MHz Radiofrequency Electromagnetic Radiation Research Articles

Effect of 900 MHz radiofrequency electromagnetic radiation emitted from mobile phone on testicular immunity and the associated risk of testicular germ cell tumor

The emission of radiofrequency electromagnetic radiation (RF-EMR) from mobile phones has been implicated in causing inflammatory changes in the testis. Nevertheless, the direct association of these changes with the development of testicular germ cell tumors (TGCT) remains unclear. Therefore, we purposed to investigate the effect of RF-EMR exposure on inflammatory changes in the testis, cytokine gene expression levels, and the incidence of TGCT. Twenty male Wistar albino rats were randomly assigned to either the study or control groups. The study group was exposed to RF-EMR at 900 MHz, 26 V/m, and a specific absorption rate (SAR) of 0.14 W/kg for 4 h/day over 8 weeks. Histopathological analysis, vitality analysis using Annexin V, and real-time polymerase chain reaction for the analysis of interleukin 1 (IL-1), IL-4, IL-10, tumor necrosis factor-alpha, and interferon-gamma (IFN-γ) cytokine gene expressions were performed on the testicular tissue. The median testis weight (163.0 g [133.0 – 183.0] vs. 179.0 g [134.0 – 195.0], P = 0.012) and volume (0.95 cm3 [0.800 – 1.400] vs. 1.100 cm3 [1.050 – 1.500], P = 0.031) of the study group were significantly lower compared to the control group. The seminiferous tubule damage (P < 0.001) and interstitial edema (P = 0.042) were significantly higher in the study group. The tunica albuginea thickness was significantly reduced in the study group (P < 0.001). The fold changes in the expression levels of IL-4 and IFN-γ increased significantly in the study group. Our findings indicate that RF-EMR exposure causes structural, histopathological, and inflammatory toxic effects on the testis. The observed elevation in gene expression levels of IL-4 and IFN-γ cytokines following RF-EMR exposure suggests their potential role as regulators of TGCT initiation, thereby offering a viable potential therapeutic target in combination with current treatments. Nonetheless, future well-designed studies are necessary to validate our findings.

The ZIP9-centered androgen pathway compensates for the 2605 MHz radiofrequency electromagnetic radiation-mediated reduction in resistance to H2O2 damage in Sertoli cells of adult rats

The direct biological effects of radiofrequency electromagnetic radiation (RF-EMR) from wireless communication equipment on the testes are still unclear. Our previous study proved that long-term exposure to 2605 MHz RF-EMR gradually damage spermatogenesis and resulted in time-dependent reproductive toxicity by directly disrupting blood-testis barrier circulation. Although short-term exposure did not cause readily observable damage to fertility, whether it caused specific biological effects and how these effects contributed to the time-dependent reproductive toxicity of RF-EMR were currently unknown. Studies on this issue are important for elucidating the time-dependent reproductive toxicity of RF-EMR. The present study established a 2605 MHz RF-EMR (SAR=1.05 W/Kg) scrotal exposure model with rats and extracted primary Sertoli cells for exposure to investigate the direct biological effects of short-term RF-EMR exposure on the testis. The results showed that short-term RF-EMR exposure did not decrease sperm quality and spermatogenesis, but it increased the levels of testicular testosterone (T) and zinc transporter 9 (ZIP9) in Sertoli cells of rats. In vitro, 2605 MHz RF-EMR exposure did not increase the apoptosis rate of Sertoli cells, but it increased the apoptosis rate and MDA of Sertoli cells exposed to H2O2. T reversed these changes and increased ZIP9 level in Sertoli cells, whereas inhibiting ZIP9 expression significantly suppressed these T-mediated protective effects. Moreover, T increased the levels of phosphorylated inositol-requiring enzyme 1 (P-IRE1), phosphorylated protein kinase R (PKR)-like endoplasmic reticulum kinase (P-PERK), phosphorylated eukaryotic initiation factor 2a (P-eIF2a) and phosphorylated activating transcription factor 6 (P-ATF6) in Sertoli cells, and these effects were reversed by ZIP9 inhibition. With prolonged exposure time, testicular ZIP9 was gradually downregulated, and testicular MDA increased. ZIP9 level was negatively correlated with MDA level in the testes of exposed rats. Thus, although short-term exposure to 2605 MHz RF-EMR (SAR=1.05 W/kg) did not significantly disturb spermatogenesis, it suppressed the ability of Sertoli cells to resist external insults, which was rescued by enhancing the ZIP9-centered androgen pathway in the short term. Increasing the unfolded protein response might be an important downstream mechanism involved. These results promote a better understanding of the time-dependent reproductive toxicity of 2605 MHz RF-EMR.

