900 MHz pulse-modulated radiofrequency radiation induces oxidative stress on heart, lung, testis and liver tissue

Article (PDF Available)inGeneral Physiology and Biophysics 30(1):84-9 · March 2011with 1,025 Reads 
How we measure 'reads'
A 'read' is counted each time someone views a publication summary (such as the title, abstract, and list of authors), clicks on a figure, or views or downloads the full-text. Learn more
DOI: 10.4149/gpb_2011_01_84 · Source: PubMed
Cite this publication
Abstract
Oxidative stress may affect many cellular and physiological processes including gene expression, cell growth, and cell death. In the recent study, we aimed to investigate whether 900 MHz pulse-modulated radiofrequency (RF) fields induce oxidative damage on lung, heart and liver tissues. We assessed oxidative damage by investigating lipid peroxidation (malondialdehyde, MDA), nitric oxide (NOx) and glutathione (GSH) levels which are the indicators of tissue toxicity. A total of 30 male Wistar albino rats were used in this study. Rats were divided randomly into three groups; control group (n = 10), sham group (device off, n = 10) and 900 MHz pulsed-modulated RF radiation group (n = 10). The RF rats were exposed to 900 MHz pulsed modulated RF radiation at a specific absorption rate (SAR) level of 1.20 W/kg 20 min/day for three weeks. MDA and NOx levels were increased significantly in liver, lung, testis and heart tissues of the exposed group compared to sham and control groups (p < 0.05). Conversely GSH levels were significantly lower in exposed rat tissues (p < 0.05). No significantly difference was observed between sham and control groups. Results of our study showed that pulse-modulated RF radiation causes oxidative injury in liver, lung, testis and heart tissues mediated by lipid peroxidation, increased level of NOx and suppression of antioxidant defense mechanism.
Advertisement
84
900 MHz pulse-modulated radiofrequency radiation induces oxidative
stress on heart, lung, testis and liver tissues
Meric A. Esmekaya1, Cigdem Ozer2 and Nesrin Seyhan1
1 Department of Biophysics, Gazi University, Faculty of Medicine Gazi Non-ionizing Radiation Protection (GNRP) Center,
Ankara, Turkey
2 Department of Physiology, Gazi University, Faculty of Medicine, Ankara, Turkey
Abstract. Oxidative stress may affect many cellular and physiological processes including gene ex-
pression, cell growth, and cell death. In the recent study, we aimed to investigate whether 900 MHz
pulse-modulated radiofrequency (RF) fields induce oxidative damage on lung, heart andliver tissues.
We assessed oxidative damage by investigating lipid peroxidation (malondialdehyde, MDA), nitric
oxide (NOx) and glutathione (GSH) levels which are the indicators of tissue toxicity. A total of 30
male Wistar albino rats were used in this study. Rats were divided randomly into three groups; control
group (n = 10), sham group (device off, n = 10) and 900 MHz pulsed-modulated RF radiation group
(n = 10). e RF rats were exposed to 900 MHz pulsed modulated RF radiation at a specific absorp-
tion rate (SAR) level of 1.20 W/kg 20 min/day for three weeks. MDA and NOx levels were increased
significantly in liver, lung, testis and heart tissues of the exposed group compared to sham and control
groups (p < 0.05). Conversely GSH levels were significantlylower inexposed rat tissues (p < 0.05). No
significantly difference was observed between sham and control groups. Results of our study showed
that pulse-modulated RF radiation causes oxidative injury in liver, lung, testis and heart tissues mediated
by lipid peroxidation, increased level of NOx and suppression of antioxidant defense mechanism.
Key words: Radiofrequency radiation — Oxidative stress — Malondialdehyde — Glutathione
— Nitric oxide
Abbreviations: GSH, gluthatione; MDA, malondialdehyde; RF, radiofrequency; ROS, reactive
oxygen species.
Correspondence to: Meric Arda Esmekaya, Department of Biophys-
ics, Gazi University, Faculty of Medicine, 06510 Beşevler, Ankara,
Turkey
E-mail: mericarda@yahoo.com
Introduction
Oxidants can be generated in numerous exogenous ways
such as chemicals and radiation exposure through redox-
catalysis and encompass reactive oxygen species (ROS),
reactive nitrogen species (RNS), sulfur-centered radicals and
various others (Abuja and Albertini 2001). Lipid peroxidation
is the deleterious consequence of oxidative damage which
involves hydrogen abstraction from fatty acids by free radi-
cals. Malondialdehyde (MDA), the end product of the lipid
peroxidation is a highly reactive three carbon dialdehyde and
one of the most intensively aldehydes formed during lipid per-
oxidation. RNS, such as nitric oxide (NO), a free radical and
peroxynitrite (ONOO) that is an extremely potent cellular
oxidant produced with the reaction of NO with superoxide
(O2•–) act together with other ROS to damage cells, causing
nitrosative stress (Squadrito and Pryor 1998). In a healthy
human body, the generation of pro-oxidants in the form of
ROS and RNS are effectively kept in balance by the various
levels of antioxidant defense (Devasagayam et al. 2004).
However, when it gets exposed to adverse environmental
agents, this delicately maintained balance is shied in favor
of pro-oxidants resulting in oxidative stress. Sub-lethal levels
of oxidative stress may activate and inactivate transcription
factors, membrane channels, and metabolic enzymes and
promote calcium-dependent and phosphorylation signaling
pathways (Winterbourn and Hampton 2008).
Scientists have been conducting experimental studies on
whether radiofrequency (RF) radiation emitted from cellular
Gen. Physiol. Biophys. (2011), 30, 84–89
doi:10.4149/gpb_2011_01_84
85
Fluvastatin and cholestatic liver injury
mobile phones induces oxidative stress on biological tissues
or cells and others developed theoretical explanations how
these fields couldimpairfree radicalre-combinations (WHO
2006 Geneva). Moreover, some authors suggested that
mechanism of RF/MW (microwave) radiation damage may
be attributable to the induction of oxidative stress leading to
free radical generation and radical scavengers’ alterations in
biological tissues or cells as a result of the interaction of the
tissues or cells with RF/MW fields (Cleary et al.1996; Diem
et al. 2005). According to the current assumption electro-
magnetic (EM) fieldsmay initiate oxygen- and nitrogen-free
radical intermediates and several types of tissue injury may
be associated with oxidative stress process induced by these
fields. EM fields may affect biological cells by interacting
electrons during redox reactions (Blank 2008).
Although some authors pointed out the possibility that
RF radiation could affect the concentration of free radicals
through the radical pair recombination thus increase the
oxidant stress on cells or tissues, studies on some specific
tissues are very limited. So we aimed to investigate whether
low intensity 900 MHz-modulated RF radiation induces
oxidative damage on lung, heart, liver and testis tissues by as-
sessing the levels of lipid peroxidation and glutathione (GSH)
on these tissues. We also measured total NO (NOx) levels to
determine biochemical damage in tissues as an additional
parameter to lipid peroxidation and antioxidant level.
Materials and Methods
Animals and treatments
Two months old male Wistar albino rats were used in this
study. e animals were acclimatized in the temperature-
controlled conditions (22 ± 1°C) and humidity (50 ± 10%)
with light/dark cycles of 12 h and had free access to food and
drinking water. None of the animals died during the experi-
ment. Rats were divided randomly into three groups; group I:
control group (n = 10), group II: sham group (n = 10) and
group III: RF radiation group (n = 10). e RF rats were
exposed to 900 MHz pulsed-modulated RF radiation 20
min/day for three weeks. e sham rats were settled in the
exposure cage and applied the same experimental procedure
of the exposed group rats, but the exposure device was off.
