Histological and biochemical assessment of hippocampal structure, neurotransmitters, and oxidative stress markers in mice following mobile phone radiation exposure

Background: Concerns regarding potential negative impacts on human health are growing as cell phone use dramatically expands worldwide. Due to the anatomical position of the brain, cell phones emit nonionizing radiofrequency waves that may have an impact on it. Objectives: The study aims to examine the effect of mobile phone radiation in male rats on the histological structure, and sonographic imaging of the brain of rats after mobile phone radiation exposure and investigate the ameliorating role of moringa. Materials and Methods: In the study, 44 male Albino rats were used. The rats were randomly divided into six groups and exposed to cell phone radiation (in the data or calling modes) for 10 weeks. The 200 mg/kg of body weight of moringa extract was administered to evaluate the protective role of the rats for 10 weeks. Results: A sonographic and histological analysis of the rat brain showed that rats exposed to mobile phone radiation suffered serious damage to their neurons in several parts of the brain. Meanwhile, the rats given moringa extract suffered less harm. Conclusion: Rats given moringa extract had less damage to neuronal architecture in their brains.

Excessive usage of gadgets Emitting Electromagnetic Radiation (EMR), especially smartphones, by people of all age groups, and so forth chronic exposure to the radiation, were indeed sounding the alarm about a multitude of health risks. The nervous system was significantly affected, altering the brain and behavior of people and animals. Many preclinical experimental studies have been performed to uncover the pathways that lead to injury, but the results have been contradictory. A strategic search was conducted to identify studies published between 2011 and 2020, using electronic databases such as PubMed and Science Direct. Based on predefined criteria, studies were identified for study and assessed individually. All of the included studies were assessed for the risk of bias, and no study was found to be free of bias. In preclinical research, heterogenicity was detected in the exposure settings (EMF-RF type, MW, pulsed, SAR value, and length of exposure) after a thorough assessment of the studies included. Exposure to mobile phone radiation can produce oxidative stress, which can lead to the activation of apoptotic and necrotic pathways if not reversed in time. The available scientific literature is insufficient to draw particular conclusions, but the possibility of harmful impacts cannot be ruled out, according to the authors. There is a great need to restrict extensive investigations and instead conduct a systematic and complete blinded study with significant reproducibility and long-term research. This review intended to explain the potential mechanisms and risks associated with mobile phone radiation exposure.

Objective(s):The increasing rate of over using cell phones has been considerable in youths and pregnant women. We examined the effect of mobile phones radiation on genes expression variation on cerebellum of BALB/c mice before and after of the birth.Materials and Methods:In this study, a mobile phone jammer, which is an instrument to prevent receiving signals between cellular phones and base transceiver stations (two frequencies 900 and 1800 MHz) for exposure was used and twelve pregnant mice (BALB/c) divided into two groups (n=6), first group irradiated in pregnancy period (19th day), the second group did not irradiate in pregnancy period. After childbirth, offspring were classified into four groups (n=4): Group1: control, Group 2: B1 (Irradiated after birth), Group 3: B2 (Irradiated in pregnancy period and after birth), Group 4: B3 (Irradiated in pregnancy period). When maturity was completed (8-10 weeks old), mice were dissected and cerebellum was isolated. The expression level of bax, bcl-2, p21 and p53 genes examined by real-time reverse transcription polymerase chain reaction (Real-Time RT- PCR).Results:The data showed that mobile phone radio waves were ineffective on the expression level of bcl-2 and p53 genes) P>0.05(. Also gene expression level of bax decreased and gene expression level of p21 increased comparing to the control group (P<0.05).Conclusion:From the obtained data it could be concluded that the mobile phone radiations did not induce apoptosis in cells of the cerebellum and the injured cells can be repaired by cell cycle arrest.

Male infertility, often attributed to insufficient production of healthy and active sperm, can be exacerbated by electromagnetic radiation emitted from mobile phones, which disrupts normal spermatogenesis and leads to a notable decline in sperm quality. The main targets of mobile phone-induced damage in the testes are Leydig cells, seminiferous tubules, and sperm cells. The aim of this systematic literature review is to identify histopathological changes in the testes due to mobile phone radiation exposure and to examine its effects on sperm parameters in experimental animals. In this systematic review, an extensive literature search was conducted across databases such as PubMed, ScienceDirect, Hinari, and Google scholar. A total of 752 studies were identified for screening, and 18 studies were deemed eligible for data extraction. Studies have identified histopathological alterations in testicular tissue caused by mobile phone radiation, such as reduced seminiferous tubule diameter, tunica albuginea and germinal epithelial thickness, Leydig cell hypoplasia, and increased intertubular space. Consistent exposure to mobile phone radiation has been shown to significantly reduce sperm count, motility, and viability, while also increasing abnormal sperm morphology in male rats, mice, and rabbits. Animal studies indicate that electromagnetic radiation from mobile phones can negatively impact testicular tissue and sperm parameters, including sperm count, motility, viability, and morphology. As a precaution, preventive measures are recommended to minimize potential risks from mobile phone exposure, and further research is needed to fully understand its effects on human reproductive health.