THE EFFECT OF RADIOFREQUENCY ELECTROMAGNETIC RADIATION ON RAT LIVER TISSUE AND SERUM PARAOXONASE (PON1)

Aim: The development of technology increases the rate of everyone having a smartphone. Therefore, the possible biological effects of these devices are of concern. In this study, we aimed to investigate the effect of 2100 MHz radiofrequency electromagnetic radiation on rat liver tissue and serum paraoxonase 1 level. Materials and Methods: Within the scope of the study, a 2100 MHz radiofrequency electromagnetic radiation model was created. In our study, we used Sprague Dawley male rats. Two groups were made as sham-control and exposure group (5 h a day for 2 weeks). Liver tissue and serum paraoxonase were studied. Results: The paraoxonase 1 value of the exposure group was higher than the sham control group, and did not have statistically important difference in the comparison of exposure and sham control groups (p>0.05). Did not have important difference in histopathological parameters of rat liver tissue (p>0.05). Conclusion: Although it seems that radiofrequency radiation does not cause liver damage, more detailed studies with short- and long-term exposure are needed.

Effects of continuous prenatal and postnatal global system for mobile communications electromagnetic waves (GSM-EMW) exposure on the oxidative stress biomarkers in female rat liver

In light of the increased use of communication technologies, the harm caused by continuous exposure to emitted radiation on pregnancy and developing newborns is among the public concerns. Using Sprague-Dawley rats, our study investigates the effects of 24 h/day prenatal and postnatal 900 MHz radiofrequency electromagnetic radiation (RF-EMR) exposure of female rats on liver oxidative stress (OS) and other hepatic parameters at postnatal days (PND) 1, 9, and 21. Our results showed that RF-EMR exposure led to an increase in oxidative stress status as indicated by a significant elevation in MDA level at PND9 and PND21, a decrease in catalase (CAT) activity at all ages, a reduction (PND1 and PND9) in catalase amounts and mRNA expression, in addition to a decrease in GPx activity at PND21 in the exposed group. Current findings also showed a significant increase in cytoSOD at PND9 and 21 and a reduction in mitoSOD at PND21 in the exposed groups compared to the control groups. However, significant increases in glutathione peroxidase (GPx) level and mitoSOD activity were observed at all studied ages. Furthermore, cytoSOD activity showed a significant reduction in PND1, whereas in PND9 the value of this parameter increased compared to the non-exposed group. Moreover, while SOD1 mRNA expression increased at PND1, it decreased at PND9 and 21. However, GPx1 expression was shown to be always decreased in the exposed group. In addition, at PND1 and 9, exposed rats showed a similar response on Akt1, nuclear factor erythroïd 2-related factor 2 (Nrf-2), and intercellular adhesion molecule-1 (ICAM-1) expression. Therefore, an increased oxidative stress status produced from a continuous (24 h/day) GSM-modulated 900 MHz radiofrequency electromagnetic radiation (RF-EMR) exposure during the prenatal and postnatal periods may result in adverse health effects during future life stages.

Effects of Acute Exposure to 3500 MHz (5G) Radiofrequency Electromagnetic Radiation on Anxiety-Like Behavior and the Auditory Cortex in Guinea Pigs.

