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The Effect of Electromagnetic Radiation on the Rat Brain: An Experimental Study

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The aim of this study is to determine the structural changes of electromagnetic waves in the frontal cortex, brain stem and cerebellum. MATERIAL and 24 Wistar Albino adult male rats were randomly divided into four groups: group I consisted of control rats, and groups II-IV comprised electromagnetically irradiated (EMR) with 900, 1800 and 2450 MHz. The heads of the rats were exposed to 900, 1800 and 2450 MHz microwaves irradiation for 1h per day for 2 months. While the histopathological changes in the frontal cortex and brain stem were normal in the control group, there were severe degenerative changes, shrunken cytoplasm and extensively dark pyknotic nuclei in the EMR groups. Biochemical analysis demonstrated that the Total Antioxidative Capacity level was significantly decreased in the EMR groups and also Total Oxidative Capacity and Oxidative Stress Index levels were significantly increased in the frontal cortex, brain stem and cerebellum. IL-1β level was significantly increased in the EMR groups in the brain stem. EMR causes to structural changes in the frontal cortex, brain stem and cerebellum and impair the oxidative stress and inflammatory cytokine system. This deterioration can cause to disease including loss of these areas function and cancer development.
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Orgnal Investgaton
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715 707
Received: 05.08.2012 / Accepted: 30.10.2012
DOI: 10.5137/1019-5149.JTN.7088-12.2
ABSTRACT
AIM: The am of ths study s to determne the structural changes of electromagnetc waves n the frontal cortex, bran stem and cerebellum.
MATERIAL and METHODS: 24 Wstar Albno adult male rats were randomly dvded nto four groups: group I conssted of control rats, and
groups II-IV comprsed electromagnetcally rradated (EMR) wth 900, 1800 and 2450 MHz. The heads of the rats were exposed to 900, 1800
and 2450 MHz mcrowaves rradaton for 1h per day for 2 months.
RESULTS: Whle the hstopathologcal changes n the frontal cortex and bran stem were normal n the control group, there were severe
degeneratve changes, shrunken cytoplasm and extensvely dark pyknotc nucle n the EMR groups. Bochemcal analyss demonstrated that
the Total Antoxdatve Capacty level was sgnfcantly decreased n the EMR groups and also Total Oxdatve Capacty and Oxdatve Stress
Index levels were sgnfcantly ncreased n the frontal cortex, bran stem and cerebellum. IL-1β level was sgnfcantly ncreased n the EMR
groups n the bran stem.
CONCLUSION: EMR causes to structural changes n the frontal cortex, bran stem and cerebellum and mpar the oxdatve stress and
nammatory cytokne system. Ths deteroraton can cause to dsease ncludng loss of these areas functon and cancer development.
KEYWORDS: Electromagnetc waves, Bran tssue, Oxdatve stress, Actve caspase-3
ÖZ
AMAÇ: Bu çalışmanın amacı, frontal korteks, beyn sapı ve serebellumda elektromanyetk dalgaların yapısal değşklklern araştırmaktır.
YÖNTEM ve GEREÇLER: 24 Wstar Albno sıçan rastgele 4 gruba bölündü: grup 1 kontrol grubu ve grup 2-4 900, 1800 ve 2450 MHz
elektromanyetk radyasyona maruz kaldı. Sıçanların kafaları 900, 1800 ve 2450 MHz mkrodalgalara 2 ay boyunca her gün 1 saat maruz bırakıldı.
BULGULAR: Kontrol grubunda hstopatolojk değşklkler, beyn sapında ve frontal kortekste normal bulunurken elektromanyetk radyasyon
uygulanan gruplarda cdd dejeneratf değşklkler, küçülmüş stoplazma ve genş koyu pknotk nükleus mevcuttu. Byokmyasal analzde
total antoksdatf kapaste sevyes elektromanyetk grupta anlamlı olarak azalmış bulunurken, total oksdatf kapaste ve oksdatf stres ndeks
sevyeler frontal korteks, beyn sapı ve serebellumda anlamlı olarak artmış bulundu. Elektromanyetk grupta beyn sapında IL-1β sevyes
anlamlı olarak artmıştı.
SONUÇ: Elektromanyetk radyasyon beyn sapında, serebellumda ve frontal kortekste yapısal değşklklere neden olmakta ve oksdatf stres
ve namatuvar stokn sstemn bozmaktadır. Bu bozulma kanser oluşumuna ve bu bölgelern fonksyon kaybını çeren hastalıklara neden
olablr.