IntroductionIt is impossible to imagine a modern socially–active man who does not use mobile devices and/or computers with Wi–Fi function. The effect of mobile phone radiation on male fertility is the subject of recent interest and investigations. The aim of this study was to investigate the direct in vitro influence of mobile phone radiation on sperm DNA fragmentation and motility parameters in healthy subjects with normozoospermia.Material and methods32 healthy men with normal semen parameters were selected for the study. Each sperm sample was divided into two equal portions (A and B). Portions A of all involved men were placed for 5 hours in a thermostat, and portions B were placed into a second thermostat for the same period of time, where a mobile phone in standby/talk mode was placed. After 5 hours of incubation the sperm samples from both thermostats were re–evaluated regarding basic motility parameters. The presence of DNA fragmentation in both A and B portions of each sample was determined each hour using a standard sperm chromatin dispersion test.ResultsThe number of spermatozoa with progressive movement in the group, influenced by electromagnetic radiation, is statistically lower than the number of spermatozoa with progressive movement in the group under no effect of the mobile phone. The number of non–progressive movement spermatozoa was significantly higher in the group, which was influenced by cell phone radiation. The DNA fragmentation was also significantly higher in this group.ConclusionsA correlation exists between mobile phone radiation exposure, DNA–fragmentation level and decreased sperm motility.

We have examined in vitro cell response to mobile phone radiation (900 MHz GSM signal) using two variants of human endothelial cell line: EA.hy926 and EA.hy926v1. Gene expression changes were examined in three experiments using cDNA Expression Arrays and protein expression changes were examined in ten experiments using 2-DE and PDQuest software. Obtained results show that gene and protein expression were altered, in both examined cell lines, in response to one hour mobile phone radiation exposure at an average specific absorption rate of 2.8 W/kg. However, the same genes and proteins were differently affected by the exposure in each of the cell lines. This suggests that the cell response to mobile phone radiation might be genome- and proteome-dependent. Therefore, it is likely that different types of cells and from different species might respond differently to mobile phone radiation or might have different sensitivity to this weak stimulus. Our findings might also explain, at least in part, the origin of discrepancies in replication studies between different laboratories.

Significance: Excess oxidative stress and neuroinflammation are risk factors in the onset and progression of Alzheimer's disease (AD) and its association with amyloid-β plaque accumulation. Oxidative stress impairs acetylcholine (ACH) and N-methyl-d-aspartate receptor signaling in brain areas that function in memory and learning. Glutathione (GSH) antioxidant depletion positively correlates with the cognitive decline in AD subjects. Treatments that upregulate GSH and ACH levels, which simultaneously decrease oxidative stress and inflammation, may be beneficial for AD. Recent Advances: Some clinical trials have shown a benefit of monotherapy with vitamin D (VD), whose deficiency is linked to AD or with l-cysteine (LC), a precursor of GSH biosynthesis, in reducing mild cognitive impairment. Animal studies have shown a simultaneous decrease in ACH esterase (AChE) and increase in GSH; combined supplementation with VD and LC results in a greater decrease in oxidative stress and inflammation, and increase in GSH levels compared with monotherapy with VD or LC. Therefore, cosupplementation with VD and LC has the potential of increasing GSH, downregulation of oxidative stress, and decreased inflammation and AChE levels. Future Directions: Clinical trials are needed to determine whether safe low-cost dietary supplements, using combined VD+LC, have the potential to alleviate elevated AChE, oxidative stress, and inflammation levels, thereby halting the onset of AD. Goal of Review: The goal of this review is to highlight the pathological hallmarks and current Food and Drug Administration-approved treatments for AD, and discuss the potential therapeutic effect that cosupplementation with VD+LC could manifest by increasing GSH levels in patients. Antioxid. Redox Signal. 40, 663-678.

