Impact of Long-Term RF-EMF on Oxidative Stress and Neuroinflammation in Aging Brains of C57BL/6 Mice

The expansion of mobile phone use has raised questions regarding the possible biological effects of radiofrequency electromagnetic field (RF-EMF) exposure on oxidative stress and brain inflammation. Despite accumulative exposure of humans to radiofrequency electromagnetic fields (RF-EMFs) from mobile phones, their long-term effects on oxidative stress and neuroinflammation in the aging brain have not been studied. In the present study, middle-aged C57BL/6 mice (aged 14 months) were exposed to 1950 MHz electromagnetic fields for 8 months (specific absorption rate (SAR) 5 W/kg, 2 h/day, 5 d/week). Compared with those in the young group, levels of protein (3-nitro-tyrosine) and lipid (4-hydroxy-2-nonenal) oxidative damage markers were significantly increased in the brains of aged mice. In addition, levels of markers for DNA damage (8-hydroxy-2′-deoxyguanosine, p53, p21, γH2AX, and Bax), apoptosis (cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase 1 (PARP-1)), astrocyte (GFAP), and microglia (Iba-1) were significantly elevated in the brains of aged mice. However, long-term RF-EMF exposure did not change the levels of oxidative stress, DNA damage, apoptosis, astrocyte, or microglia markers in the aged mouse brains. Moreover, long-term RF-EMF exposure did not alter locomotor activity in aged mice. Therefore, these findings indicate that long-term exposure to RF-EMF did not influence age-induced oxidative stress or neuroinflammation in C57BL/6 mice.

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Oxidative Stress and NADPH Oxidase: Connecting Electromagnetic Fields, Cation Channels and Biological Effects

International Journal of Molecular Sciences ◽

10.3390/ijms221810041 ◽

2021 ◽

Vol 22 (18) ◽

pp. 10041

Author(s):

Christos D. Georgiou ◽

Lukas H. Margaritis

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Ion Channels ◽

Nadph Oxidase ◽

Electromagnetic Fields ◽

Biological Effects ◽

Cation Channels ◽

Cellular Functions ◽

Voltage Gated ◽

Voltage Gated Ion Channels

Electromagnetic fields (EMFs) disrupt the electrochemical balance of biological membranes, thereby causing abnormal cation movement and deterioration of the function of membrane voltage-gated ion channels. These can trigger an increase of oxidative stress (OS) and the impairment of all cellular functions, including DNA damage and subsequent carcinogenesis. In this review we focus on the main mechanisms of OS generation by EMF-sensitized NADPH oxidase (NOX), the involved OS biochemistry, and the associated key biological effects.

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Biological Effects of Environmental Electromagnetic Fields

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.183-185.532 ◽

2011 ◽

Vol 183-185 ◽

pp. 532-536 ◽

Cited By ~ 3

Author(s):

Gun Li ◽

Xiao Feng Pang

Keyword(s):

Electromagnetic Field ◽

Electromagnetic Fields ◽

Human Body ◽

Geomagnetic Field ◽

Biological Effects ◽

Long Term Effects ◽

Negative Effects ◽

The Past ◽

Theoretical Results

Each of us are exposed to the environmental electromagnetic fields, such as the geomagnetic field, electromagnetic field from power line, and antenna radiation etc. all the time, when the biological tissue exposure in the electromagnetic fields may lead some certain effects, and many effects are studied during the past few years, most of these studies concentrated on negative effects of electromagnetic fields. It is necessary to explore effects of these environmental electromagnetic fields on human body comprehensively, some effects of environmental electromagnetic fields are studied theoretically in the following paper, and attenuate characteristics of several environmental electromagnetic fields propagate in human body is discussed. The theoretical results expressed the penetration depth of several environmental electromagnetic fields, and the possible effects of long term effects are analyzed.

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Mechanisms of aging-induced impairment of endothelium-dependent relaxation: role of tetrahydrobiopterin

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00248.2004 ◽

2004 ◽

Vol 287 (6) ◽

pp. H2448-H2453 ◽

Cited By ~ 69

Author(s):