ANAHTAR SÖZCÜKLER: Elektromanyetk dalga, Beyn dokusu, Oksdatf stres, Aktf kaspaz-3
Corresponding Author: Olcay ESER / E-mal: drolcayeser@hotmal.com
Olcay ESER1, Ahmet SONGUR2, Cevat AKTAS3, Ergun KARAVELIOGLU4, Vel CAGLAR2, Frdevs AYLAK5,
Fehm OZGUNER6, Mehmet KANTER7
1Afyon Kocatepe University, Faculty of Medicine, Department of Neurosurgery, Afyonkarahisar, Turkey
2Afyon Kocatepe University, Faculty of Medicine, Department of Anatomy, Afyonkarahisar, Turkey
3Namik Kemal University, Faculty of Medicine, Department of Histology and Embryology, Tekirdag, Turkey
4Bolvadin Dr. H.I.Ozsoy State Hospital, Department of Neurosurgery, Afyonkarahisar, Turkey
5Suleyman Demirel University, Faculty of Medicine, Department of Biochemistry, Isparta, Turkey
6Suleyman Demirel University, Faculty of Medicine, Department of Physiology, Isparta, Turkey
7Istanbul Medeniyet University, Faculty of Medicine, Department of Histology and Embryology, Istanbul, Turkey
e Eect of Electromagnetic Radiation on the
Rat Brain: An Experimental Study
Elektromanyetik dalgaların Sıçan Beyin dokusu Üzerine Etkileri:
deneysel Çalışma
INTRODUCTION
The frequent using of mobile and cordless phones in our
daily life has led to concern regarding possible health
eects, cancer risk in particular, from frequent exposure to
radiofrequency radiation. However, scientic evidence on
a possible mobile phone–cancer relation has still not clear
enough. Therefore, investigators have still been showing
high performance to clarify this topic (3). Electromagnetic
radiation (EMR) is emitted by both cellular mobile phones and
their base stations. Unfortunately, exposure to EMR may have
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715708
Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
detrimental eects on the body, depending on the frequency
and power of the EMR (27). Analogue phones use frequencies
of 400–450 MHz, and digital mobile phones use frequencies
of 850–900 MHz (similarly used in our study), and 1850–1990
MHz, whereas microwave ovens use a frequency of 2450 MHz
(24).
During embryogenesis, and throughout the lifespan of a
multi-cellular organism, apoptosis plays a key role in normal
tissue homeostasis (1,8). Perturbations in apoptotic pathways
can cause human disease (30). There are several markers
currently used to detect apoptosis. In particular, the active
(cleaved) caspase-3 is a well-characterized component typi-
cally observed during apoptosis, making it an ideal marker
for this cellular process (9). Defects in apoptosis signaling
pathways are common in cancer cells. Since apoptosis elimi-
nates cells with damaged DNA or dysregulated cell cycle (as is
the case for cells with increased malignant potential), decits
in apoptotic signaling may play an important role in tumor
initiation (3). Decits in apoptosis may also promote tumor
progression and metastasis by enhancing the survival of tu-
mor cells during transit through the bloodstream and growth
in ectopic tissues (17).
Dasdag et al. (4) intended to examine the eects of 900
MHz mobile phone exposure on p53 in the rat brain. They
found that 900 MHz microwave radiation emitted from
mobile phones do not aect these apoptotic parameters
(4). Leszczynski et al. (18) reported that mobile phone
exposure can alter heat shock protein-27 (hsp27) by causing
a transient increase in its phosphorylation. Hsp27 has many
known functions that suggest that mobile phone radiation-
induced activation of hsp27 may (i) promote brain cancer by
inhibiting the cytochrome c/caspase-3 apoptotic pathway
and (ii) enhance the permeability of the blood-brain barrier
by stabilizing stress bers of endothelial cells.
EMR or radiofrequency elds of cellular mobile phones may
also aect individuals by increasing free radicals, which
enhance lipid peroxidation, or by promoting oxidative stress
by changing the antioxidant defense systems of human tissues
(24). Oxidative stress is caused by relatively high levels of toxic
reactive species, consisting mostly of reactive oxygen species
(ROS), reactive nitrogen species (RNS), and the antioxidative
defense mechanisms (23). Electromagnetic radiation causes
oxidative stress, which in turn induces apoptosis. The signal
for apoptosis is possibly generated via lipid peroxidation
when radiation acts on cell membranes (23).