Sham- and RF-exposed animals were kept in the same condi-
tions as the control ones when sham and RF exposures were
not performed. At the end of the last day of the exposure,
rats were sacrificed by injection of ketamine (50 mg/kg)
and xylazine (5 mg/kg) combination. e investigation was
performed following European Community guidelines and
approval by the ethics committee of Gazi University Faculty
of Medicine.
Radiofrequency radiation exposure system
A rectangular horn antenna (Ets-Lindgren, St. Louis, MO,
USA) was used as a transmitting antenna which generates
RF signals inside polymethyl methacrylate plastics cages
(15 cm × 20 cm × 20 cm) where the rats were restrained.
Antenna was fed by a properly selected RF power generator
(Agilent Technologies, Santa Clara, CA, USA) that delivers
900 MHz carrier RF waves and connected to a power ampli-
fier (Hittite, Chelmsford, MA, USA) which amplifies the RF
signals. e signals were pulse-modulated by rectangular
pulses (repetition frequency 217 Hz, pulse width 0.576 ms)
by using a function generator (andar, Cambridgeshire,
UK). Cages were placed symmetrically along the axis that is
perpendicular to the antenna (Fig. 1) and constantly venti-
Figure 1. Schematic diagram of the RF exposure system.
86 Lotková et al.
lated to eliminate the external stress and avoid the possibility
of any temperature increase inside them.
e applied electric field was measured by using an elec-
tric field isotropicprobe along thehorn antennas axis.At the
beginning of exposure, average power density was observed
at a reference point which was the midpoint of the bottom of
the cage wall facing horn the antenna. emaximum power
density was on the axis of the antenna and it was observed
that the power density was decreased uniformly with the
distance from the antennas axis. Whole body specific absorp-
tion rate (SAR) was approximately calculated according to
the formulary of SAR = σ/ρ·|ERMS|2 (W/kg). Where σ is the
mean electrical conductivity of the whole body (S/m), ρ is
the mass density (kg/m3) and ERMS is the root mean square
value of the electric field (V/m). e whole body average
SAR was calculated to be 1.20 W/kg.
Measurement of tissue lipid peroxidation and GSH levels
Tissue samples were obtained aer measuring lesion areas
and frozen immediately by liquid nitrogen then kept in
–70°C deep-freeze until the assay. Lipid peroxidation was
quantified by measuring the formation of thiobarbituric
acid reactive substances (TBARS). Samples were homog-
enized in ice-cold trichloroacetic acid (1 g tissue in 10 ml
10% trichloroacetic acid) in a tissue homogenizer (Hei-
deloph Diax 900, Germany). Following centrifugation of
the homogenate at 3000 × g for 10 min (Hermle Z 323 K,
Germany), 750 µl of supernatant was added to an equal
volume of 0.67% (m/v) thiobarbituric acid and heated
at 100°C for 15 min. e absorbance of the samples was
measured at 535 nm. Lipid peroxide levels are expressed in
terms of MDA equivalents using an extinction coefficient
of 1.56 × 105 l·mol–1·cm–1.
e GSH levels were determined by Ellman method with
some modifications. Briefly, aer centrifugation of the ho-
mogenates at 3 000 × g for 10 min, 0.5 ml of supernatant was
added to 2 ml of 0.3 M Na2HPO4·2 H2O solution. A 0.2 ml
solution of dithiobisnitrobenzoate (0.4 mg/ml 1% sodium
citrate) was added and aer mixing, the absorbance at 412
nm was measured using a spectrophotometer (UV 1208,
Shimadsu, Japan) at room temperature immediately. e
GSH levels were calculated using an extinction coefficient
of 13 600 l·mol–1·cm–1.
Determination of NOx (Griess assay)
NOx levels were obtained from Elisa reader by vanadium
chloride (VCl3)/Griess assay. Before NOx determination, tis-
sues were homogenized in five volumes of phosphate buffer
saline (pH = 7) and centrifuged at 2000 × g for 5 min. Aer
centrifugation, 0.25 ml of 0.3 M NaOH was added to 0.5 ml
supernatant. e incubationof the samples for5 minatroom
temperature was followed by addition of 0.25 ml of 5% (w/v)
ZnSO4 for deproteinization. is mixture was then centri-
fuged at 3000 × g for 20 min and supernatants were used for
the assays. Nitrate standard solution was serially diluted and
the plates were loaded with samples (100 μl). en Vanadium
III chloride (VCl3) (100 μl) and Griess reagents sulphanila-
mide (SULF) (50 μl) and N-(1-naphthyl) ethylenediamine
dihydrochloride (NEDD) (50 μl) were added to each well.
Aer incubation in 37°C for 45 min, samples were measured
at 540 nm using ELISA reader (Miranda et al. 2001).
Statistical Analysis
All data were presented as mean values ± SD. Differences
among three groups were analyzed by one way analysis of
variance (ANOVA). Mann-Whitney U test was used for
pairwise comparisons among groups. e accepted level
of significance was set at p < 0.05. Data were analyzed with
statistical package (SPSS) version 13.0.
Results
e MDA levels of heart, liver and lung tissues
Tissue MDA level of liver (Table 1) and lung (Table 2) tissues
was significantly higher (p < 0.001) in RF-exposed group
in comparison with sham and control tissues. A significant
increase was observed also in heart MDA level of RF-exposed
rats compared to sham and control rats (p < 0.05) (Table 3).
e most dramatic increase in the MDA level of the tissues
was observed in testis tissue. MDA level of testis was mar-
ginally higher in RF exposed group than sham and control
groups (p < 0.001) (Table 4). No significant difference was
observed in terms of tissue MDA level between sham and
control groups in each tissue.
NOx levels in heart, liver and lung tissues
Liver NOx level was significantly higher in RF-exposed
group than sham and control groups (p < 0.001) (Table 1).
e level of NOx increased significantlyin RF-exposed lung
Table 1. Mean liver tissue levels of MDA, total NO and GSH in
control, sham and RF-exposed groups
Group MDA (nmol/g) NOx (µmol/g) GSH (nmol/g)
control 9.02 ± 1.1 12.44 ± 1.96 3.36 ± 0.45
sham 9.31 ± 0.91 11.35 ± 1.42 3.14 ± 0.31
RF-exposed* 14.78 ± 1.2 16.00 ± 2.99 2.09 ± 0.26
e values are means ± SD; n = 10. * p < 0.01, RF-exposed vs.
control or sham groups.
87
tissues (p < 0.01) (Table 2). NOx level of heart increased in
RF-exposed group compared to sham and control groups
(p < 0.001) (Table 3). Tissue level of NOx was quite high
in RF-exposed testis tissues (p < 0.001) (Table 4). No sta-
tistically difference was seen between sham and control
groups.
e GSH levels of heart, liver and lung tissues
GSH level of liver decreased following to RF exposure in
exposed group compared to sham and control groups (p <
0.001) (Table 1). Lung GSH level reduced significantly in
RF-exposed group (p < 0.01) (Table 2). A significant decrease
in GSH level of heart was observed in RF-exposed group
in comparison with sham and control groups (p < 0.001)
(Table 3). Exposure to RF radiation reduced GSH level of
testis tissues about 50% compared to those of sham and
control groups (p < 0.001) (Table 4). ere was no statisti-
cally significant difference in GSH levels between shamand
control groups.