Numerous studies have shown that radiofrequency electromagnetic radiation (RF-EMR) may negatively affect human health. We detected the effect of 3500 MHz RF-EMR on anxiety-like behavior and the auditory cortex (ACx) in guinea pigs. Forty male guinea pigs were randomly divided into four groups and exposed to a continuous wave of 3500 MHz RF-EMF at an average specific absorption rate (SAR) of 0, 2, 4, or 10 W/kg for 72 h. After exposure, malondialdehyde (MDA) levels, antioxidant enzyme activity, anxiety-like behavior, hearing thresholds, cell ultrastructure, and apoptosis were detected. Our results revealed that hearing thresholds and basic indexes of animal behavior did not change significantly after exposure (P > 0.05). However, the MDA levels of ACx were increased (P < 0.05), and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) activities were decreased (P < 0.05) in the exposure groups compared to the sham group. Ultrastructural changes of ACx, including swollen mitochondria and layered myelin sheaths, were observed. Cytochrome-c relocalization, caspase-9, and cleaved caspase-3 activation were detected in the exposure groups. In conclusion, these results suggest that oxidative stress is an important mechanism underlying the biological effects of RF-EMR, which can induce ultrastructural damage to the ACx and cell apoptosis through a mitochondria-dependent mechanism. Moreover, oxidative stress, apoptosis induction and ultrastructural damage increase in a SAR-dependent manner. However, RF-EMR does not increase hearing thresholds or induce anxiety. Bioelectromagnetics. 43:106-118, 2022. © 2021 Bioelectromagnetics Society.

Molecular Mechanism of Malignant Transformation of Balb/c-3T3 Cells Induced by Long-Term Exposure to 1800 MHz Radiofrequency Electromagnetic Radiation (RF-EMR).

Purpose: We aimed to investigate RF-EMR-induced cell malignant transformation. Methods: We divided Balb/c-3T3 cells into sham and expo groups. The expo groups were exposed to a 1800 MHz RF continuous wave for 40 and 60 days, for 4 h per day. The sham group was sham-exposed. Cells were harvested for a cell transformation assay, transplantation in severe combined immune deficient (SCID) mice, soft agar clone formation detection, and a transwell assay. The mRNA microarray assay was used to declare key genes and pathways. Results: The exposed Balb/c-3T3 cells showed a strong increase in cell proliferation and migration. Malignant transformation was observed in expo Balb/c-3T3 cells exposed for 40 days and 60 days, which was symbolized with visible foci and clone formation. Expo Balb/c-3T3 cells that were exposed for 40 days and 60 days produced visible tumors in the SCID mice. Lipid metabolism was the key biological process and pathway involved. The mevalonate (MVA) pathway was the key metabolic pathway. The interacted miRNAs could be further research targets to examine the molecular mechanism of the carcinogenic effects of long-term exposure. Conclusion: Exposure for 40 and 60 days to 1800 MHz RF-EMR induced malignant transformation in Balb/c-3T3 cells at the SAR of 8.0 W/kg. We declared that lipid metabolism was the pivotal biological process and pathway. The MVA pathway was the key metabolic pathway.

The Effects of Exposure to 900 MHz Radiofrequency Radiation and Nicotine on Apoptotic Ratio of Human Fetal Cells

AIM: The present study purposes to examine the effects of radiofrequency electromagnetic radiation (RF-EMR) and nicotine exposures on apoptosis and necrosis ratio of cultured amniocytes. METHODS: Amniotic fluid samples were gained from 48 pregnant women and, after culturing procedure, samples were analyzed by flow cytometry. RESULTS: Significant increases were observed in ratios of necrotic (UL), early (LR), and late apoptotic cells (UR) in the exposure groups of RF-EMR, nicotine, and RF-EMR + nicotine groups (p &lt; 0.01 and p &lt; 0.001), along with significant changes in ratios of viable (LL) cells (p &lt; 0.001). CONCLUSION: Our results showed that nicotine exposure, alone or in combination with 900 MHz RF-EMR, led to increased apoptotic cell ratios. Amniocytes were even more severely affected by nicotine, when nicotine was administered in combination with 900 MHz RF-EMR, due to created synergistic effect. More studies with different settings, exposure times, frequencies, and doses are needed to clarify net effects of exposures to nicotine and RF-EMR radiation, alone or in combination.