IL-1β, an important component of the cytokine network,
and is one of the inammatory cytokines that introduces
prostaglandin E1, matrix metalloproteinase-3, nitrous oxide
(NO), and other substances into the intervertebral discs
(22). IL-1β is a pro-inammatory cytokine elicited following
traumatic brain injury; behavioral outcome is improved when
this cytokine is decreased (27).
We investigated the eects of cell phone exposure on the
antioxidants, oxidants, oxidative stress index, interleukin-1β
levels and histological structure of rat brain tissue, caspase-3
immunoreactivity in this study.
MATERIAL and METHODS
Animal Model
Twenty-four male Spraque-Dawley rats (8-week-old, 150–
200 g body weight) obtained from the Laboratory Animal
Production Unit of Suleyman Demirel University were used in
the study. The animals were procured, maintained, and used
in accordance with the Animal Welfare Act and the Guide
for the Care and Use of Laboratory Animals prepared by the
Suleyman Demirel University, Animal Ethical Committee.
They were kept in a temperature- and humidity-controlled
environment (temperature, 24–26°C; humidity, 55–60%), on
a 12:12-h light/darkness cycle for 1 week before the start of
experiments. A commercially balanced diet (Hasyem Ltd.,
Isparta, Turkey) and tap water were provided ad libitum.
Experimental Design
The animals were randomly divided into four equal groups
(consisting of 6 rats each): Group I rats were used as the
control group (without exposure to EMR); these rats were
held in the EMR tube for 60 minutes a day for 60 days (two
months) under the same environmental conditions. EMR
groups: group II rats were exposed to 900 MHz, group III rats
were exposed to 1800 MHz, and group IV rats were exposed
to 2450 MHz. All of the rats in the EMR groups were exposed
to EMR from the generator for 60 minutes a day for 60 days.
The EMR exposure time was from 11:00–12:00 a.m. on each
day. At the end of the study, the rats in all of the groups were
anesthetized with intraperitoneal administration of ketamine
(50 mg/kg)-xylazine (6 mg/kg) after the last dose exposure to
EMR. The rats were sacriced by collecting blood samples from
the posterior vena cava. After removing the cranial bones,
cerebral cortex and brain stem removed and the brain stem,
right frontal cortex and cerebellum tissue were kept in -86°C
for biochemical study. Left frontal cortex, cerebellum and
brain stem were taken in neutral buered formalin solution
for histopathological study. Histopathological evaluation of
left cerebellum was unsuccessful due to staining failure.
Exposure Device
Radiation for the study (900, 1800, 2450 MHz) was provided by
an electromagnetic generator continuously for 60 min each
day for 2 months (peak power, 2 W; average power density,
1.04 mW/cm2). The predicted average specic absorption rate
(SAR) value was measured at 1.04 W/kg. The power density
measurements were made with an electromagnetic eld meter
(Holaday Industries Inc.) produced at the electromagnetic
compatibility (EMC) laboratory of the School of Electronic
Engineering (Suleyman Demirel University, Isparta, Turkey).
The exposure system consisted of a plastic tube cage (length:
12 cm, diameter: 5.5 cm) and a dipole antenna. The entire
body of each rat was positioned in close contact above the
dipole antenna, and the tube was ventilated from head-to-tail
to decrease the stress of the rat while in the tube.
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715 709
Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
Biochemical Analysis Tissue Sampling and Homogeni-
zation
On the last day of the study, brains were removed immediately
after euthanization to determine total antioxidative capacity
(TAC), total oxidant status (TOS), and oxidative stress index
(OSI). Prior to biochemical assays, all tissues were weighed
and placed in empty glass tubes. Ten milliliters of 140 mM KCl
solution per 1 g of tissue were added to each tube containing
tissue samples, and the tissue was homogenized in a motor-
driven homogenizer. The homogenate was centrifuged at
2800 g for 10 min at 4°C, placed in labeled vials and stored
at −80°C. Microprotein levels were measured using the Lowry
method (20).
