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Journal ArticleDOI

2.45-GHz microwave irradiation adversely affects reproductive function in male mouse, Mus musculus by inducing oxidative and nitrosative stress

TL;DR: It is observed that MW irradiation induced a significant decrease in sperm count and sperm viability along with the decrease in seminiferous tubule diameter and degeneration of seminiferously tubules, which suggest that chronic exposure to nonionizing MW radiation may lead to infertility via free radical species-mediated pathway.
Abstract: Electromagnetic radiations are reported to produce long-term and short-term biological effects, which are of great concern to human health due to increasing use of devices emitting EMR especially microwave (MW) radiation in our daily life. In view of the unavoidable use of MW emitting devices (microwaves oven, mobile phones, Wi-Fi, etc.) and their harmful effects on biological system, it was thought worthwhile to investigate the long-term effects of low-level MW irradiation on the reproductive function of male Swiss strain mice and its mechanism of action. Twelve-week-old mice were exposed to non-thermal low-level 2.45-GHz MW radiation (CW for 2 h/day for 30 days, power density = 0.029812 mW/cm(2) and SAR = 0.018 W/Kg). Sperm count and sperm viability test were done as well as vital organs were processed to study different stress parameters. Plasma was used for testosterone and testis for 3β HSD assay. Immunohistochemistry of 3β HSD and nitric oxide synthase (i-NOS) was also performed in testis. We observed that MW irradiation induced a significant decrease in sperm count and sperm viability along with the decrease in seminiferous tubule diameter and degeneration of seminiferous tubules. Reduction in testicular 3β HSD activity and plasma testosterone levels was also noted in the exposed group of mice. Increased expression of testicular i-NOS was observed in the MW-irradiated group of mice. Further, these adverse reproductive effects suggest that chronic exposure to nonionizing MW radiation may lead to infertility via free radical species-mediated pathway.
Citations
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Journal ArticleDOI
TL;DR: In this paper, the authors summarized key experimental findings on oxidative stress related to electromagnetic field exposure from animal and cell studies of the last decade and discussed in the context of molecular mechanisms and functionalities relevant to health such as neurological function, genome stability, immune response, and reproduction.
Abstract: Concomitant with the ever-expanding use of electrical appliances and mobile communication systems, public and occupational exposure to electromagnetic fields (EMF) in the extremely-low-frequency and radiofrequency range has become a widely debated environmental risk factor for health. Radiofrequency (RF) EMF and extremely-low-frequency (ELF) MF have been classified as possibly carcinogenic to humans (Group 2B) by the International Agency for Research on Cancer (IARC). The production of reactive oxygen species (ROS), potentially leading to cellular or systemic oxidative stress, was frequently found to be influenced by EMF exposure in animals and cells. In this review, we summarize key experimental findings on oxidative stress related to EMF exposure from animal and cell studies of the last decade. The observations are discussed in the context of molecular mechanisms and functionalities relevant to health such as neurological function, genome stability, immune response, and reproduction. Most animal and many cell studies showed increased oxidative stress caused by RF-EMF and ELF-MF. In order to estimate the risk for human health by manmade exposure, experimental studies in humans and epidemiological studies need to be considered as well.

53 citations

Journal ArticleDOI
TL;DR: Exposure to CW MW radiation leads to oxidative/nitrosative stress induced p53-dependent/independent activation of hippocampal neuronal and nonneuronal apoptosis associated with spatial memory loss, and learning and spatial memory deficit which increases with the increased duration of MW exposure is correlated with a decrease in hippocampal subfield neuronal arborization and dendritic spines.

38 citations


Cites methods from "2.45-GHz microwave irradiation adve..."

  • ...In the first step, after initial deparafinization in xylene and rehydration in graded series of alcohol, slides were incubated with goat- full length p53 antisera (dilution 1:100), rabbit- Bax antisera (dilution 1:100), rabbit- proCaspase-3 antisera (dilution 1:100) and mouse- full length/uncleaved PARP-1 antisera (dilution 1:100) for 24 h in humid chamber respectively (Shahin et al., 2014)....

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  • ...The SAR value was estimated for body length parallel to the electric field, as per actual placement of the mouse (Gandhi et al., 1977; Shahin et al., 2013, 2014)....