1,800 MHz Radiofrequency Electromagnetic Irradiation Impairs Neurite Outgrowth With a Decrease in Rap1-GTP in Primary Mouse Hippocampal Neurons and Neuro2a Cells.

Background: With the global popularity of communication devices such as mobile phones, there are increasing concerns regarding the effect of radiofrequency electromagnetic radiation (RF-EMR) on the brain, one of the most important organs sensitive to RF-EMR exposure at 1,800 MHz. However, the effects of RF-EMR exposure on neuronal cells are unclear. Neurite outgrowth plays a critical role in brain development, therefore, determining the effects of 1,800 MHz RF-EMR exposure on neurite outgrowth is important for exploring its effects on brain development.Objectives: We aimed to investigate the effects of 1,800 MHz RF-EMR exposure for 48 h on neurite outgrowth in neuronal cells and to explore the associated role of the Rap1 signaling pathway.Material and Methods: Primary hippocampal neurons from C57BL/6 mice and Neuro2a cells were exposed to 1,800 MHz RF-EMR at a specific absorption rate (SAR) value of 4 W/kg for 48 h. CCK-8 assays were used to determine the cell viability after 24, 48, and 72 h of irradiation. Neurite outgrowth of primary hippocampal neurons (DIV 2) and Neuro2a cells was observed with a 20 × optical microscope and recognized by ImageJ software. Rap1a and Rap1b gene expressions were detected by real-time quantitative PCR. Rap1, Rap1a, Rap1b, Rap1GAP, and p-MEK1/2 protein expressions were detected by western blot. Rap1-GTP expression was detected by immunoprecipitation. The role of Rap1-GTP was assessed by transfecting a constitutively active mutant plasmid (Rap1-Gly_Val-GFP) into Neuro2a cells.Results: Exposure to 1,800 MHz RF-EMR for 24, 48, and 72 h at 4 W/kg did not influence cell viability. The neurite length, primary and secondary neurite numbers, and branch points of primary mouse hippocampal neurons were significantly impaired by 48-h RF-EMR exposure. The neurite-bearing cell percentage and neurite length of Neuro2a cells were also inhibited by 48-h RF-EMR exposure. Rap1 activity was inhibited by 48-h RF-EMR with no detectable alteration in either gene or protein expression of Rap1. The protein expression of Rap1GAP increased after 48-h RF-EMR exposure, while the expression of p-MEK1/2 protein decreased. Overexpression of constitutively active Rap1 reversed the decrease in Rap1-GTP and the neurite outgrowth impairment in Neuro2a cells induced by 1,800 MHz RF-EMR exposure for 48 h.Conclusion: Rap1 activity and related signaling pathways are involved in the disturbance of neurite outgrowth induced by 48-h 1,800 MHz RF-EMR exposure. The effects of RF-EMR exposure on neuronal development in infants and children deserve greater focus.

1800MHz Radiofrequency electromagnetic radiation: Does it affect heat shock genes expression levels in the rat brain?

The brain could recognizethe cell phone radiation as environmental stress and may alter stress-related gene expression levels. Heat shock proteins (HSP) are a family of proteins that are produced by cells in response to the exposure of stressful conditions. We investigated whether exposure to 1800MHz Radiofrequency Electromagnetic Radiation (RF-EMR) recognize the expression levels of some HSPs (Cryaa, Crybb, Hsp20, Hsp25, Hsp70) in mature rat’s brain tissue. The experimental group was exposed to 1.800MHz RF-EMR in restrainer for eight weeks with 2 h/day. The specific absorption rate (SAR) was 0.06 W/kg. The sham group was kept in restrainer but not exposed to radiation. The Control group was kept under their condition. Whole brain was homogenized.ViA7 Real-Time-PCR software was used to measure CT values of the genes and ΔΔCT values were also calculated. Cryaa (p=0.02), Crybb (p=0.01), and Hsp20 (p

Probing the Origins of 1,800 MHz Radio Frequency Electromagnetic Radiation Induced Damage in Mouse Immortalized Germ Cells and Spermatozoa in vitro.

