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(Database last updated on Mar 27, 2024)
| ID Number | 2325 | |
| Study Type | In Vivo | |
| Model | Observations on circadian rhythms, spatial memory, DNA damage in brain cells, blood cell counts, reproduction and oxidative stress in mice exposed at 2.45 GHz. | |
| Details | AUTHORS' ABSTRACT: Chaturvedi et al. 2011 IEEE #5346): Present study examines biological effects of 2.45 GHz microwave radiation in Parkes strain mice. Forty-day-old mice were exposed to CW (continuous wave) microwave radiation (2 h/day for 30 days). Locomotor activity was recorded on running wheel for 12 days prior to microwave exposure (pre-exposure), 7 days during the ¯rst week of exposure (short-term exposure) and another 7-day spell during the last week of the 30-day exposure period (long-term exposure). Morris water maze test was performed from 17th to 22nd day of exposure. At the termination of the exposure, blood was processed for hematological parameters, brain for comet assay, epididymis for sperm count and motility and serum for SGOT (serum glutamate oxaloacetate transaminase) and SGPT (serum glutamate pyruvate transaminase). The results show that long-term radiation-exposed group exhibited a positive ª (phase angle difference) for the onset of activity with reference to lights-o® timing and most of the activity occurred within the light fraction of the LD (light:dark) cycle. Microwave radiation caused an increase in erythrocyte and leukocyte counts, a significant DNA strand break in brain cells and the loss of spatial memory in mice. This report for the first time provides experimental evidence that continuous exposure to low intensity microwave radiation may have an adverse effect on the brain function by altering circadian system and rate of DNA damage. AUTHORS' ABSTRACT: Shahin et al. 2013 (IEEE #6180): The present experiment was designed to study the 2.45 GHz low-level microwave (MW) irradiation-induced stress response and its effect on implantation or pregnancy in female mice. Twelve-week-old mice were exposed to MW radiation (continuous wave for 2 h/day for 45 days, frequency 2.45 GHz, power density=0.033549 mW/cm(2), and specific absorption rate=0.023023 W/kg). At the end of a total of 45 days of exposure, mice were sacrificed, implantation sites were monitored, blood was processed to study stress parameters (hemoglobin, RBC and WBC count, and neutrophil/lymphocyte (N/L) ratio), the brain was processed for comet assay, and plasma was used for nitric oxide (NO), progesterone and estradiol estimation. Reactive oxygen species (ROS) and the activities of ROS-scavenging enzymes- superoxide dismutase, catalase, and glutathione peroxidase-were determined in the liver, kidney and ovary. We observed that implantation sites were affected significantly in MW-irradiated mice as compared to control. Further, in addition to a significant increase in ROS, hemoglobin (p<0.001), RBC and WBC counts (p<0.001), N/L ratio (p<0.01), DNA damage (p<0.001) in brain cells, and plasma estradiol concentration (p<0.05), a significant decrease was observed in NO level (p<0.05) and antioxidant enzyme activities of MW-exposed mice. Our findings led us to conclude that a low level of MW irradiation-induced oxidative stress not only suppresses implantation, but it may also lead to deformity of the embryo in case pregnancy continues. We also suggest that MW radiation-induced oxidative stress by increasing ROS production in the body may lead to DNA strand breakage in the brain cells and implantation failure/resorption or abnormal pregnancy in mice. AUTHORS' ABSTRACT: Shahin et al. 2017 (IEEE #6822): Present study investigated the long-term effects of mobile phone (1800MHz) radiation in stand-by, dialing and receiving modes on the female reproductive function (ovarian and uterine histo-architecture, and steroidogenesis) and stress responses (oxidative and nitrosative stress). We observed that mobile phone radiation induces significant elevation in ROS, NO, lipid peroxidation, total carbonyl content and serum corticosterone coupled with significant decrease in antioxidant enzymes in hypothalamus, ovary and uterus of mice. Compared to control group, exposed mice exhibited reduced number of developing and mature follicles as well as corpus lutea. Significantly decreased serum levels of pituitary