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  • ...…alcohol, slides were incubated with goat- full length p53 antisera (dilution 1:100), rabbit- Bax antisera (dilution 1:100), rabbit- proCaspase-3 antisera (dilution 1:100) and mouse- full length/uncleaved PARP-1 antisera (dilution 1:100) for 24 h in humid chamber respectively (Shahin et al., 2014)....

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Journal ArticleDOI
TL;DR: Long term EMR exposure resulted in testicular physiopathology via oxidative damage and inflammation through mitotic activity, and the regenerative reaction increased in seminiferous tubules cells of the testes in EMR+GA group.
Abstract: The aim of this study was to investigate electromagnetic radiation (EMR) transmitted by wireless devices (2.45 GHz), which may cause physiopathological or ultrastructural changes, in the testes of rats. We addressed if the supplemental gallic acid (GA) may reduce these adverse effects. Six-week-old male Sprague Dawley rats were used in this study. Forty eight rats were equally divided into four groups, which were named: Sham, EMR only (EMR, 3 h day-1 for 30 days), EMR + GA (30 mg/kg/daily), and GA (30 mg/kg/daily) groups. Malondialdehyde (MDA) and total oxidant status (TOS) levels increased (p = 0.001 for both) in EMR only group. TOS and oxidative stress index (OSI) levels decreased in GA treated group significantly (p = 0.001 and p = 0.045, respectively). Total antioxidant status (TAS) activities decreased in EMR only group and increased in GA treatment group (p = 0.001 and p = 0.029, respectively). Testosterone and vascular endothelial growth factor (VEGF) levels decreased in EMR only group, but this was not statistically significant. Testosterone and VEGF levels increased in EMR+GA group, compared with EMR only group (p = 0.002), and also increased in GA group compared with the control and EMR only group (p = 0.044 and p = 0.032, respectively). Prostaglandin E2 (PGE2 ) and calcitonin gene releated peptide (CGRP) staining increased in tubules of the testes in EMR only group (p < 0.001 for both) and decreased in tubules of the testes in EMR+GA group (p < 0.001 for all parameters). In EMR only group, most of the tubules contained less spermatozoa, and the spermatozoon counts decreased in tubules of the testes. All these findings and the regenerative reaction, characterized by mitotic activity, increased in seminiferous tubules cells of the testes in EMR+GA group (p < 0.001). Long term EMR exposure resulted in testicular physiopathology via oxidative damage and inflammation. GA may have ameliorative effects on the prepubertal rat testes physiopathology. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1771-1784, 2016.

34 citations


Cites background from "2.45-GHz microwave irradiation adve..."

  • ...Shahin et al. (2014) exposed rats to the nonthermal low-level 2.45 GHz EMR (CW for 2 h day21 during 30 days, power density 0.029812 mW cm22 and SAR 0.018 W kg21), and they observed that EMR irradiation induced a significant decrease in a sperm count and sperm viability, along with the decrease in a…...

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  • ...Shahin et al. (2014) applied 2.45-GHz microwave irradiation for 2 h day21 during 30 days and found a decrease in testosterone levels in the exposed group of mice....