Katherine A. Blackwell ◽

Joseph P. Sorenson ◽

Darcy M. Richardson ◽

Leslie A. Smith ◽

Osamu Suda ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Anion ◽

Carotid Arteries ◽

Serum Levels ◽

Oxidation Products ◽

Aged Mouse ◽

No Donor ◽

Aged Mice ◽

Vasomotor Function ◽

Endothelium Dependent Relaxation

Oxidative stress has been implicated as an important mechanism of vascular endothelial dysfunction induced by aging. Previous studies suggested that tetrahydrobiopterin (BH4), an essential cofactor of endothelial NO synthase, could be a molecular target for oxidation. We tested the hypothesis that oxidative stress, in particular oxidation of BH4, may contribute to attenuation of endothelium-dependent relaxation in aged mice. Vasomotor function of isolated carotid arteries was studied using a video dimension analyzer. Vascular levels of BH4 and its oxidation products were measured via HPLC. In aged mice (age, 95 ± 2 wk), endothelium-dependent relaxation to ACh (10−5 to 10−9 M) as well as endothelium-independent relaxation to the NO donor diethylammonium ( Z)-1-( N, N-diethylamino)diazen-1-ium -1,2-diolate (DEA-NONOate, 10−5 to 10−9 M) were significantly reduced compared with relaxation detected in young mice (age, 23 ± 0.5 wk). Incubation of aged mouse carotid arteries with the cell-permeable SOD mimetic Mn(III)tetra(4-benzoic acid)porphyrin chloride normalized relaxation to ACh and DEA-NONOate. Furthermore, production of superoxide anion in aorta and serum levels of amyloid P component, which is the murine analog of C-reactive protein, was increased in old mice. In aorta, neither the concentration of BH4 nor the ratio of reduced BH4 to the oxidation products were different between young and aged mice. Our results demonstrate that in mice, aging impairs relaxation mediated by NO most likely by increased formation of superoxide anion. Oxidation of BH4 does not appear to be an important mechanism underlying vasomotor dysfunction in aged mouse arteries.

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Karate Training Improves Metabolic Health in Overweight and Obese Adolescents: A Randomized Clinical Trial

Pediatric Exercise Science ◽

10.1123/pes.2020-0193 ◽

2021 ◽

pp. 1-11

Author(s):

Fabricio de Souza ◽

Luciano Acordi da Silva ◽

Gisele Santinoni Ferreira ◽

Márcia Mendonça Marcos de Souza ◽

Franciane Bobinski ◽

...

Keyword(s):

Oxidative Stress ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Overweight And Obesity ◽

Lipoprotein Cholesterol ◽

Psychological Interventions ◽

Long Term Effects ◽

Low Density Lipoprotein Cholesterol ◽

Stress Markers

Purpose: This study evaluated the effects of 12 weeks of karate training on cardiometabolic parameters, oxidative stress, and inflammation in adolescents with overweight and obesity. Method: Seventy adolescents were randomized into 2 groups: control received nutritional and psychological interventions once a week for 12 weeks, and treatment received nutritional and psychological interventions once a week, plus 3 karate sessions per week, for 12 weeks. The main outcome measure was improvement in cardiometabolic parameters, oxidative stress, and inflammation. Results: After the intervention period, the treatment group showed a reduction in resting heart rate (77.86 [10.89]), high-density lipoprotein cholesterol (40.86 [8.31]), and triglycerides (75.18 [32.29]) and an increase in low-density lipoprotein cholesterol (95.64 [42.53]) in relation to pretraining. Regarding oxidative stress markers, there was a reduction in protein carbonylation (0.07 [0.06]) and nitric oxide (1.39 [1.11]) and an increase in superoxide dismutase (0.68 [0.31]) and glutathione (0.11 [0.08]) compared with pretraining. With respect to inflammation, adiponectin increased (14.54 [5.36]) after the intervention when compared with preintervention. Conclusion: The study concluded that the intervention may improve cardiometabolic parameters, oxidative stress, and inflammation in adolescents with overweight and obesity. Long-term effects need to be evaluated.

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BIOLOGICAL EFFECTS OF 131I AND 125I ISOTOPES OF IODINE IN THE RAT

Journal of Endocrinology ◽

10.1677/joe.0.0710109 ◽

1976 ◽

Vol 71 (1) ◽

pp. 109-114 ◽

Cited By ~ 6

Author(s):

I. DONIACH ◽

D. J. SHALE

Keyword(s):

Thyroid Function ◽

Biological Effects ◽

Female Rats ◽

Long Term Effects ◽

Significant Elevation ◽

Radioiodine Uptake ◽

Male And Female ◽

Male And Female Rats ◽

Serum Tsh

SUMMARY From the differences in radiation profiles between 131I and 125I isotopes of iodine it would be expected that they would show different effects on thyroid function. The differences should lead to lower rates of thyroid gland destruction with 125I and hence less post-irradiation hypothyroidism. This difference in biological effect has been demonstrated in rats by indirect assessment of thyroid function. In this report the long-term effects of a range of similar doses of 131I and 125I were compared, in male and female rats, by direct assessment of thyroid function. Seventeen months after receiving 25 and 125 μCi of 131I, male and female rats showed significant elevation of serum TSH concentration and a reduction in 3 h radioiodine uptake. Rats receiving 1 and 5 μCi of 131I and all doses of 125I showed no significant changes in thyroid function. These findings confirm the previously reported differences in effect between the 131I and 125I isotopes of iodine in the rat.