Worldwide, the number of mobile phone users has increased from 5.57billion in 2011 to 6.8billion in 2019. However, short- and long-term impact of the electromagnetic radiation emitting from mobile phones on tissue homeostasis with particular to brain proteome composition needs further investigation. In this study, we attempted a global proteome profiling study of rat hippocampus exposed to mobile phone radiation for 20 weeks (for 3h/day for 5 days/week) to identify deregulated proteins and western blot analysis for validation. As a result, we identified 358 hippocampus proteins, of which 16 showed deregulation (log2 (exposed/sham) ≥ ±1.0, p-value <.05). Majority of these deregulated proteins grouped into three clusters sharing similar molecular pathways. A set of four proteins (Succinate-semialdehyde dehydrogenase: Aldh5a1, Na+ K+ transporting ATPase: Atp1b2, plasma membrane calcium transporting ATPase: PMCA and protein S100B) presenting each functional pathway were selected for validation. Western blot analysis of these proteins, in an independent sample set, corroborated the mass spectrometry findings. Aldh5a1 involve in cellular energy metabolism, both Atp1b2 and PMCA responsible for membrane transport and protein S100B have a neuroprotective role. In conclusion, we present a deregulated hippocampus proteome upon mobile phone radiation exposure, which might influence the healthy functioning of the brain.

The relationship between radiofrequency electromagnetic fields emitted from mobile phone and infertility is a matter of continuing debate. It is postulated that these radiations may affect the reproduction pattern spell by targeting biochemistry of sperm. In an attempt to expedite the issue, 70 days old Wistar rats (n = 6) were exposed to mobile phone radiofrequency (RF) radiation for 2 h per day for 45 days and data compared with sham exposed (n = 6) group. A significant decrease (P < 0.05) in the level of testosterone and an increase in caspase-3 activity were found in the RF-exposed animals. Distortions in sperm head and mid piece of sperm mitochondrial sheath were also observed as captured by Transmission Electron Microscope (TEM). In addition, progeny from RF-exposed rats showed significant decreases in number and weight as compared with that of sham-exposed animals. A reduction in testosterone, an increase in caspase-3, and distortion in spermatozoa could be caused by overproduction of reactive oxygen species (ROS) in animals under mobile phone radiation exposure. Our findings on these biomarkers are clear indications of possible health implications of repeated exposure to mobile phone radiation.

Chronic glaucoma is a multifactorial disease among which oxidative stress may play a major pathophysiological role. We conducted a systematic review and meta-analysis to evaluate the levels of oxidative and antioxidative stress markers in chronic glaucoma compared with a control group. The PubMed, Cochrane Library, Embase and Science Direct databases were searched for studies reporting oxidative and antioxidative stress markers in chronic glaucoma and in healthy controls using the following keywords: “oxidative stress” or “oxidant stress” or “nitrative stress” or “oxidative damage” or “nitrative damage” or “antioxidative stress” or “antioxidant stress” or “antinitrative stress” and “glaucoma”. We stratified our meta-analysis on the type of biomarkers, the type of glaucoma, and the origin of the sample (serum or aqueous humor). We included 22 case-control studies with a total of 2913 patients: 1614 with glaucoma and 1319 healthy controls. We included 12 studies in the meta-analysis on oxidative stress markers and 19 on antioxidative stress markers. We demonstrated an overall increase in oxidative stress markers in glaucoma (effect size = 1.64; 95%CI 1.20–2.09), ranging from an effect size of 1.29 in serum (95%CI 0.84–1.74) to 2.62 in aqueous humor (95%CI 1.60–3.65). Despite a decrease in antioxidative stress marker in serum (effect size = –0.41; 95%CI –0.72 to –0.11), some increased in aqueous humor (superoxide dismutase, effect size = 3.53; 95%CI 1.20–5.85 and glutathione peroxidase, effect size = 6.60; 95%CI 3.88–9.31). The differences in the serum levels of oxidative stress markers between glaucoma patients and controls were significantly higher in primary open angle glaucoma vs primary angle closed glaucoma (effect size = 12.7; 95%CI 8.78–16.6, P < 0.001), and higher in pseudo-exfoliative glaucoma vs primary angle closed glaucoma (effect size = 12.2; 95%CI 8.96–15.5, P < 0.001). In conclusion, oxidative stress increased in glaucoma, both in serum and aqueous humor. Malonyldialdehyde seemed the best biomarkers of oxidative stress in serum. The increase of some antioxidant markers could be a protective response of the eye against oxidative stress.