Discussion
Increasing evidence has indicated that RF radiation has the
potential of inducing oxidative stress in biological systems
via free radicals by enhancing lipid peroxidation and re-
ducing antioxidant levels. In the recent study, we showed
that chronic exposure to 900 MHz pulse-modulated RF
radiation can cause lipid peroxidation, nitrogenic stress and
antioxidant suppression in various tissues. MDA levels of
liver, heart, lung and testis tissues increased significantly in
RF group compared to sham and control groups. Similarly
tissue NOx levels were significantly higher in RF-exposed
tissues. However, GSH levels showed significant reduction
in exposed tissues. e results of our study verified the hy-
pothesis that RF radiation may cause oxidative damage in
biological tissues. Moreover, we observed that the magnitude
of the damage depended on type of the tissue.
e change in MDA and GSH levels in exposed rats
reflected pathophysiological effects of pulse modulated RF
fields on liver tissue. Oxidative stress may accelerate the
peroxidation reactions of lipids in liver (Yasa et al. 1999). It
has been reported that patients diagnosed with degenerative
liver diseases have higher level of lipoperoxide in their liver
tissues and several forms of liver diseases have been shown
to be associated with oxidative tissue injury (Suematsu et al.
1981). Dasdag et al. (2008) reported increased levels of MDA
and of the total oxidant status in liver tissue of the Wistar
albino rats exposed to 900 MHz RF radiation. However,
they found no significant endpoints in terms of catalase,
myeloperoxidase, total antioxidant capacity levels. Koyu et
al. (2005) investigated the effects of MW radiation on the
liver oxidant/antioxidant system, and the possible protective
effects of caffeic acid phenethyl ester (CAPE) on liver tissue.
ey observed increased level of lipid peroxidation and
decreased activity of GSH-Px in the liver tissue of the 1800
MHz RF radiation exposed rats. Moreover the authors noted
that CAPE prevented the oxidative injury in liver tissue due
to RF radiation exposure. e significant increase in lipid
peroxidation level in exposed rat liver tissues may be due to
increase of NOx level in the recent study. Overproduction
of NO is one of the most important sources of oxidative
damage in liver (Beckman et al. 1990). e reaction of NO
with O2•– can produce the ONOO which can cause lipid
peroxidation.
e results of our study also showed that the levels of
MDA and NOx may be increased in heart tissue due to RF ra-
diation exposure. ese indicate thatRF radiation mayact as
a stressor on heart tissue as well. Our results were consistent
with those of Ozgüner et al. (2005), who observed increased
level of NO and MDA in rat myocardial tissue as a result of
the exposure to 900 MHz RF radiation. NO is a major intra-
Table 2. Mean lung tissue levels of MDA, total NO and GSH in
control, sham and RF-exposed groups
Group MDA (nmol/g) NOx (µmol/g) GSH (nmol/g)
control 10.95 ± 2.56 16.21 ± 1.63 3.24 ± 0.27
sham 11.45 ± 2.16 15.23 ± 1.56 3.22 ± 0.34
RF-exposed* 23.62 ± 4.14 19.97 ± 2.71 2.99 ± 0.25
e values are means ± SD; n = 10. * p < 0.01, RF-exposed vs.
control or sham groups.
Table 3. Mean heart tissue levels of MDA, total NO and GSH in
control, sham and RF-exposed groups
Group MDA (nmol/g) NOx (µmol/g) GSH (nmol/g)
control 6.07 ± 1.11 7.83 ± 1.39 1.84 ± 0.1
sham 5.93 ± 0.86 6.96 ± 1.37 1.72 ± 0.29
RF-exposed* 7.3 ± 0.93 13.09 ± 2.6 1.01 ± 0.11
e values are means ± SD; n = 10. * p < 0.01, RF-exposed vs.
control or sham groups.
Table 4. Mean testis tissue levels of MDA, total NO and GSH in
control, sham and RF-exposed groups
Group MDA (nmol/g) NOx (µmol/g) GSH (nmol/g)
control 6.48 ± 0.93 9.92 ± 1.72 4.1 ± 0.37
sham 6.49 ± 0.92 11.87 ± 2.07 4.14 ± 0.42
RF-exposed* 15.11 ± 1.37 32.99 ± 3.83 2.25 ± 0.39
e values are means ± SD; n = 10. * p < 0.01, RF-exposed vs.
control or sham groups.
88 Esmekaya et al.
cellular messenger synthesized by NO synthetase in vascular
endothelium and converted into more stable forms nitrite
(NO2) and nitrate (NO3) in plasma. It mediates a variety
of biological functions including cardiovascular homeostasis,
yet overproduction of NO has been implicated as a cytotoxic
factor in a variety of pathophysiological processes. Olsen
et al. (1977) observed bradycardia in isolated and perfused
rat hearts that were maintained in 20°C and exposed to 960
MHz continuous MW radiation.
Lung is a major ROS production organ having a large
surface that is constantly in contact with pollutants. is
makes lung to need a strong antioxidant defense system
to protect it against oxidative/nitrosative stressors. e
oxidant/antioxidant imbalance in lung may activate redox-
sensitive transcription factors which regulate the protective
antioxidant genes. GSH is a major extracellular protective
antioxidant against oxidative/nitrosative stresses, which plays
a key role in the control of pro-inflammatory processes in
the lung. e decrease GSH levelin the lungof exposed rats
showed that this protective mechanism was reduced due to
RF radiation exposure. e low level of GSH in lung tissues
of the RF-exposed rats may be associated with increase of
the production of lipid peroxidation and NO. It is known
that increased level of ROS can alter the GSH redox state.
Moreover, increased level of lipid peroxidation impairs mem-
brane function and inactivates membrane-bound receptors
and enzymes that result in increase in the tissue permeability
which has been implicated in the pathogenesis inflammatory
lung disorders (Rahman and MacNee 2000).
e most dramatic increase in lipid peroxidation and
decrease in antioxidant levels of the RF-exposed rats were
observed in testis tissue. e obtained results indicated that
900 MHz pulse-modulated RF radiation exposure is quite
detrimental on testis tissue and RF fields induce an unbalance
between production and the neutralization of prooxidant and
antioxidant processes and cause oxidative damage in testis.
Similar to our study, Mailankot et al. (2009) demonstrated
increased lipid peroxidation and reduced GSH content in the
testis and epididymis of 10–12 weeks old male Wistar rats
exposed to GSM mobile phone radiation 1 h/day for 28 days.
ey also observed reduced percentage of motile sperm. De
Iuliis et al. (2009) found increased level of ROS and higher
DNA damage due to RF radiation exposure. Agarwal et al.
(2009) reported significant increasein ROSlevel andsignifi-
cant decrease in ROS-TAC score in unprocessed ejaculated
human semen which were taken from each patient that were
exposed to cellular phone radiation for 1 h.
Due to rich polyunsaturated fatty acid content human
spermatozoa plasma membranes are highly sensitive to ROS-
induced damage. It is considered that lipid peroxidation is the
key factor in ROS-induced sperm damage leading to decrease
in sperm count, loss of motility, abnormal morphology and
reduced capacity of sperm oocyte penetration and infertility
(Sikka 1996; Storey 1997). ere is strong clinical evidence
that men diagnosed with infertility have significantlyhigher
levels of ROS (Pasqualotto et al. 2000). Some of the reports
have suggested a possible linkage between mobile phone
usage and male infertility (Baste et al. 2008). Decreased
sperm count and capacity of quails were reported by McRee
et al. (1983) as a result of MW exposure. Cleary et al. (1996)
showed that RF radiation may reduce fertilizing capacity of
spermatozoa. Agarwal et al. (2009) suggested that RF EMR-
induced oxidative stress in semen may be responsible for
decreased sperm motility and viability.