As the use of mobile phone devices is now highly prevalent, many studies have sought to evaluate the effects of the radiofrequency-electromagnetic radiation (RF-EMR) on both human health and biology. While several such studies have shown RF-EMR is capable of inducing cellular stress, the physicobiological origin of this stress remains largely unresolved. To explore the effect of RF-EMR on the male reproductive system, we exposed cultured mouse spermatogonial GC1 and spermatocyte GC2 cell lines, as well as cauda epididymal spermatozoa to a waveguide generating continuous wave RF-EMR (1.8 GHz, 0.15 and 1.5 W/kg). This study demonstrated that a 4 h exposure is capable of inducing the generation of mitochondrial reactive oxygen species (ROS) in populations of GC1 (7 vs. 18%; p < 0.001) and GC2 cells (11.5 vs. 16 %; p < 0.01), identifying Complex III of the electron transport chain (ETC) as the potential source of electrons producing ROS. Assessing the generation of ROS in the presence of an antioxidant, penicillamine, as well as measuring lipid peroxidation via 4-hydroxynonenal levels, indicated that the elevated incidence of ROS generation observed under our exposure conditions did not necessarily induce an overt cellular oxidative stress response. However, exposure to RF-EMR at 0.15 W/kg for 3 h did induce significant DNA fragmentation in spermatozoa (that was no longer significant after 4 h), assessed by the alkaline comet assay (p < 0.05). Furthermore, this fragmentation was accompanied by an induction of oxidative DNA damage in the form of 8-hydroxy-2′-deoxyguanosine, which was significant (p < 0.05) after spermatozoa were exposed to RF-EMR for 4 h. At this exposure time point, a decline in sperm motility (p < 0.05) was also observed. This study contributes new evidence toward elucidating a mechanism to account for the effects of RF-EMR on biological systems, proposing Complex III of the mitochondrial ETC as the key target of this radiation.

1800 MHz radio-frequency electromagnetic radiation induces oxidative stress in rat liver, kidney and brain tissues

1800 MHz radio-frequency electromagnetic radiation induces oxidative stress in rat liver, kidney and brain tissues

Effects of acute and chronic exposure to both 900 MHz and 2100 MHz electromagnetic radiation on glutamate receptor signaling pathway

Purpose: To demonstrate the molecular effects of acute and chronic exposure to both 900 and 2100 MHz radiofrequency electromagnetic radiation (RF-EMR) on the hippocampal level/activity of some of the enzymes – including PKA, CaMKIIα, CREB, and p44/42 MAPK – from N-methyl-D-aspartate receptor (NMDAR)-related signaling pathways.Materials and methods: Rats were divided into the following groups: sham rats, and rats exposed to 900 and 2100 MHz RF-EMR for 2 h/day for acute (1 week) or chronic (10 weeks), respectively. Western blotting and activity measurement assays were used to assess the level/activity of the selected enzymes.Results: The obtained results revealed that the hippocampal level/activity of selected enzymes was significantly higher in the chronic groups as compared to the acute groups at both 900 and 2100 MHz RF-EMR exposure. In addition, hippocampal level/activity of selected enzymes was significantly higher at 2100 MHz RF-EMR than 900 MHz RF-EMR in both acute and chronic groups.Conclusions: The present study provides experimental evidence that both exposure duration (1 week versus 10 weeks) and different carrier frequencies (900 vs. 2100 MHz) had different effects on the protein expression of hippocampus in Wistar rats, which might encourage further research on protection against RF-EMR exposure.