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Journal ArticleDOI
TL;DR: The findings suggest that PTY-2r exerted the nephroprotective potential against STZ induced DN rats via suppressing oxidative stress and apoptosis due to the presence of different bioactive compounds.
Abstract: Oxidative stress and renal apoptosis play a significant role in the progression of diabetic nephropathy. The tubers of Pueraria tuberosa (Roxb. ex Willd.) DC. has been traditionally used as anti-ageing and health promotive tonic. The purpose of this study was to investigate its nephroprotective effect and mechanism via antioxidant and antiapoptotic potential in Streptozotocin-induced diabetic nephropathy (DN) in rats. The chemical composition of aqueous extract of Pueraria tuberosa (PTY-2r) was analyzed by gas chromatography-mass spectrometry (GC-MS). Diabetes was induced by intraperitoneal injection of streptozotocin (STZ) (55 mg/kg body weight) in rats. After 60 days, the rats were randomly divided into 3 groups (n = 6/each group), namely DN control (DN) group-2, DN rats treated with PTY-2r at the dose of 50 mg/100 g, group-3 and 100 mg/100 g, group-4 p.o. for 20 days. The normal rats were chosen as a normal control (NC) group-1. PTY-2r was orally given to the rats for 20 days. Reactive oxygen species (ROS), lipid peroxidation (LPO) and the activity of ROS-scavenging enzymes – superoxide dismutase (SOD), catalase (CAT) & glutathione peroxidase (GPx) were determined in the kidney tissue of DN rats. The expression of apoptosis-related proteins was measured by immunofluorescence. GC-MS analysis of PTY-2r indicated the presence of 37 compounds among them 5-Hydroxymethylfurfural (17.80%), 2,3-dihydro-3,5-dihydroxy-6-methyl-4H-pyran-4-one (17.03%), n-Hexadecanoic acid (5.18%) and 9-Octadecenoic acid (Z) - (6.69%) were found in the higher amount. A significant increase in ROS and LPO was observed along with the decreased activity of antioxidant enzymes, responsible for oxidative stress in the kidney of DN rats. Since, high oxidative stress induces apoptosis in target cells, as shown by significantly decreased expression of Bcl-2 along with increased expression of Bax, active Caspase-3 & cleaved PARP-1 in DN control rats, suggesting apoptosis. The PTY-2r treatment significantly raised the activity of antioxidant enzymes, suppressed oxidative stress and apoptosis thus, prevented urinary albumin excretion in a dose-dependent manner. The findings suggest that PTY-2r exerted the nephroprotective potential against STZ induced DN rats via suppressing oxidative stress and apoptosis due to the presence of different bioactive compounds. ᅟ

33 citations


Additional excerpts

  • ...2000 [27] with slight modification [28]....

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Journal ArticleDOI
TL;DR: 2.45 GHz MW radiation exposure induced local stress suppresses signaling mechanism(s) of hippocampal memory formation in adult male mice, leading to slow learning and significantly increased number of working and reference memory errors in radial maze task.

33 citations


Cites background or methods from "2.45-GHz microwave irradiation adve..."

  • ...The SAR value was estimated for body length parallel to the electric field, as per actual placement of the mouse (Gandhi et al., 1977; Shahin et al., 2013, 2014)....

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  • ...…and other laboratories have demonstrated MW radiation as one of the strongest environmental stressor, responsible for inducing oxidative/nitrosative stress by havoc generation of free radicals (reactive oxygen [ROS]/nitrogen species [RNS]) (Shahin et al., 2013, 2014, 2015; Yakymenko et al., 2016)....

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"2.45-GHz microwave irradiation adve..." refers methods in this paper

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TL;DR: Studies with scavengers of reactive oxygen species revealed that, while reagents directed against singlet oxygen and the hydroxyl radical were without effect, cytochrome C reduced the response to A23187 by about 50%, suggesting that the superoxide anion radical is a major product of the activated human spermatozoon.
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Journal ArticleDOI
TL;DR: It is proposed that mitochondrial ROS is a major determinant of telomere-dependent senescence at the single-cell level that is responsible for cell-to-cell variation in replicative lifespan.
Abstract: Aging is an inherently stochastic process, and its hallmark is heterogeneity between organisms, cell types, and clonal populations, even in identical environments. The replicative lifespan of primary human cells is telomere dependent; however, its heterogeneity is not understood. We show that mitochondrial superoxide production increases with replicative age in human fibroblasts despite an adaptive UCP-2–dependent mitochondrial uncoupling. This mitochondrial dysfunction is accompanied by compromised [Ca2+]i homeostasis and other indicators of a retrograde response in senescent cells. Replicative senescence of human fibroblasts is delayed by mild mitochondrial uncoupling. Uncoupling reduces mitochondrial superoxide generation, slows down telomere shortening, and delays formation of telomeric γ-H2A.X foci. This indicates mitochondrial production of reactive oxygen species (ROS) as one of the causes of replicative senescence. By sorting early senescent (SES) cells from young proliferating fibroblast cultures, we show that SES cells have higher ROS levels, dysfunctional mitochondria, shorter telomeres, and telomeric γ-H2A.X foci. We propose that mitochondrial ROS is a major determinant of telomere-dependent senescence at the single-cell level that is responsible for cell-to-cell variation in replicative lifespan.

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"2.45-GHz microwave irradiation adve..." refers background in this paper

  • ...Free radicals are also implicated in the induction of apoptosis [23] and cellular senescence [24]....

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