We observed an enormous increase in the level of NOx in
testis tissue due to pulse-modulated RF radiation exposure
for 21 days. Tissue level of NOx was marginally higher in
RF-exposed testis tissues (32.99 µmol/g) than sham (11.87
µmol/g) and control tissues (9.92 µmol/g). Although
a continent amount of NO in seminal plasma is essential for
normal reproductive function and sperm motility, at supra
physiological levels it may lead to testicular abnormalities by
inhibiting sperm production and motility (Rosselli et al. 1995;
Donnelly et al. 1997; Balercia et al. 2004) through formation of
ONOO (Kisa et al. 2004). Human studies showed that infer-
tile males have higher concentration of NO in seminal plasma
than the healthy males (Nobunago et al. 1996). Furthermore,
high amount of NO in seminal plasma is an important factor
in sperm DNA damage (Saleh et al. 2002).
In the recent study, we showed that 900 MHz pulse-modu-
lated RF radiation is capable of inducing oxidative stress. is
induction was mediated by increase of lipid peroxidation and
the reduction of GSH. e study also gave evidence that RF
radiation might enhance NO production. e results of our
study are evident that pulse-modulated RF emissions may act
as an environmental stressor and cause oxidative and nitro-
genic damage in lung, liver, testis and heart tissues. Oxidative
stress is known to underlie many human diseases including
atherosclerosis, heart failure, myocardial infarction, chronic
liver and lung diseases, infertility, etc. Our results suggested
that mobile phone use should be limited.
References
Abuja P. M., Albertini R. (2001): Methods for monitoring oxidative
stress, lipid peroxidation and oxidation resistance of lipopro-
teins. Clin. Chim. Acta. 306, 1–17
doi:10.1016/S0009-8981(01)00393-X
Agarwal A., Desai N. R., Makker K., Varghese A., Mouradi R., Sabanegh
E., Sharma R. (2009): Effects of radiofrequency electromagnetic
waves (RF-EMW) from cellular phones on human ejaculatedse-
men: an in vitro pilot study. Fertil. Steril. 92, 1318–1325
doi:10.1016/j.fertnstert.2008.08.022
Balercia G., Moretti S., Viynini A., Mayaynini M., Mantero F.,
Boscaro M. (2004): Role of nitric oxide concentrations on hu-
man sperm motility. J. Androl. 25, 245–249
89
Radiofrequency radiation induces oxidative stress
Baste V., Riise T., Moen B. (2008): Radiofrequency electromagnetic
fields; male infertility and sex ratio of offspring. Eur. J. Epide-
miol. 23, 369–377
doi:10.1007/s10654-008-9236-4
Beckman J. S., Beckman T. W., Chen J. (1990): Apparent hydroxyl
radical production by peroxynitrite: implications for endothe-
lial injury from nitric oxide and superoxide. Proc. Natl. Acad.
Sci. 87, 1620–1624
doi:10.1073/pnas.87.4.1620
Blank M. (2008): Protein and DNA reactions stimulated by electro-
magnetic fields. Electromagn. Biol. Med. 27, 3–23
doi:10.1080/15368370701878820
Cleary S. F., Du Z., Cao G., Liu L. M., McCrady C. (1996): Effect
of isothermal radiofrequency radiation on cytolytic T lym-
phocytes. FASEB J. 10, 913–919
Dasdag S., Bilgin H. M., Akdag M. Z., Celik H., Aksen F. (2008):
Effect of long term mobile phone exposure on oxidative-
antioxidative processes and nitric oxide in rats. Biotechnol. &
Biotechnol. 22, 992–997
De Iuliis G. N., Newey R. J., King B. V., Aitken R. J. (2009): Mobile phone
radiation induces reactive oxygen species production and DNA
damage in human spermatozoa in vitro. PLoS One 4, 6446
doi:10.1371/journal.pone.0006446
Devasagayam T. P., Tilak J. C., Boloor K. K., Sane K. S., Lele R.
D., Ghaskadbi, R. D. (2004): Free radicals and antioxidants in
human health: Current status and future prospects. J. Assoc.
Physicians India 52, 794–804
Diem E., Schwarz C., Adlkofer F., Jahn O., Rudiger H. (2005):
Non-thermal DNA breakage by mobile-phone radiation (1800
MHz) in human fibroblasts and in transformed GFSH-R17rat
granulosa cells in vitro. Mutat. Res. 583, 178–183
Donnelly E., Lewis S. H., Tompson W., Chakaravarty U. (1997): Sperm
nitric oxide and motility: the effectsofnitric oxidesynthase stimu-
lation and inhibition. Mol. Hum. Reprod. 3, 755–762
doi:10.1093/molehr/3.9.755
Kisa U., Basar M. M., Ferhat M., Yilmaz E., Basar, H (2004): Testicu-
lar tissue nitric oxide and thiobarbituric acid reactive substance
levels: evaluation with respect to the pathogenesis of varicocele
Urol. Res. 32, 196–199
doi:10.1007/s00240-004-0401-2
Koyu A., Naziroglu M., Özgüner F. (2005): Caffeic acid phenethyl
ester modulates 1800 MHz microwave-induced oxidative stress
in rat liver. Electromagn. Biol. Med. 24, 135–142
doi:10.1080/15368370500253787
Mailankot M., Kunnath A. P., Jayalekshmi H., Koduru B., Valsalan
R. (2009): Radio frequency electromagnetic radiation (RF-EMR)
from GSM (0.9/1.8GHz) mobile phones induces oxidative stress
and reduces sperm motility in rats. Clinics 64, 561–565
doi:10.1590/S1807-59322009000600011
McRee D. I., oxton J. P., Parkhurst C. R. (1983): Reproduction
in male Japanese quail exposed to microwave radiation during
embryogeny. Radiat. Res. 96, 51–58
doi:10.2307/3576163
Miranda K. M., Espey M. G., Wink D. A. (2001): A rapid, simple
spectrophotometric method for simultaneous detection of
nitrate and nitrite. Nitric Oxide 5, 62–71
doi:10.1006/niox.2000.0319
Nobunago T., Tokugawa Y., Hashimoto K., Kubota Y., Sawai K.
(1996): Elevated nitric oxide concentration in the seminal
plasma of infertile males: nitric oxide inhibits sperm motility.
Am. J. Reprod. Immunol. 36, 193–197
Olsen R. G., Lords J. L., Durney C. H. (1977): Microwave-induced
chronotropic effects in the isolated rat heart. Ann. Biomed.
Eng. 5, 395–409
doi:10.1007/BF02367318
Ozguner F., Altinbas A., Ozaydin M., Dogan A., Vural H., Kisioglu
A. N., Cesur G., Yildirim N. G. (2005): Mobile phone-induced
myocardial oxidative stress: protection by a novel antioxidant
agent caffeic acid phenethyl ester. Toxicol. Ind. Health 21,
223–230
doi:10.1191/0748233705th228oa
Pasqualotto F. F., Sharm R. K., Nelson D. R., omas A.J., Agarwal
A. (2000): Relationship between oxidative stress, semen char-
acteristics, and clinical diagnosis in men undergoing infertility
investigation. Fertil. Steril. 73, 459–464
doi:10.1016/S0015-0282(99)00567-1
Rahman I., MacNee W. (2000): Oxidative stress and regulation of
glutathione in lung inflammation. Eur Respir. J. 16, 534–554
doi:10.1034/j.1399-3003.2000.016003534.x
Rosselli M., Dubey R. K., Imthurn B., Macas E., Keller P. J. (1995):
Effects of nitric oxide on human spermatozoa: evidence that
nitric oxide decreases sperm motility and induces sperm toxic-
ity. Hum. Reprod. 10, 1786–1790
Saleh R. A., Agarwal A., Nelson D. R., Nada E. A., El-Tonsy M.