gonadotrophins (LH, FSH), sex steroids (E2 and P4) and expression of SF-1, StAR, P-450scc, 3²-HSD, 17²-HSD, cytochrome P-450 aromatase, ER-± and ER-² were observed in all the exposed groups of mice, compared to control. These findings suggest that mobile phone radiation induces oxidative and nitrosative stress, which affects the reproductive performance of female mice. AUTHORS' ABSTRACT: Shahin et al. 2017 (IEEE #6863): Microwave (MW) radiation induced oxidative stress reduces dendritic arborization, spine density and number of hippocampal pyramidal neurons and hence, impair learning and spatial memory through p53-dependent/independent apoptosis of hippocampal neuronal and non-neuronal cells. However, the mechanisms responsible for MW radiation induced impairment in memory formation remains still unknown. Present study elucidates the effect of short (15 days) and long-term (30 and 60 days) low level 2.45 GHz MW radiation induced local stress on the hippocampal spatial memory formation pathway in adult male mice. Twelve-weeks old mice were exposed to 2.45 GHz MW radiation [continuous-wave (CW) with overall average Power density of 0.0248 mW/cm 2 and overall average whole body SAR value of 0.0146 W/Kg] @ 2h/day for 15, 30 and 60 days. Learning and spatial memory was assessed by eight-arm radial maze (RAM). We have investigated the alterations in serum corticosterone level and the expression of GR, CRH, i-NOS, iGluRs, PSD-95-nNOS system, PKA-PKCµ-ERK1/2-pERK1/2 in all the hippocampal subregions, viz. CA1, CA2, CA3 and DG through immunohistochemistry/immunofluorescence and alterations in the expression of hippocampal GR, CRH-R1, CREB and p-CREB through western blot analysis. We observed that 2.45 GHz MW irradiated mice showed slow learning and significantly increased number of working and reference memory errors in RAM task. Further, 2.45 GHz MW radiation exposure increases serum corticosterone level and the expression of CRH, CRH-R1 and i-NOS, while the expression of iGluRs, n-NOS, PSD-95, PKCµ, PKA, ERK-p-ERK, CREB and p-CREB decreases in above mentioned hippocampal subregions in a duration dependent manner. Our findings led us to conclude that 2.45 GHz MW radiation exposure induced local stress suppresses signaling mechanism(s) of hippocampal memory formation. AUTHORS' ABSTRACT: Shahin et al. 2018 (IEEE #7143): Present study was carried out to investigate the effect of long-term mobile phone radiation exposure in different operative modes (Dialing, Receiving, and Stand-by) on immature male mice. Three-week old male mice were exposed to mobile phone (1800 MHz) radiation for 3 hr/day for 120 days in different operative modes. To check the changes/alteration in testicular histoarchitecture and serum testosterone level, HE staining and ELISA was performed respectively. Further, we have checked the redox status (ROS, NO, MDA level, and antioxidant enzymes: SOD, CAT, and GPx) by biochemical estimation, alteration in the expression of pro-apoptotic proteins (p53 and Bax), active executioner caspase-3, full length/uncleaved PARP-1 (DNA repair enzyme), anti-apoptotic proteins (Bcl-2 and Bcl-xL ) in testes by immunofluorescence and cytosolic cytochrome-c by Western blot. Decreased seminiferous tubule diameter, sperm count, and viability along with increased germ cells apoptosis and decreased serum testosterone level, was observed in the testes of all the mobile phone exposed mice compared with control. We also observed that, mobile phone radiation exposure in all the three different operative modes alters the testicular redox status via increasing ROS, NO, and MDA level, and decreasing antioxidant enzymes levels leading to enhanced apoptosis of testicular cells by increasing the expression of pro-apoptotic and apoptotic proteins along with decreasing the expression of anti-apoptotic protein. On the basis of results, it is conclude that long-term mobile phone radiation exposure induced oxidative stress leads to apoptosis of testicular cells and thus impairs testicular function. |
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| Findings | Effects | |
| Status | Completed With Publication | |
| Principal Investigator | Banaras Hindu U, Varanasi, India | |
| Funding Agency | India, Council of Scientific and Industrial Resear | |
| Country | INDIA | |
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