Measurement of TAC
TAC levels of all tissues were measured using a novel
automated colorimetric measurement method developed by
Erel (6,7). This method is based on the Fenton reaction, which
involves the colorless substrate O-dianisidine reacting with
the hydroxyl radical to produce the dianisyl radical, which
is bright yellowish-brown. Upon the addition of a plasma
sample, hydroxyl radicals present in the reaction mix initiate
oxidative reactions that are suppressed by the antioxidant
components within the homogenates. This prevents the
color change, providing an eective measure of the total
antioxidant capacity of the plasma. The assay has excellent
precision values (<3% error). Assay results are expressed as
mol Trolox equiv/g protein.
Measurement of TOS
TOS levels of all tissues were determined using a novel
automated measurement method developed by Erel (7).
Oxidants present in the sample oxidize the ferrous iono-
dianisidine complex to ferric ion. Glycerol molecules present
in the reaction medium enhance the oxidation reaction. In
an acidic medium with xylenol orange, the ferric ion forms
a colored complex. Spectrophotometric measurement of
the color intensity represents the total amount of oxidant
molecules present in the sample. Hydrogen peroxide (H2O2)
is used to calibrate the assay, and the results are expressed
as micromolar H2O2 equivalents per g protein (mol H2O2
equiv/g protein).
OSI Calculation
OSI is the percent ratio of TOS to TAC and an indicator of the
degree of oxidative stress (7). The OSI value was calculated
according to the formula: OSI = ((TOS, mol H2O2 Equiv/g
protein)/(TAC, mol Trolox equiv/g protein)).
Interleukin-1β Determination
Brain stem tissue weighed in phosphate buer (pH 7.4)
was diluted in 10 volumes. Tissue samples were separated
by centrifugation (Eppendorf 5415-R (Germany) brand
refrigerated centrifuge) and 4000 rev/min for 15 min, and the
supernatant from the IL-1β was studied. The supernatants
were stored at −20°C until the cytokine assays were performed.
Cytokines in the supernatant of tissue homogenates were
measured using commercially available enzyme-linked
immunosorbent assay according to the manufacturer’s
instructions. The assay kits for IL-1β were purchased from
RayBio mark (USA).
Histopathologic Evaluation
Frontal cortex and brainstem tissues were harvested and
xed in 10% neutral buered formalin solution, embedded
in paran, sectioned at a thickness of 5 µm, and then
stained with hematoxylin and eosin (H&E). Sections were
photographed and were evaluated using a bright-eld
microscope (Optiphot 2; Nikon, Tokyo, Japan).
Microscopic Examination
Tissue sections were examined using a bright-eld microscope,
and the number of neurons was counted within random
high-power elds using a Nikon Optiphot-2 light microscope
tted with a square graticule in the eyepiece (eyepiece x10,
objective x40, a total side length of 0.25 µm2). The number
of neurons was assessed by counting the number of cells in
the frontal cortex and brainstem in 400 high-power elds. The
number of neurons/µm2 in each region was determined. The
tissue compartments were used to record neuron distribution
in the frontal cortex and brain stem tissues.
Immunohistochemistry
Frontal cortices and brain stems were xed in 10% neutral
buered formalin solution, embedded in paran, and
sectioned at a thickness of 5 µm. Immunocytochemistry
was performed according to the ABC technique described
previously (13). The procedure involved the following steps:
(1) incubation in 3% H2O2 in distilled water for 30 min to inhibit
endogenous peroxidase activity; (2) washing in distilled water
for 10 min; (3) incubation in normal goat serum (DAKO X
0907, Carpinteria, CA) with phosphate-buered saline (PBS)
(diluted 1:4) to block non-specic binding of antibodies; (4)
incubation in rabbit polyclonal anti-Caspase-3 antibody
(1:50; ab13847, Abcam, USA) for 1 h at room temperature;
(5) washing in PBS 3 × 3 min; (6) incubation in biotinylated
anti-mouse IgG (DAKO LSAB 2 Kit); (7) washing in PBS 3
× 3 min; (8) incubation in ABC complex (DAKO LSAB 2 Kit);
(9) washing in PBS 3 × 3 min; (10) detection of peroxidase
using an aminoethylcarbazole substrate kit (AEC kit; Zymed
Laboratories); (11) washing in tap water for 10 min, followed
dehydration; (12) hematoxylin staining to visualize the nuclei;
and (13) mounted in DAKO Paramount. All dilutions and
washes between steps were performed using PBS and were
carried out at room temperature unless otherwise specied.
As a negative control, the primary antibody was replaced with
PBS.