Effects of GSM-like radiofrequency irradiation during the oogenesis and spermiogenesis of Xenopus laevis

We aimed to evaluate the effect of GSM-like radiofrequency electromagnetic radiation (RF-EMR) on the oogenesis, and spermiogenesis of Xenopus laevis, and so the development of the embryos obtained from Normal Females+Normal Males (i.e. “N(F)+N(M)”); Normal Females+RF-exposed Males (i.e. “N(F)+RF(M)”); RF-exposed Female+Normal Male (i.e. “RF(F)+N(M)”); and RF-exposed Female+RF-exposed Male (i.e. “RF(F)+RF(M)”. Various, assessments were performed to determine potential teratogenic effects and mortality, body growth and behavior on first generation embryos. After exposing adults frogs of both sexes to 900MHz RF-EMR (at 1.0W/kg) for 8h a day over a 5-week period, the embryos' specific energy absorption rate (SAR) was calculated.In our present study (control group; 2.2% abnormal, 0.0% dead); with the N(F)+RF(M) combination, the long-term exposure of adult males to GSM-like radiation at 900MHz (RF: 2W) for 5 week/8h/day resulted in normal, abnormal and dead embryo ratios of 88.3%, 3.3% and 8.3%, respectively (p<0.001). In the RF(F)+N(M) combination, long-term exposure (5 week/8h/day) of adult females led to normal, abnormal and dead embryo ratios of 76.7%, 11.7%, and 11.7%, respectively (p<0.001). And in the RF(F)+RF(M) combination, long-term exposure (5 week/8h/day) of both adult males and females led to normal, abnormal and dead embryo ratios of 73.3%, 11.7%, and 15%, respectively (p<0.001).With the exception RF(F)+RF(M) group (p<0.001), no significant changes were observed on body growth (lengths) in comparison to the control group. It was also observed that the offspring of female adult Xenopus exposed to RF-EMR during oogenesis exhibited a more aggressive behavior compared to the control group. Cell phones radiation can thus lead to detrimental effects in humans' male and female reproductive cells.

8-oxoG DNA Glycosylase-1 Inhibition Sensitizes Neuro-2a Cells to Oxidative DNA Base Damage Induced by 900 MHz Radiofrequency Electromagnetic Radiation

Background/Aims: The purpose of this study was to explore the in vitro putative genotoxicity during exposure of Neuro-2a cells to radiofrequency electromagnetic fields (RF-EMFs) with or without silencing of 8-oxoG DNA glycosylase-1 (OGG1). Methods: Neuro-2a cells treated with or without OGG1 siRNA were exposed to 900 MHz Global System for Mobile Communication (GSM) Talk signals continuously at a specific absorption rate (SAR) of 0, 0.5, 1 or 2 W/kg for 24 h. DNA strand breakage and DNA base damage were measured by the alkaline comet assay and a modified comet assay using formamidopyrimidine DNA glycosylase (FPG), respectively. Reactive oxygen species (ROS) levels and cell viability were monitored using the non-fluorescent probe 2, 7-dichlorofluorescein diacetate (DCFH-DA) and CCK-8 assay. Results: Exposure to 900 MHz RF-EMFs with insufficient energy could induce oxidative DNA base damage in Neuro-2a cells. These increases were concomitant with similar increases in the generation of reactive oxygen species (ROS). Without OGG1 siRNA, 2 W/kg RF-EMFs induced oxidative DNA base damage in Neuro-2a cells. Interestingly, with OGG1 siRNA, RF-EMFs could cause DNA base damage in Neuro-2a cells as low as 1 W/kg. However, neither DNA strand breakage nor altered cell viability was observed. Conclusion: Even if further studies remain conducted we support the hypothesis that OGG1 is involved in the process of DNA base repair and may play a pivotal role in protecting DNA bases from RF-EMF induced oxidative damage.

The protective effect of autophagy on mouse spermatocyte derived cells exposure to 1800 MHz radiofrequency electromagnetic radiation

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 1800MHz Global System for Mobile Communication (GSM) signals in GSM-Talk mode at specific absorption rate (SAR) values of 1w/kg, 2w/kg or 4w/kg for 24h, 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 Chloroquine (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 1800MHz 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.

