Mobile phone (1800 MHz) radiation impairs female reproduction in mice, Mus musculus , through stress induced inhibition of ovarian and uterine activity

Shahin, Saba; Singh, S. P.; Chaturvedi, Chandra Mohini

doi:10.1016/j.reprotox.2017.08.001

Cited by 16 publications

(16 citation statements)

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“…The significance of such changes is valuable for elucidating the mechanism of action of the MP radiation, as it implicates that a specific lipid composition aggravates certain cell communication abnormalities caused by MP radiation. Studies showing hippocampal genome profile alterations associated with membrane functions (Nittby, Widegren, et al., ) and lipid peroxidation changes (Saikhedkar et al., ; Shahin, Singh, & Chaturvedi, ) following EMR exposure support our observations.…”

Section: Discussionsupporting

confidence: 88%

“…Importantly, the altered expression of genes implicated in the lipid metabolism may be associated with the changes that we observed on the fatty acid levels in the lipidomics analysis. Particularly, Acadl, the product of which catalyzes the initial step of mitochondrial beta-oxidation of straight-chain fatty acids, was found (Nittby, Widegren, et al, 2008) and lipid peroxidation changes (Saikhedkar et al, 2014;Shahin, Singh, & Chaturvedi, 2017) following EMR exposure support our observations.…”

Section: Discussionsupporting

confidence: 88%

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Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study

et al. 2018

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BackgroundThe widespread use of wireless devices during the last decades is raising concerns about adverse health effects of the radiofrequency electromagnetic radiation (RF‐EMR) emitted from these devices. Recent research is focusing on unraveling the underlying mechanisms of RF‐EMR and potential cellular targets. The “omics” high‐throughput approaches are powerful tools to investigate the global effects of RF‐EMR on cellular physiology.MethodsIn this work, C57BL/6 adult male mice were whole‐body exposed (nE xp = 8) for 2 hr to GSM 1800 MHz mobile phone radiation at an average electric field intensity range of 4.3–17.5 V/m or sham‐exposed (nSE = 8), and the RF‐EMR effects on the hippocampal lipidome and transcriptome profiles were assessed 6 hr later.ResultsThe data analysis of the phospholipid fatty acid residues revealed that the levels of four fatty acids [16:0, 16:1 (6c + 7c), 18:1 9c, eicosapentaenoic acid omega‐3 (EPA, 20:5 ω3)] and the two fatty acid sums of saturated and monounsaturated fatty acids (SFA and MUFA) were significantly altered (p < 0.05) in the exposed group. The observed changes indicate a membrane remodeling response of the tissue phospholipids after nonionizing radiation exposure, reducing SFA and EPA, while increasing MUFA residues. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p < 0.05) between the two groups, revealing an impact on genes involved in critical biological processes, such as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis.ConclusionsThis study provides preliminary evidence that mobile phone radiation induces hippocampal lipidome and transcriptome changes that may explain the brain proteome changes and memory deficits previously shown by our group.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 88%

Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study

et al. 2018

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“…Testicular protein samples (50 µg) from each group were resolved on 15% SDS‐PAGE at constant setting of 50 V for 30 min and then at 100 V for 1 hr, using the Mini‐PROTEAN tetra system, BIO‐RAD, The United States as mentioned elsewhere . Proteins were transferred from the polyacrylamide gels to PVDF membranes (Millipore, The United States) by electro‐blotting for 15 min in a Semi‐Dry blotting apparatus (TRANS‐BLOT SD, Semi‐dry transfer cell, BIO‐RAD, The United States) at constant setting of 15 V. Membrane was then blocked by 5% fat free skimmed (dry) milk in Tris buffered saline with 0.1% Tween‐20 (TBST) for 2 hr at room temperature.…”

Section: Methodsmentioning

confidence: 99%

2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular apoptosis: Involvement of a p53 dependent bax‐caspase‐3 mediated pathway

Shahin

Singh

Chaturvedi

2018

Environmental Toxicology

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Deleterious effects of MW radiation on the male reproduction are well studied. Previous reports although suggest that 2.45 GHz MW irradiation induced oxidative and nitrosative stress adversely affects the male reproductive function but the detailed molecular mechanism occurring behind it has yet to be elucidated. The aim of present study was to investigate the underlying detailed pathway of the testicular apoptosis induced by free radical load and redox imbalance due to 2.45 GHz MW radiation exposure and the degree of severity along with the increased exposure duration. Twelve-week old male mice were exposed to 2.45 GHz MW radiation [continuous-wave (CW) with overall average Power density of 0.0248 mW/cm and overall average whole body SAR value of 0.0146 W/kg] for 2 hr/day over a period of 15, 30, and 60 days. Testicular histology, serum testosterone, ROS, NO, MDA level, activity of antioxidant enzymes, expression of pro-apoptotic proteins (p53 and Bax), anti-apoptotic proteins (Bcl-2 and Bcl-x ), cytochrome-c, inactive/active caspase-3, and uncleaved PARP-1 were evaluated. Findings suggest that 2.45 GHz MW radiation exposure induced testicular redox imbalance not only leads to enhanced testicular apoptosis via p53 dependent Bax-caspase-3 mediated pathway, but also increases the degree of apoptotic severity in a duration dependent manner.

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“…Mice of experimental group were exposed to 1800 MHz mobile phone radiation at Power density of 1.15 W/m 2 and Specific Absorption Rate (SAR) value of 0.05 W/Kg. Detailed design of exposure set‐up, exposure cage, Power density, and SAR value calculation (at a point near to testes) has been described in our recent study (Shahin et al, ). Rectal temperature of all the mice were measured before and after the exposure during the first, middle (i.e., after 60 days of exposure) and the last 3 days of exposure.…”

Section: Methodsmentioning

confidence: 99%

1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53 dependent Bax mediated testicular apoptosis in mice, Mus musculus

Shahin

Singh

Chaturvedi

2018

Journal Cellular Physiology

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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-x ) 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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Mobile phone (1800 MHz) radiation impairs female reproduction in mice, Mus musculus , through stress induced inhibition of ovarian and uterine activity

Cited by 16 publications

References 64 publications

Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study

Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study

2.45 GHz microwave radiation induced oxidative and nitrosative stress mediated testicular apoptosis: Involvement of a p53 dependent bax‐caspase‐3 mediated pathway

1800 MHz mobile phone irradiation induced oxidative and nitrosative stress leads to p53 dependent Bax mediated testicular apoptosis in mice, Mus musculus

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