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Longstanding Eosinophilic Gastroenteritis of More Than 20 Years

Canadian Journal of Gastroenterology ◽

10.1155/2009/565293 ◽

2009 ◽

Vol 23 (9) ◽

pp. 632-634 ◽

Cited By ~ 8

Author(s):

Hugh J Freeman

Keyword(s):

Inflammatory Process ◽

Biological Effects ◽

Eosinophilic Gastroenteritis ◽

Gastric Body ◽

Clinical Relapse ◽

Long Term Effects ◽

Mucosal Folds ◽

Erosive Change ◽

Symptomatic Benefit

Eosinophilic gastroenteritis (EGE) is an eosinophil-predominant inflammatory process that may be detected in endoscopic gastric or intestinal biopsies. The long-term natural history and effects of EGE treatment are not known. A 44-year-old man with abdominal pain was treated with oral ketotifen and followed for more than 20 years. Ketotifen provided symptomatic benefit, with prompt clinical relapse if the drug was discontinued. However, despite the use of ketotifen, the endoscopic abnormalities persisted and appeared to progress. Gastric body and antral mucosal folds appeared thickened, erythematous and friable, with minimal erosive change. Later, even during long asymptomatic periods suggesting clinical ‘remission’, inflammatory polypoid change, previously described in children with EGE, developed with mucosal ‘pock-marking’ and apparent scarring. Ketotifen treatment does not appear to prohibit or reverse the inflammatory process in the gastric mucosa in EGE, although long-term effects of steroids may be avoided. In the future, treatment of EGE may involve monoclonal antibody agents that target the specific biological effects of the eosino-phil, apparently central to this unusual inflammatory process.

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The ATM Cofactor ATMIN Protects against Oxidative Stress and Accumulation of DNA Damage in the Aging Brain

Journal of Biological Chemistry ◽

10.1074/jbc.m110.145896 ◽

2010 ◽

Vol 285 (49) ◽

pp. 38534-38542 ◽

Cited By ~ 33

Author(s):

Nnennaya Kanu ◽

Kay Penicud ◽

Mariya Hristova ◽

Barnaby Wong ◽

Elaine Irvine ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Aging Brain

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Severe but not moderate hyperoxia of newborn mice causes an emphysematous lung phenotype in adulthood without persisting oxidative stress and inflammation

BMC Pulmonary Medicine ◽

10.1186/s12890-019-0993-5 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 2

Author(s):

Anke Kindermann ◽

Leonore Binder ◽

Jan Baier ◽

Beate Gündel ◽

Andreas Simm ◽

...

Keyword(s):

Oxidative Stress ◽

Later Life ◽

Lung Compliance ◽

Elastic Fibers ◽

Newborn Mouse ◽

Long Term Effects ◽

Newborn Mice ◽

Functional Changes ◽

Oxygen Concentrations

Abstract Background Preterm newborns typically require supplemental oxygen but hyperoxic conditions also damage the premature lung. Oxygen-induced lung damages are mainly studied in newborn mouse models using oxygen concentrations above 75% and looking at short-term effects. Therefore, we aimed at the investigation of long-term effects and their dependency on different oxygen concentrations. Methods Newborn mice were exposed to moderate vs. severe hyperoxic air conditions (50 vs. 75% O2) for 14 days followed by a longer period of normoxic conditions. Lung-related parameters were collected at an age of 60 or 120 days. Results Severe hyperoxia caused lower alveolar density, enlargement of parenchymal air spaces and fragmented elastic fibers as well as higher lung compliance with peak airflow limitations and higher sensitivity to ventilation-mediated damages in later life. However, these long-term lung structural and functional changes did not restrict the voluntary physical activity. Also, they were not accompanied by ongoing inflammatory processes, increased formation of reactive oxygen species (ROS) or altered expressions of antioxidant enzymes (superoxide dismutases, catalase) and lung elasticity-relevant proteins (elastin, pro-surfactant proteins) in adulthood. In contrast to severe hyperoxia, moderate hyperoxia was less lung damaging but also not free of long-term effects (higher lung compliance without peak airflow limitations, increased ROS formation). Conclusions Severe but not moderate neonatal hyperoxia causes emphysematous lungs without persisting oxidative stress and inflammation in adulthood. As the existing fragmentation of the elastic fibers seems to play a pivotal role, it indicates the usefulness of elastin-protecting compounds in the reduction of long-term oxygen-related lung damages.

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