Evaluation of oxidant stress and antioxidant defense in discrete brain regions of rats exposed to 900 MHz radiation

In the current study, the effects of 900 MHz radio-frequency electromagnetic radiation (RF-EMR) on levels of thiobarbituric acid-reactive substances (TBARS), total antioxidants (TA), and glutathione S-transferase (GST) activity in discrete brain regions were studied in adolescent rats.Thirty-six male Wistar rats (6-8 weeks old) were allotted into three groups (n = 12 in each group). Control group (1) remained undisturbed in their home cage; sham group (2) was exposed to mobile phone in switch off mode for four weeks; RF-EMR-exposed group (3) was exposed to 900 MHz of RF-EMR (1 hr/day with peak power density of 146.60 µW/cm2) from an activated Global System for Mobile communication (GSM) mobile phone (kept in silent mode; no ring tone and no vibration) for four weeks. On 29th day, behavioral analysis was done. Followed by this, six animals from each group were sacrificed and biochemical parameters were studied in amygdala, hippocampus, frontal cortex, and cerebellum.Altered behavioral performances were found in RF-EMR-exposed rats. Additionally, elevated TBARS level was found with all brain regions studied. RF-EMR exposure significantly decreased TA in the amygdala and cerebellum but its level was not significantly changed in other brain regions. GST activity was significantly decreased in the hippocampus but, its activity was unaltered in other brain regions studied.RF-EMR exposure for a month induced oxidative stress in rat brain, but its magnitude was different in different regions studied. RF-EMR-induced oxidative stress could be one of the underlying causes for the behavioral deficits seen in rats after RF-EMR exposure (Fig. 5, Ref. 37).

Exposure to 1800 MHz radiofrequency electromagnetic radiation induces oxidative DNA base damage in a mouse spermatocyte-derived cell line

Whether exposure to radiofrequency electromagnetic radiation (RF-EMR) emitted from mobile phones can induce DNA damage in male germ cells remains unclear. In this study, we conducted a 24h intermittent exposure (5min on and 10min off) of a mouse spermatocyte-derived GC-2 cell line to 1800MHz Global System for Mobile Communication (GSM) signals in GSM-Talk mode at specific absorption rates (SAR) of 1W/kg, 2W/kg or 4W/kg. Subsequently, through the use of formamidopyrimidine DNA glycosylase (FPG) in a modified comet assay, we determined that the extent of DNA migration was significantly increased at a SAR of 4W/kg. Flow cytometry analysis demonstrated that levels of the DNA adduct 8-oxoguanine (8-oxoG) were also increased at a SAR of 4W/kg. These increases were concomitant with similar increases in the generation of reactive oxygen species (ROS); these phenomena were mitigated by co-treatment with the antioxidant α-tocopherol. However, no detectable DNA strand breakage was observed by the alkaline comet assay. Taking together, these findings may imply the novel possibility that RF-EMR with insufficient energy for the direct induction of DNA strand breaks may produce genotoxicity through oxidative DNA base damage in male germ cells.

Impact of radio frequency electromagnetic radiation on DNA integrity in the male germline

Concern has arisen over human exposures to radio frequency electromagnetic radiation (RFEMR), including a recent report indicating that regular mobile phone use can negatively impact upon human semen quality. These effects would be particularly serious if the biological effects of RFEMR included the induction of DNA damage in male germ cells. In this study, mice were exposed to 900 MHz RFEMR at a specific absorption rate of approximately 90 mW/kg inside a waveguide for 7 days at 12 h per day. Following exposure, DNA damage to caudal epididymal spermatozoa was assessed by quantitative PCR (QPCR) as well as alkaline and pulsed-field gel electrophoresis. The treated mice were overtly normal and all assessment criteria, including sperm number, morphology and vitality were not significantly affected. Gel electrophoresis revealed no gross evidence of increased single- or double-DNA strand breakage in spermatozoa taken from treated animals. However, a detailed analysis of DNA integrity using QPCR revealed statistically significant damage to both the mitochondrial genome (p < 0.05) and the nuclear beta-globin locus (p < 0.01). This study suggests that while RFEMR does not have a dramatic impact on male germ cell development, a significant genotoxic effect on epididymal spermatozoa is evident and deserves further investigation.