H., Alvarez J. G., omas A. J., Sharma R. (2002): Increased
sperm nuclear DNA damage in normozoospermic infertile
men: a prospective study. Fertil. Steril. 78, 313–318
doi:10.1016/S0015-0282(02)03219-3
Sikka S. C. (1996): Oxidative stress and role of antioxidants in nor-
mal and abnormal sperm function. Front. Biosci. 1, 78–86
Storey B. T. (1997): Biochemistry of the induction and prevention
of lipoperoxidative damage in human spermatozoa. Mol. Hum.
Reprod. 3, 203–213
doi:10.1093/molehr/3.3.203
Suematsu T., Matsumura T., Sato N., Miyamoto T., Ooka T., Kamada
T., Abe H. (1981): Lipid peroxidation in alcoholic liver disease
in humans. Alcohol. Clin. Exp. Res. 5, 427–430
doi:10.1111/j.1530-0277.1981.tb04926.x
Squadrito G. L., Pryor W. A. (1998): Oxidative chemistry of nitric
oxide: the roles of superoxide, peroxynitrite, and carbon diox-
ide. Free Radic. Biol. Med. 25, 392–403
doi:10.1016/S0891-5849(98)00095-1
Winterbourn C. C., Hampton M. B. (2008): iol chemistry
and specificity in redox signaling. Free Radic. Biol. Med. 45,
549–561
doi:10.1016/j.freeradbiomed.2008.05.004
World Health Organization. (2006): WHO research agenda for
radio frequency fields. Geneva, pp. 1–10
Yasa M. H., Kacmaz M., Ozturk H. S., Durak I. (1999): Antioxidant
status of erythrocytes from patients with cirrhosis. Hepatogas-
troenterology 46, 2460–2463
Received: March 24, 2010
Final version accepted: September 14, 2010

Supplementary resource

  • ... This is no longer the case. The basic low-grade inflammation and oxidative/nitrosative stress-related states we showed in EHS patients [10,11,22] are remarkable since they confirm the detrimental health effects of (1) non-thermal or weak thermal non-ionizing radiation, which were proven experimentally in animals [37][38][39] and in humans [11] exposed to different environmental stressors including ELF and RF EMFs, and (2) multiple man-made environmental chemicals [40][41][42], especially in the brain [43,44]. Figure 6 summarizes the different steps of the model we have so far been able to construct from the presently available published data, including our own. ...
    ... Hence, on this basis, and because of the experimental evidence provided by studies in animals [37][38][39]43,44] and in humans [11,14,23,24] have shown the detrimental impact of EMF on health we believe, there is presently no sufficiently robust scientific data to refute a role of EMF exposure in inducing the previously described clinical symptoms and biological alterations in EHS patients. ...
    ... Here too, such observations certainly dismiss the hypothesis of a nocebo effect as the initial cause of EHS. In fact, the inflammation and oxidative/nitrosative states we showed in EHS patient are remarkable since they confirm the data obtained experimentally in animals exposed to these two types of non-ionizing frequencies [37][38][39], especially in the brain [43,44]. Furthermore, the limbic system-associated capsulo-thalamic abnormalities that we showed to characterize these patients [12,33] may likely correspond to the hippocampal neuronal alterations caused by EMF exposure in rats [51][52][53]. ...
    Article
    Full-text available
    Since 2009, we built up a database which presently includes more than 2000 electrohypersensitivity (EHS) and/or multiple chemical sensitivity (MCS) self-reported cases. This database shows that EHS is associated in 30% of the cases with MCS, and that MCS precedes the occurrence of EHS in 37% of these EHS/MCS-associated cases. EHS and MCS can be characterized clinically by a similar symptomatic picture, and biologically by low-grade inflammation and an autoimmune response involving autoantibodies against O-myelin. Moreover, 80% of the patients with EHS present with one, two, or three detectable oxidative stress biomarkers in their peripheral blood, meaning that overall these patients present with a true objective somatic disorder. Moreover, by using ultrasonic cerebral tomosphygmography and transcranial Doppler ultrasonography, we showed that cases have a defect in the middle cerebral artery hemodynamics, and we localized a tissue pulsometric index deficiency in the capsulo-thalamic area of the temporal lobes, suggesting the involvement of the limbic system and the thalamus. Altogether, these data strongly suggest that EHS is a neurologic pathological disorder which can be diagnosed, treated, and prevented. Because EHS is becoming a new insidious worldwide plague involving millions of people, we ask the World Health Organization (WHO) to include EHS as a neurologic disorder in the international classification of diseases.
  • ... Reproduction is an important function of a living creature, which involves both female and male genital organs. Recently, evidence showed that both nonionizing and ionizing radiations induce epigenetic changes, genomic instability and oxidative stress in reproductive tissues (1,2). Radiofrequency (RF) radiation is part of the electromagnetic spectrum with frequencies ranging from 3 kHz to 300 GHz, which is below visible light and above extremely low-frequency fields (ELF-MFs) (3). ...
    Article
    Full-text available
    Objectives: The placenta provides nutrients and oxygen to embryo and removes waste products from embryo's blood. As far as we know, the effects of exposure to Wi-Fi (2.4 GHz) signals on placenta have not been evaluated. Hence, we examined the effect of prenatal exposure to Wi-Fi signals on anti-oxidant capacity, expressions of CDKNA1, and GADD45a as well as apoptosis in placenta and pregnancy outcome. Materials and methods: Pregnant mice were exposed to Wi-Fi signal (2.4 GHz) for 2 and 4 hr. Placenta tissues were examined to measure the MDA and SOD levels. To measure SOD, CDKNA1, GADD45a, Bax, and Bcl-2 expressions were compared by real-time PCR analysis. TUNEL assay was used to assess apoptosis in placenta tissues. The results were analyzed by one-way analysis of variance (ANOVA) using Prism version 6.0 software. Results: MDA and SOD levels had significantly increased in exposed Wi-Fi signal groups (P-value< 0.05). Also, quantitative PCR experiment showed that SOD mRNA expression significantly increased in Wi-Fi signal groups. The data showed that CDKN1A and GADD45a genes were increased in Wi-Fi groups (P-value<0.05). The quantitative PCR and the TUNEL assay showed that apoptosis increased in Wi-Fi groups (P-value<0.05). Conclusion: Our results provide evidence that Wi-Fi signals increase lipid peroxidation, SOD activity (oxidative stres), apoptosis and CDKN1A and GADD45a overexpression in mice placenta tissue. However, further experimental studies are warranted to investigate other genes and aspects of pregnancy to determine the role of Wi-Fi radiation on fertility and pregnancy.
  • ... Which were very marked in the 24 h group if compared with the 6 h group. Some studies were in accordance with this study such as Mohamed [20] and Esmekaya et al. [21] who stated that the exposure to radiofrequency caused high level of nitric oxide in lung, liver, testes and heart, so dilatation of blood vessels might be due to increased nitric oxide production, which is a vasodilator. In the exposed groups of this study, there were obvious thickening of inter-alveolar septa which increased in the septa of the 24 h group than the 6 h group. ...