Immunohistochemical staining was scored in a semiquan-
titative manner to determine dierences between the control
group and the experimental groups. Weak (±), mild (+),
moderate (++), strong (+++), and very strong (++++) signals
was observed and recorded. This analysis was performed in
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715710
Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
Figure 1: Representative light microphotographs showing the morphology (a1–d1) and apoptosis (a2–d2) of the frontal cortex tissue
in control and EMR groups (900, 1800, 2450 MHz) by hematoxylin-eosin and caspase-3 immunohistochemistry. (Immunoperoxidase,
haematoxylin counterstain, scale bar, 50 µm) .
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715 711
Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
Figure 2: Representative light microphotographs showing the morphology (a1–d1) and apoptosis (a2–d2) of the brain stem tissue
in control and EMR groups (900, 1800, 2450 MHz) by hematoxylin-eosin and caspase-3 immunohistochemistry. (Immunoperoxidase,
haematoxylin counterstain, scale bar, 50 µm) 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16.
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715712
Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
The determination of TAC, TOS and OSI values in the brain
stem are shown in Table IV. The brainstem in the EMR groups
TAC were lower than in the control group (p<0.05), TOS and
OSI were higher than in the control group (p<0.05). In the
EMR groups, the group II TAC was not signicantly dierent
from that of groups III and IV (P>0.05). The group II TOS was
signicantly dierent from that of groups II and III (P<0.05),
whereas the group III TOS was not signicantly dierent from
that of group IV (P>0.05). For the OSI comparisons, the OSI
group II was not signicantly dierent from that of group III
and IV (P>0.05).
The determination of TAC, TOS and OSI values in the
cerebellum are shown in Table V. The cerebellum in the EMR
groups TAC were lower than in the control group (p<0.05), TOS
and OSI were higher than in the control group (p<0.05). In the
EMR groups, the group II TAC was not signicantly dierent
from that of groups III (P>0.05), whereas the group IV TAC was
signicantly dierent from that of group II (P<0.05). The group
II TOS was signicantly dierent from that of groups III (P<0.05),
whereas the group II TOS was not signicantly dierent from
that of group IV (P>0.05). For the OSI comparisons, the OSI
group II was not signicantly dierent from that of group III
and IV (P>0.05), and the group III OSI was not signicantly
dierent from that in group IV (P>0.05).
Measurement of Brain Stem IL-1β levels
The brain stem IL-1β levels are showed in table 4. IL-1β levels
in the EMR groups were signicantly dierent from those in
at least 8 areas from the frontal cortex and brain stem, in 2
sections from each animal at x400 magnication.
Statistical analysis
Data were expressed as the mean ± standard deviation
(SD). Data from controls and each of the groups were
compared using the Mann–Whitney non-parametric test for
independent samples. Statistical analyses were performed
using the Statistical Package for the Social Sciences (SPSS) for
Windows version 11.5 (SPSS Inc. Chicago, IL, USA) and a p <
0.05 was considered signicant.
RESULTS
Histopathological Findings
The morphology of neurons in the frontal cortex and brain
stem were normal in H&E-stained sections taken from the
control group (Figure 1A1; 2A1). In the EMR groups (900,
1800, and 2450 MHz), the most consistent observations
were severe degenerative changes, shrunken cytoplasm, and
extensively dark pyknotic nuclei in neurons of the frontal
cortex and brain stem tissues (Figure 1B1, C1, D1; 2B1, C1,
D1). In the EMR groups (900 and 1800 MHz) frontal cortex and
brain stem tissues, the intensity of neuronal changes was less
than in the EMR group (2450 MHz). The number of neurons in
the frontal cortex and brain stem tissues of the EMR groups
(900, 1800, 2450 MHz) were also signicantly less than in the
control group (P < 0.05, P < 0.01 and P < 0.001) (Table I).
Immunohistochemical Findings
Weak caspase-3 immunoreactivity was observed in the
cytoplasm of neurons in control rats (Figure 1A2; 2A2). Light
micrographs of caspase-3 immunohistochemistry revealed
apoptotic neurons after EMR exposure. The caspase-3 signal
was more intense in degenerating neurons of the frontal
cortex and brain stem tissues following EMR exposure (Figure
1B2D2; 2B2D2). In the cytoplasm of neurons in EMR (2450
MHz) group, the strong caspase-3 immunoreactivity was
observed (Figure 1D2; 2D2) (Table II).