Recently, there have been several reports referring to detrimental effects due to radio frequency electromagnetic fields (RF-EMF) exposure. Special attention was given to investigate the effect of mobile phone exposure on the rat brain. Since the integrative mechanism of the entire body lies in the brain, it is suggestive to analyze its biochemical aspects. For this, 35-day old Wistar rats were exposed to a mobile phone for 2 h per day for a duration of 45 days where specific absorption rate (SAR) was 0.9 W/Kg. Animals were divided in two groups: sham exposed (n = 6) and exposed group (n = 6).Our observations indicate a significant decrease (P < 0.05) in the level of glutathione peroxidase, superoxide dismutase, and an increase in catalase activity. Moreover, protein kinase shows a significant decrease in exposed group (P < 0.05) of hippocampus and whole brain. Also, a significant decrease (P < 0.05) in the level of pineal melatonin and a significant increase (P < 0.05) in creatine kinase and caspase 3 was observed in exposed group of whole brain as compared with sham exposed. Finally, a significant increase in the level of ROS (reactive oxygen species) (P < 0.05) was also recorded.The study concludes that a reduction or an increase in antioxidative enzyme activities, protein kinase C, melatonin, caspase 3, and creatine kinase are related to overproduction of reactive oxygen species (ROS) in animals under mobile phone radiation exposure. Our findings on these biomarkers are clear indications of possible health implications.

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.

Anti-inflammatory and antioxidant effect of methanol extract of latex of Calotropis procera in rat model of colorectal cancer

To investigate oxidative stress markers and antioxidants in bipolar disorder (BD). Electronic MEDLINE/PubMed/Cochrane-Library/Scopus/TripDatabase search until 06/30/2019 for studies comparing antioxidant or oxidative stress markers between BD and healthy controls (HCs). Standardized mean differences (SMD) and 95% confidence intervals (CIs) were calculated for≥3 studies. Forty-four studies (n=3,767: BD=1,979; HCs=1,788) reported on oxidative stress markers malondialdehyde (MDA), thiobarbituric acid reactive substances (TBARS), and total nitrites; antioxidants glutathione (GSH), uric acid, and zinc; or antioxidantenhancing enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and GSH-transferase (GST). Compared with HCs, BD was associated with higher GST (P=.01), CAT (P=.02), nitrites (P<.0001), TBARS (P<.0001), MDA (P=.01), uric acid (P<.0001), and lower GSH (P=.006), without differences in SOD, GPX, and zinc. Compared to HCs, levels were higher in BD-mania for TBARS (P<.0001) and uric acid (P<.0001); in BD-depression for TBARS (P=.02); and BD-euthymia for uric acid (P=.03). Uric acid levels were higher in BD-mania vs BD-depression (P=.002), but not vs BD euthymia. TBARS did not differ between BD-mania and BD-depression. Medication-free BD-mania patients had higher SOD (P=.02) and lower GPX (P<.0001) than HCs. After treatment, BD did not differ from HCs regarding SOD and GPX. Beyond a single biomarker of oxidative stress, the combination of several parameters appears to be more informative for BD in general and taking into account illness polarity. BD is associated with an imbalance in oxidative stress with some phase-specificity for uric acid and TBARS and possible treatment benefits for SOD and GPX. Future studies should take into account confounding factors that can modify oxidative stress status and simultaneously measure oxidative stress markers and antioxidants including different blood sources.

Oxidative stress is the critical marker of neurological complications such as Alzheimer's disease (AD). Apple cider vinegar (ACV) is known to have health benefits due to its antidiabetic, anti-inflammatory, and high antioxidant properties. Therefore, we hypothesized that regular consumption of ACV would protect against AD-like neurological diseases via inhibition of oxidative stress. Authors have compared the efficacy of ACV with that of Chrysin and Rivastigmine in cellular and animal studies. In the cellular study, oxidative stress was induced in Neuro2A cells (1 × 107 ) via H2 O2 (50 μM) treatment. Subsequently, acetylcholinesterase (AChE) activity was performed, and cell viability, SOD, GSH, lipid peroxidation (MDA) levels were measured. Similarly, in the animal study, oxidative stress was introduced in Swiss albino mice (10-11 weeks old, 20-25 g, n=30) via scopolamine (1mg/kg). Subsequently, histopathological experiments were performed; cognitive ability, AChE activity, and SOD, GSH, and MDA levels were measured. The in vitro results indicated that ACV (2μM) provided better protection than Chrysin and Rivstigmine in cell viability. ACV has also performed better in restoring the antioxidants markers (SOD, GSH levels) and reducing MDA and AChE levels. In the in vivo study, test compounds (ACV, Chrysin, and Rivastigmine) improved cognitive impairment, increased the SOD and GSH level, reduced the MDA level and AChE activity, and protected the cortex-hippocampal neurons from degeneration. Here also, ACV (0.7%) showed better neuroprotection than the other two compounds. Therefore, these results supported our hypothesis that moderate consumption of ACV might prove to be beneficial prophylaxis against AD-like neurological diseases.