    Article
    Introduction: Recent years have witnessed a marked increase in use of Wi-Fi devices in daily life. This new technology was approved to cause many health hazards. Aim of the Work: To investigate the histological structure changes occurred in the lung of the adult male albino rats after short and long time exposure of Wi-Fi router devices. Materials and Method: This study was carried out on 30 adult male albino rats. They were exposed to the 2.45 GHz radiation from Wi-Fi router device which was placed at 25 cm from the animals. Animals were divided into 3 groups 10 rats each: Group I (control): Rats were isolated in a room away from router device. Group II (6 hours): Rats were exposed to router device for 6 hours per day for 30 days. Group III (24 hours): Rats were exposed to router device for 24 hours per day for 30 days. Histological, immune-histochemical (Caspase 3 and iNOS antibodies), and morphometric studies were done. Results: Both 6 hours and 24 hours groups showed marked histological and immune-histochemical changes in the lung tissues when compared with the control group, however, changes in the 24 hours group is more severe when compared with the 6 hours group. Conclusion: Nowadays, the utilization of Wi-Fi routers devices becomes unavoidable in work and inside our homes. So, if we fail to control the radiation exposure time many people are likely to become sick. From this study, the exposure to such devices can cause bad effects on the lung tissue which increases with prolonged exposure time. So we should control the usage of these devices to save our health.
  • ... These might be related to the production of reactive oxygen species (ROS) by lipid peroxidation [Hanci et al., 2015;Çelik et al., 2016]. Oxidants can be generated in numerous exogenous ways such as chemical and radiation exposure through redox catalysis [Esmekaya et al., 2011]. These can block the activities of cell membrane enzymes and thereby affect cell functions, resulting in massive cell death and possibly the death of the organism [Achudume et al., 2012]. ...
    Article
    Full-text available
    The use of devices, including mobile phones, generating electromagnetic fields (EMF) is widespread and is progressively increasing. It has also been shown that EMF may have detrimental effects. This is the first study to investigate the postnatal biochemical and histological effects of prenatal exposure of rat livers to 1,800-MHz EMF at different time intervals in uteroplacental life. The 3 EMF groups of rats were exposed to 1,800-MHz EMF for 6, 12, or 24 h daily for 20 days. Unexposed rats served as control group. All rats were subjected to anesthesia, and on postnatal day 60, the livers were excised, and blood was collected for histological and biochemical analyses. Malondialdehyde levels were significantly higher in the exposed groups than the unexposed controls (p < 0.05). In contrast, EMF-exposed groups had lower liver tissue glutathione levels than controls (p < 0.05). Serum Ca2+, alanine transaminase, and aspartate aminotransferase levels were higher in EMF-exposed groups than controls (p < 0.05). In addition, liver tissue total oxidant status levels were increased (p < 0.05), and liver tissue total antioxidant status levels were decreased (p < 0.05) compared to the control group. Furthermore, in the EMF groups, extensive vacuolation and degeneration of the hepatocytes in the portal area, as well as those surrounding the sinusoids, were evident. Affected hepatocytes had polygonally shaped nuclei and vacuolic cytoplasm imparting eosinophilic staining. Loss of cellular membrane integrity and invaginations, as well as picnotic nuclei, was prominent. This study has shown that intrauterine liver damage caused by 1,800-MHz EMF exposure persists into puberty in rats.
  • ... However, FPP has been shown to produce some anti-inflammatory and anti-oxidant effects in chronic degenerative disease such as Alzheimer disease [12]. Similar favorable effects have also been observed for the treatment of diabetes [9] and for the prevention of psychological stress-induced acute gastric mucosal lesions [10], oxidative stress-induced oral cavity mucosal inflammation [11], and oxidative stressassociated occupational burn out [51]. ...
    Article
    Full-text available
    Citation: Philippe I., Catherine G., Carine H., Pierre M., Dominique B. Beneficial effects of a Fermented Papaya Preparation for the treatment of electrohypersensitivity self-reporting patients: results of a phase I-II clinical trial with special reference to cerebral pulsation measurement and oxidative stress analysis. ABSTRACT Background: Electromagnetic Field Intolerance Syndrome (EMFIS), also termed Idiopathic Environmental Intolerance (IEI) attributed to Electromagnetic Fields (IEI-EMF) by WHO, is a newly identified pathological disorder occurring in electrohypersensitivity (EHS) self-reporting patients. To date, there has been no recognized treatment of this disorder. We have shown that EHS self-reporting patients experience some degree of oxidative stress, inflammation, and autoimmune response. Additionally, Fermented Papaya Preparation (FPP) has some antioxidant, anti-inflammation, and immuno-modulating properties. The objective of this phase I-II clinical trial was thus to test whether FPP treatment is well tolerated, can improve clinical outcomes, and can normalize biological abnormalities. Methods: 32 EMFIS-bearing patients were serially included in this trial, among which 26 and 16 of them were evaluable after 3 and 6 months of FPP treatment, respectively. Clinical assessment was conducted during a specific face to face interview by using a validated pre-established questionnaire. Biological assessment consisted of measuring intracerebral tissue pulsometric index (PI) in the temporal lobes with ultrasonic cerebral tomosphygmography (UCTS), in addition to oxidative stress and inflammation with a battery of oxidative stress and inflammation-related peripheral blood tests.
  • ... Which were very marked in the 24 h group if compared with the 6 h group. Some studies were in accordance with this study such as Mohamed [20] and Esmekaya et al. [21] who stated that the exposure to radiofrequency caused high level of nitric oxide in lung, liver, testes and heart, so dilatation of blood vessels might be due to increased nitric oxide production, which is a vasodilator. In the exposed groups of this study, there were obvious thickening of inter-alveolar septa which increased in the septa of the 24 h group than the 6 h group. ...
