damage of DNA and changes in the activity of antioxidant enzymes. It indicates that among 100 currently available peer-reviewed studies dealing with oxidative effects of low-intensity RFR, in general, 93 confirmed that RFR induces oxidative effects in biological systems. A wide pathogenic potential of the induced ROS and their involvement in cell signaling pathways explains a range of biological/health effects of low-intensity RFR, which include both cancer and non-cancer pathologies. In conclusion, our analysis demonstrates that low-intensity RFR is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.
    Electromagnetic Biology and Medicine 07/2015; DOI:10.3109/15368378.2015.1043557 · 1.19 Impact Factor
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    • "ROS production is an important intracellular inducer of autophagy (Garg et al., 2013). Recent studies have reported that RF exposure could increase ROS production in sperm in vitro (Agarwal et al., 2009; De Iuliis et al., 2009), which is considered to be one of the primary mechanisms involved in the bio-effects mediated by RF-EMR (Desai et al., 2009). Based on these evidences, we hypothesized that autophagy might be induced by RF-EMR as an underlying adaptive response mechanism and ROS could play a vital role in this process. "
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    ABSTRACT: The increasing exposure to radiofrequency (RF) radiation emitted from mobile phone use has raised public concern regarding the biological effects of RF exposure on the male reproductive system. Autophagy contributes to maintaining intracellular homeostasis under environmental stress. To clarify whether RF exposure could induce autophagy in the spermatocyte, mouse spermatocyte-derived cells (GC-2) were exposed to 1800 MHz Global System for Mobile Communication (GSM) signals in GSM-Talk mode at specific absorption rate (SAR) values of 1 w/kg, 2w/kg or 4w/kg for 24 h, respectively. The results indicated that the expression of LC3-II increased in a dose- and time-dependent manner with RF exposure, and showed a significant change at the SAR value of 4w/kg. The autophagosome formation and the occurrence of autophagy were further confirmed by GFP-LC3 transient transfection assay and transmission electron microscopy (TEM) analysis. Furthermore, the conversion of LC3-I to LC3-II was enhanced by co-treatment with Chloroqrine (CQ), indicating autophagic flux could be enhanced by RF exposure. Intracellular ROS levels significantly increased in a dose- and time-dependent manner after cells were exposed to RF. Pretreatment with anti-oxidative NAC obviously decreased the conversion of LC3-I to LC3-II and attenuated the degradation of p62 induced by RF exposure. Meanwhile, phosphorylated extracellular-signal-regulated kinase (ERK) significantly increased after RF exposure at the SAR value of 2w/kg and 4w/kg. Moreover, we observed that RF exposure did not increase the percentage of apoptotic cells, but inhibition of autophagy could increase the percentage of apoptotic cells. These findings suggested that autophagy flux could be enhanced by 1800 MHz GSM exposure (4w/kg), which is mediated by ROS generation. Autophagy may play an important role in preventing cells from apoptotic cell death under RF exposure stress.
    Toxicology Letters 08/2014; 228(3). DOI:10.1016/j.toxlet.2014.05.004 · 3.26 Impact Factor
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