Biochemical Analysis
Determination of total antioxidative capacity (TAC), total
oxidative status (TOS) and Oxidative Stress Index (OSI):
The determination of TAC, TOS and OSI values in the frontal
cortex are shown in Table III. The frontal cortex in the EMR
groups TAC were lower than in the control group (p<0.05), TOS
and OSI were higher than in the control group (p<0.05). In the
EMR groups, the group II frontal cortex TAC was signicantly
dierent from that of groups III and IV (P<0.05), whereas the
group III TAC was not signicantly dierent from that of group
IV (P>0.05). The group IV frontal cortex TOS was signicantly
dierent from that of groups II and III (P<0.05), whereas the
group II TOS was not signicantly dierent from that of group
III (P>0.05). For the OSI comparisons, the OSI in frontal cortex
group II was signicantly dierent from that of group III and IV
(P<0.05), and the group III OSI was not signicantly dierent
from that in group IV (P>0.05).
Table I: The Numbers (Number/mm2) of Neurons n the Frontal
Cortex and Bran Stem Tssue of Control and EMR Groups (900,
1800, 2450 MHz)
Groups Frontal cortex Bran stem
Control 77.38±5.13 35.31±1.54
900 MHz 63.82±4.64a28.12±1.32a
1800 MHz 51.44±3.86b23.14±1.11b
2450 MHz 42.16±2.98c18.12±0.94c
Kruskal-Wallis test was used for statistical analysis. Values are expressed as
means ± SD, n = 6 for each group; aP<0.05 compared to A group, bP<0.01
compared to A group, cP<0.001 compared to A group.
Table II: Semquanttatve Comparson of the Intensty n Neurons
of Caspase-3 Immunoreactivity n the Frontal Cortex and Bran
Stem Tssue of Control and EMR Groups (900, 1800, 2450 MHz),
(n: 6 for Each Group)
Frontal cortex Bran stem
Control ± ±
900 MHz + +
1800 MHz ++ ++
2450 MHz +++ +++
The ntensty of the stanng was recorded as weak (±), mld (+), moderate
(++), strong (+++) and very strong (++++).
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Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
initiation because cells with damaged DNA or dysregulated
cell cycle (i.e., cells with increased malignant potential) are
normally eliminated (17). Moreover, impaired apoptotic
function may enhance tumor progression and promote
metastasis by enhancing the ability of tumor cells to survive in
the circulatory system and to grow in ectopic tissue sites (17).
Therefore, the result of this study is of importance in terms of
its implication on the dysregulation of apoptotic machinery.
Because we found that 900/1800/2400 MHz radiation used
in this study altered the number of apoptotic cells, this may
potentially be dangerous in the networking of the brain cells.
Radiation is known to induce oxidative stress, which in turn
activates the apoptotic pathway (23). Oxidative stress is a
cellular or physiological condition of elevated concentrations
of reactive oxygen species that cause molecular damage to
vital structures and functions (32). It has been reported that
the eects of radiation on cell membranes induces apoptotic
signal via lipid peroxidation (23). Radiation may also mediate
the control group (P<0.05). In the EMR groups, group II IL-1β
levels were signicantly dierent from those in group III and IV
(P<0.05), whereas group III IL-1β levels were not signicantly
dierent from those in group IV (P>0.05).
DISCUSSION
The frequent using of mobile phones and base stations in
our daily life has led to concern regarding possible health
eects, cancer risk in particular, from frequent exposure to
radiofrequency radiation. However, scientic evidence on
a possible mobile phone–cancer relation has still not clear
enough (3). There fore we aimed to investigate experimentally
the biological eect of EMR on the cranial structure. In this
study, we demonstrated that EMR aect the oxidative stress,
levels of cytokine and induction of the apoptosis on the brain
tissue.
Cancer cells often exhibit decits in apoptotic signaling
pathways. These decits may play a signicant role in tumor
Table V: The Levels of Total Antoxdatf Capacty (TAC), Total Oxdant Status (TOS and Oxdant Stres Index (OSI) n Cerebellum Groups
Parameters Control 900MHz 1800MHz 2450MHz
TAC 0.58±0.08 0.27±0.01 0.27±0.02 0.24±0.01
TOS 2.30±0.21 3.01±0.35 2.59±0.18 2.59±0.20
OSI 400.85± 80.75 1110.03± 146.43 950.38± 94.75 1077.33± 154.62
The value represent the mean±SD.
TAC compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900- 1800 MHz (p>0.05), 900-2450 MHz (p<0.05), 1800-2450 MHz (p>0.05).