  • Article
    The excessive exposure of patients with type 2 diabetes mellitus (T2DM) to electromagnetic radiation (EMR) from mobile phones or their base stations antenna may influence oxidative stress and development of diabetic complications. Here, we investigated the effects of exposing type 2 diabetic rats to EMR of 900 MHz emitted from GSM mobile phone antenna for 24 hours/day over a period of 28 days on hyperglycemia and hepatic oxidative stress. Male Sprague-Dawley rats were divided into 4 groups (12 rats/group): control rats, normal rats exposed to EMR, T2DM rats generated by nicotinamide/streptozotocin administration, and T2DM rats exposed to EMR. Our results showed that the exposure of T2DM rats to EMR nonsignificantly reduced the hyperglycemia and hyperinsulinemia compared to unexposed T2DM rats. The exposure of T2DM rats to EMR for 28 days increased the hepatic levels of MDA and Nrf-2 as well as the activities of superoxide dismutase (SOD) and catalase but decreased phosphorylated Akt-2 (pAkt-2) as compared to unexposed T2DM rats. Therefore, the decrease in the hepatic pAkt-2 in T2DM rats after the exposure to EMR may result in elevated level of hepatic MDA, even though the level of Nrf-2 and the activities of SOD and catalase were increased. Abbreviations: BGL: blood glucose level; EMR: electromagnetic radiation; GSM: global system for mobile communication; H2O2: hydrogen peroxide; LSD: least significance difference; MDA:malondialdehyde; Nrf-2: nuclear factor erythroid 2- related factor 2; PI3K: phosphoinositide-3-kinase; pAkt-2: phosphorylated Akt-2; Akt-2: protein kinase; ROS: reactive oxygen species; SEM: standard error of the mean; STZ: streptozotocin; SOD: superoxide dismutase ; O2⁻: superoxide radical; CT: threshold cycle; T2DM: type 2 diabetes mellitus
  • Article
    Despite their benefits, technological devices such as cell phones may also have deleterious effects on human health. Considerable debate continues concerning the effects of the electromagnetic field (EMF) emitted during cell phone use on human health. We investigated the effects of exposure to 900 megahertz (MHz) EMF during mid to late adolescence on the rat liver. Control (ContGr), sham (ShmGr) and EMF (EMFGr) groups of female rats were established. We exposed the EMFGr rats daily to 900 MHz EMF on postnatal days 35−59. ShmGr rats underwent sham procedures. No procedure was performed on ContGr rats. Rats were sacrificed on postnatal day 60 and the livers were extracted. One part of the liver was stained with Masson’s trichrome or hematoxylin and eosin. The remaining tissue was used to measure oxidative stress markers including malondialdehyde, glutathione, catalase, superoxide dismutase, 8-hydroxydeoxyguanosine (8-OHdG) and nitrotyrosine. Total antioxidant status and total oxidant status were used to calculate the oxidative stress index. We found normal hepatic morphology in the ContGr and ShmGr groups. The EMFGr group exhibited occasional irregularities in the radial arrangement of hepatocytes, cytoplasmic vacuolization, hemorrhage, sinusoid expansion, hepatocyte morphology and edema. Biochemical analysis revealed that 8-OHdG and SOD levels in EMFGr decreased significantly compared to the ContGr and ShmGr groups. Exposure to a continuous 900 MHz EMF for 1 h daily during mid to late adolescence may cause histopathological and biochemical alterations in hepatic tissue.
  • Article
    The non-intrusive polynomial chaos (NIPC) expansion method is used to quantify the uncertainty of a stochastic system. It potentially reduces the number of numerical simulations in modelling process, thus improving efficiency, whilst ensuring accuracy. However, the number of polynomial bases grows substantially with the increase of random parameters, which may render the technique ineffective due to the excessive computational resources. To address such problems, methods based on the sparse strategy such as the least angle regression (LARS) method with hyperbolic index sets can be used. This paper presents the first work to improve the accuracy of the original LARS method for uncertainty quantification (UQ). We propose an adaptive LARS method in order to quantify the uncertainty of the results from the numerical simulations with higher accuracy than the original LARS method. The proposed method outperforms the original LARS method in terms of accuracy and stability. The L2 regularisation scheme further reduces the number of input samples while maintaining the accuracy of the LARS method.
  • Article
    In the present study, the effect of 900 MHz radiation exposure on blood biochemical and reproductive parameters was evaluated in adolescent rats. Male albino Wistar rats (8-10 weeks of age) were exposed to 900 MHz radiation (1hr/day, power density-146.60 μW/cm 2) from a mobile phone for 28 days. On 29th day the animals were euthanized and malondialdehyde (MDA), total antioxidants (TA) levels and Glutathione-S transfer-ase (GST) activity were studied in the blood. Reproductive parameters such as total sperm count, percentage of non-motile sperms, and sperm morphology were determined. Testes sections were stained with H&E staining and their cellular integrity was evaluated. Caspase-3 activity in the testes was also determined. MDA concentration was increased but TA levels and GST activity were not found to be different in 900 MHz group compared to controls. Sperm motility was found to be slightly reduced in 900 MHz group. Percentage of abnormal sperm was signifi cantly elevated in 900 MHz group. Additionally, loss of germ cells particularly spermatocytes and spermatids was found in the testes of 900 MHz group. Testes caspase-3 activity was slightly elevated in 900 MHz exposed rats. Chronic 900 MHz exposure induced oxidative damage in the blood and lead to alterations in reproductive parameters in rats (Fig. 4, Ref. 33). Text in PDF www.elis.sk.
  • Article
    Nitric oxide (NO) is synthesized from L-arginine by a family of enzymes known as the nitric oxide synthases (NOS). We have recently shown a NOS similar to constitutive brain NOS (bNOS) and endothelial NOS (ecNOS) to be present in spermatozoa. The aim of this study is to investigate NO production by human spermatozoa and the effects of stimulation and inhibition of NOS. This was carried out using the Iso‐NO, an isolated NO meter and sensor, which provides rapid, accurate and direct measurements of NO. Semen samples with normozoospermic and asthenozoospermic profiles were prepared using a direct swim-up technique. Basal concentrations of NO and stimulated NO production were measured after exposure to the calcium ionophore (A23187; 0.01‐10 mM) a potent activator of constitutive NOS. NO production in human spermatozoa was significantly increased by the addition of A23187 30 seconds after stimulation. Furthermore, this response was greatly diminished by pre-incubating the samples with competitive inhibitors of L-arginine, the substrate for NOS, before treatment with calcium ionophore. In the presence of N G -nitro-L-arginine methyl ester (L-NAME), N G -nitro-L-arginine (L-NA) or N G -methyl-L-arginine (L-NMMA; all at 10 mM), NO production
  • Article
    Full-text available
    The effects of radiation emitted from cellular phones on humans are an emerging area of investigation. The previous studies have shown the role of oxidative stress and NO at radiofrequency exposed rats. Therefore, the purpose of this study was to investigate the effect of microwave/radiofrequency emitted from mobile phones and its possible oxidative damage. Wistar Albino rats were divided into three groups as exposure, sham and cage control. Rats in exposure group were exposed to 900 MHz microwave radiation (0.0782 mW/cm2) in a carousel for 2 hours/7 days in a week during ten months. The same process was applied to sham group but the generator was turned off. Rats in cage control group were kept in cage only during the study. The levels of catalase (CAT), myeloperoxidase (MPO), malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI) in liver and nitric oxide (NO) levels in serum were determined to demonstrate the role of oxidative mechanisms. The increase of nitric oxide levels in exposure and sham groups were found significant compared to cage control group (p
  • Article
    Microwaves (MW) from cellular phones may affect biological systems by increasing free radicals, which may enhance lipid peroxidation (LP), and by changing the antioxidative activities of the liver, thus leading to oxidative damage. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties and several studies suggest that supplementation with antioxidant can influence MW induced hepatotoxicity. The present study was designed to determine the effects of MW on the liver oxidant/antioxidant system, and the possible protective effects of CAPE on liver toxicity induced by MW. Twenty nine male Spraque- Dawley rats were divided into three groups: control (n = 9), 1800 MHz MW (n = 10) and 1800 MHz MW + CAPE (n = 10). CAPE was injected intraperitoneally for 30 days before exposure to MW. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO) and the levels of LP. The activities of XO, CAT and level of LP increased in MW group compared with the control group although XO and LP levels were decreased by MW + CAPE administration. The activities of SOD and GSH-Px decreased in MW group compared with the control group. Their levels were increased by MW + CAPE administration. We conclude that CAPE may prevent MW-induced oxidative changes in liver by strengthening the antioxidant defense system, by reducing reactive oxygen species, and by increasing antioxidant enzyme activities.
  • Article
    Exposure of cells to sublethal oxidative stress results in the modulation of various signaling pathways. Oxidants can activate and inactivate transcription factors, membrane channels, and metabolic enzymes, and regulate calcium-dependent and phosphorylation signaling pathways. Oxidation and reduction of thiol proteins are thought to be the major mechanisms by which reactive oxidants integrate into cellular signal transduction pathways. This review focuses on mechanisms for sensing and transmitting redox signals, from the perspective of their chemical reactivity with specific oxidants. We discuss substrate preferences for different oxidants and how the kinetics of these reactions determines how each oxidant will react in a cell. This kinetic approach helps to identify initial oxidant-sensitive targets and elucidate mechanisms involved in transmission of redox signals. It indicates that only those proteins with very high reactivity, such as peroxiredoxins, are likely to be direct targets for hydrogen peroxide. Other more modestly reactive thiol proteins such as protein tyrosine phosphatases are more likely to become oxidized by an indirect mechanism. The review also examines oxidative changes observed during receptor-mediated signaling, the strengths and limitations of detection methods for reactive oxidant production, and the evidence for hydrogen peroxide acting as the second messenger. We discuss areas where observations in cell systems can be rationalized with the reactivity of specific oxidants and where further work is needed to understand the mechanisms involved.
  • Article
    Objective: To determine whether particular semen characteristics in various clinical diagnoses of infertility are associated with high oxidative stress and whether any group of infertile men is more likely to have high seminal oxidative stress. Reactive oxygen species (ROS) play an important role in sperm physiological functions, but elevated levels of ROS or oxidative stress are related to male infertility. Design: Measurement of sperm concentration, motility, morphology, seminal ROS, and total antioxidant capacity (TAC) in patients seeking infertility treatment and controls. Setting: Male infertility clinic of a tertiary care center. Patient(s): One hundred sixty-seven infertile patients and 19 controls. Intervention(s): None. Main outcome measure(s): Semen characteristics, seminal ROS, and TAC in samples from patients with various clinical diagnoses and controls. Result(s): Fifteen patients (9.0%) were Endtz positive and 152 (91.0%) Endtz negative. Sperm concentration, motility, and morphology were significantly reduced in all groups compared with the controls (P =.02), except in varicocele associated with infection group. Mean (+/-SD) ROS levels in patient groups ranged from 2.2 +/- 0.13 to 3.2 +/- 0.35, significantly higher than controls (1.3 +/- 0.3; P<.005). Patient groups had a significantly lower mean (+/-SD) TAC from 1014.75 +/- 79.22 to 1173.05 +/- 58.07 than controls (1653 +/- 115.28, P<.001), except in the vasectomy reversal group (1532.02 +/- 74.24). Sperm concentration was negatively correlated with ROS both overall and within all groups (P</=.007), with the exception of idiopathic infertility. Conclusion(s): Irrespective of the clinical diagnosis and semen characteristics, the presence of seminal oxidative stress in infertile men suggests its role in the pathophysiology of infertility. Medical or surgical treatments for infertility in these men should include strategies to reduce oxidative stress.
  • Article
    The World Health Organization (WHO) has recently published a new research agenda for radiofrequency fields. The document lists high priority and other research needs for health effects research, subdivided into epidemiology, human studies, animal studies, cellular studies and mechanisms, and for social science research.
  • Article
    Full-text available
    BACKGROUND: In recent times there has been some controversy over the impact of electromagnetic radiation on human health. The significance of mobile phone radiation on male reproduction is a key element of this debate since several studies have suggested a relationship between mobile phone use and semen quality. The potential mechanisms involved have not been established, however, human spermatozoa are known to be particularly vulnerable to oxidative stress by virtue of the abundant availability of substrates for free radical attack and the lack of cytoplasmic space to accommodate antioxidant enzymes. Moreover, the induction of oxidative stress in these cells not only perturbs their capacity for fertilization but also contributes to sperm DNA damage. The latter has, in turn, been linked with poor fertility, an increased incidence of miscarriage and morbidity in the offspring, including childhood cancer. In light of these associations, we have analyzed the influence of RF-EMR on the cell biology of human spermatozoa in vitro. PRINCIPAL FINDINGS: Purified human spermatozoa were exposed to radio-frequency electromagnetic radiation (RF-EMR) tuned to 1.8 GHz and covering a range of specific absorption rates (SAR) from 0.4 W/kg to 27.5 W/kg. In step with increasing SAR, motility and vitality were significantly reduced after RF-EMR exposure, while the mitochondrial generation of reactive oxygen species and DNA fragmentation were significantly elevated (P
  • Article
    Full-text available
    Mobile phones have become indispensable in the daily lives of men and women around the globe. As cell phone use has become more widespread, concerns have mounted regarding the potentially harmful effects of RF-EMR from these devices. The present study was designed to evaluate the effects of RF-EMR from mobile phones on free radical metabolism and sperm quality. Male albino Wistar rats (10-12 weeks old) were exposed to RF-EMR from an active GSM (0.9/1.8 GHz) mobile phone for 1 hour continuously per day for 28 days. Controls were exposed to a mobile phone without a battery for the same period. The phone was kept in a cage with a wooden bottom in order to address concerns that the effects of exposure to the phone could be due to heat emitted by the phone rather than to RF-EMR alone. Animals were sacrificed 24 hours after the last exposure and tissues of interest were harvested. One hour of exposure to the phone did not significantly change facial temperature in either group of rats. No significant difference was observed in total sperm count between controls and RF-EMR exposed groups. However, rats exposed to RF-EMR exhibited a significantly reduced percentage of motile sperm. Moreover, RF-EMR exposure resulted in a significant increase in lipid peroxidation and low GSH content in the testis and epididymis. Given the results of the present study, we speculate that RF-EMR from mobile phones negatively affects semen quality and may impair male fertility.
  • Article
    To evaluate effects of cellular phone radiofrequency electromagnetic waves (RF-EMW) during talk mode on unprocessed (neat) ejaculated human semen. Prospective pilot study. Center for reproductive medicine laboratory in tertiary hospital setting. Neat semen samples from normal healthy donors (n = 23) and infertile patients (n = 9). After liquefaction, neat semen samples were divided into two aliquots. One aliquot (experimental) from each patient was exposed to cellular phone radiation (in talk mode) for 1 h, and the second aliquot (unexposed) served as the control sample under identical conditions. Evaluation of sperm parameters (motility, viability), reactive oxygen species (ROS), total antioxidant capacity (TAC) of semen, ROS-TAC score, and sperm DNA damage. Samples exposed to RF-EMW showed a significant decrease in sperm motility and viability, increase in ROS level, and decrease in ROS-TAC score. Levels of TAC and DNA damage showed no significant differences from the unexposed group. Radiofrequency electromagnetic waves emitted from cell phones may lead to oxidative stress in human semen. We speculate that keeping the cell phone in a trouser pocket in talk mode may negatively affect spermatozoa and impair male fertility.
  • Article
    Continuous wave (cw) microwave irradiation at 960 MHz has caused bradycardia in isolated, perfused rat hearts maintained at 20C. The observed bradycardia occurred at microwave dose rates that should have caused mild tachycardia in the heart based on the thermogenic properties of the irradiation. The observed bradycardia, moreover, exhibited neurologic features because atropinized hearts showed strong tachycardia during irradiation and hearts treated with propranolol showed significantly stronger bradycardia during irradiation than that seen without drugs. Use of the liquid-crystal optical-fiber (LCOF) temperature probe has shown, by calorimetric methods, that the microwave-induced bradycardia occurred at dose rates of 1.3 and 2.1 mW/g. We hypothesize that microwave energy interacts with the remaining portion of the autonomic nervous system within the heart to produce the observed chronotropic effects.