TOS compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900- 1800 MHz (p<0.05), 900- 2450 MHz (p>0.05), 1800-2450 MHz (p>0.05).
OSI compares; Control- 900/1800/2450 MHz (p<0.05), 900-1800/ 2450 MHz (p>0.05), 1800-2450 MHz (p>0.05) Arbtrary Unts (AU).
Table III: The Levels of Total Antoxdatf Capacty ( TAC), Total Oxdant Status (TOS) and Oxdant Stres Index (OSI n Frontal Cortex
Groups
Parameters Control 900MHz 1800MHz 2450MHz
TAC 0.90±0.05 0.59±0.01 0.74±0.02 0.78±0.03
TOS 3.29±0.35 4.77±0.40 4.71±0.24 6.15±0.99
OSI 418.48± 41.38 808.52± 69.15 629.38± 28.78 678.01± 83.53
The value represent the mean±SD.
TAC compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900- 1800/2450 MHz (p<0.05), 1800- 2450 MHz (p>0.05).
TOS compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900- 1800 MHz (p>0.05), 900- 2450 MHz (p<0.05), 1800-2450 MHz (p<0.05).
OSI compares; Control- 900/1800/2450 MHz (p<0.05), 900-1800/ 2450 MHz (p<0.05), 1800-2450 MHz (p>0.05) Arbtrary Unts (AU).
Table IV: The Levels of Interleukn-1Β (Il-1Β), Total Antoxdatf Capacty (TAC), Total Oxdant Status ( TOS) and Oxdant Stres Index (OSI)
n Bran Stem Groups
Parameters Control 900MHz 1800MHz 2450MHz
IL-1β 5061.57± 418.75 8189.23± 1151.21 6055.58± 648.34 6039.02± 710.64
TAC 0.37±0.01 0.26±0.02 0.27±0.01 0.28±0.00
TOS 2.22±0.13 3.71±0.30 3.03±0.14 2.68±0.11
OSI 661.82± 36.16 1094.94± 108.29 1080.30± 78.29 1074.16± 63.23
The value represent the mean±SD.
IL-1β compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900-1800/2450 MHz (p<0.05), 1800-2450 MHz (p>0.05).
TAC compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900- 1800/2450 MHz (p>0.05), 1800- 2450 MHz (p>0.05).
TOS compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900- 1800/2450 MHz (p<0.05), 1800-2450 MHz (p<0.05).
OSI compares; Control- 900/ 1800/ 2450 MHz (p<0.05), 900-1800/ 2450 MHz (p>0.05), 1800-2450 MHz (p>0.05) Arbtrary Unts (AU).
Turksh Neurosurgery 2013, Vol: 23, No: 6, 707-715714
Eser O. et al: e Eect of Electromagnetic Radiation on the Rat Brain
clinical outcome, it plays a key role in injury response. Hirose
et al. (12) demonstrated that there was no dierences of IL-1β
level between control and 1950 MHz groups in rat brain. Also
Rasouli et al (27) demonstrated no dierences in IL-1β level
between pulsed electromagnetic elds treated and control
groups in brain homogenates after traumatic brain injury in
rats. In this study, IL-1β level was signicantly increased in
brain stem in EMR groups compared to the control group.
CONCLUSION
Biochemical analysis of this study demonstrated that TAC
level was signicantly decreased in EMR groups compared
to control group while TOS and OSI level were signicantly
increased. This result revealed that EMR is aective on
the oxidant-antioxidant system. The frontal cortex was
signicantly more aected in 900 MHz EMR. There was not
signicant dierence between other groups. Also in the brain
stem and frontal cortex there was not signicantly dierences
between EMR groups. IL-1β level was signicantly increased at
brain stem in EMR group compared to control group. EMR in
terms of IL-1β levels most aected group was 900 MHz. There
were severe degenerative changes, shrunken cytoplasm and
extensively dark pyknotic nuclei and less neuron in the EMR
groups compared to control groups. The most aected EMR
group was the 2450 MHz group. In the frontal cortex and
brain stem of the EMR groups, caspase-3 immunoreactivity
was increased compared to the control group. The most
aected group was again the 2450 MHz group.
DECLARATION of INTEREST
This study was supported by the Turkish Neurosurgery
Society Scientic Research Committee. The authors alone are
responsible for the content and writing of the paper.
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