Protective Effect of Alpha Lipoic Acid on Rat Sciatic Nerve Ischemia Reperfusion Damage.

BACKGROUND: Alpha lipoic acid is a potent antioxidant that plays numerous roles in human health. This study examined the effect of ALA on rat sciatic nerve ischemia reperfusion damage. AIMS: Protective effect of alpha lipoic acid (ALA) on sciatic nerve following ischemia-reperfusion in rats was investigated by using light microscopy and biochemical methods. Provided that the protective effect of ALA on sciatic nerve is proven, we think the damage to the sciatic nerve that has already occurred or might occur in patients for various reasons maybe prevented or stopped by giving ALA in convenient doses. STUDY DESIGN: Animal experiment. METHODS: Forty-two adult male Sprague-Dawley rats (250-300 grams) were used in this study. Rats were randomly divided into six groups including one control (Group 1), one sham (Group 2), two ischemia-reperfusion (Groups 3 and 4) and two treatment groups (Groups5 and 6). Doses of 60 and 100 mg/kg ALA were given (Group 5 and 6) intra peritoneally twice, 1 and 24 hours before the ischemia to each treatment group. Ischemia was carried out the abdominal aorta starting from the distal part of the renal vein for two hours followed by reperfusion for three hours. In immunohistochemical methods, fibronectin immunoreactivity was analyzed. For biochemical analyses, the tissues were taken in eppendorf microtubes and superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) enzyme activities as well as malondialdehyde (MDA) and nitricoxide (NO) levels were measured. RESULTS: Fibronectin was observed to have increased significantly in the ischemia group; on the other hand, it was observed to have decreased in parallel to the doses in the ALA groups. Biochemical studies showed that SOD and GSHPx declined with ischemia-reperfusion, but the activities of these enzymes were increased in the treatment groups in parallel with the dose. It was found that increased MDA levels with ischemia-reperfusion were decreased in parallel with ALA dose. There were no statistically significant changes in NO. CONCLUSION: Increased fibronectin observed after ischemia/reperfusion of rat sciatic nerve is reduced after the administration of ALA. This indicates that the function of fibronectin, to reconnect cut nerve segments and regenerate nerves, is more prominent than its function in tissue healing after ischemia. ALA administered before ischemia decreases MDA and increases SOD and GSHPx. We think that ALA may protect against the pathological changes in ischemic nerve and may be used to devise more efficient treatments.

Association analyses of depression, anxiety, and physical fitness parameters in Turkish obese adults.

OBJECTIVE: This study aims to investigate the associations among depression, anxiety, aerobic exercise capacity, body fat percentage, sum of skinfolds, abdomen circumference, and waist to hip ratio on the basis of body mass index (BMI) in adults. METHODS: The subjects of the study were 60 obese participants (30 women, 30 men) with BMIs over 30 kg/m{2}and 60 healthy controls (30 women, 30 men) with BMIs of 18-25 kg/m{2}. Body fat percentage was calculated from the skinfold thicknesses using the formula. Body circumference measurements were performed using a tape measure. Maximal aerobic capacity (VO(2)max) was determined by Astrand submaximal exercise protocol. Two self-reported questionnaires, Beck Depression Inventory (BDI) and Beck Anxiety Inventory (BAI), were administered to all participants. RESULTS: BMI, body fat percentage, sum of skinfolds, abdomen circumference, and waist to hip ratio were found to be higher in obese groups as compared to the controls, while VO(2)max (ml/kg/min) values were lower in both genders. In males, BAI scores and mild-level anxiety percentage values were higher in the obese group than in the control group. There was no significant difference for BDI scores and levels between the obese and control groups in both genders. There was also no significant difference in BAI scores and levels between the obese and control groups in women. CONCLUSION: The fact that physical fitness being found poor in obese shows the existence of a condition that might constitute an increased tendency for obesity-related disorders. In addition, it was suggested that, in Turkey, attitudes toward obesity change depending on gender.

The protective effect of avocado soybean unsaponifilables on brain ischemia/reperfusion injury in rat prefrontal cortex.

OBJECT: We investigated the protective effects of avocado/soybean unsaponifiables (ASU) on the prefrontal cortex (PFC) after global brain ischemia/reperfusion (I/R) injury in rats. METHODS: Rats were randomly divided into three experimental groups as follows: Group I was control rats, Group II was ischemia rats, Group III was Isch + ASU rats. Brain ischemia was produced via four-vessel occlusion model. These processes followed by reperfusion for 30 min for both II and III groups. Rats were sacrificed and their brains were removed immediately. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in left PFC, levels of TNF-α concentration were measured in the plasma. The number of apoptotic neurons was assayed in histological samples of the right PFC. RESULTS: MDA and TNF-α levels as well as the number of apoptotic neurons were observed to have decreased significantly in Group III compared to Group II, while SOD activities have been found to have increased significantly in Group III in comparison to Group II, significantly. CONCLUSIONS: We think that ASU might have an antioxidant and neuroprotective effects in brain I/R injured rats.

Novel approach for the prevention of contrast nephropathy.

OBJECTIVE: To date, there is no effective treatment of contrast medium (CM)-induced nephropathy. Multiple studies documented a protective role of hydration and N-acetylcystein (NAC) as prophylactic agents against CM-induced nephropathy in a high-risk population. In the present study, we investigated a new antioxidant agent, caffeic acid phenethyl ester (CAPE), and compare with NAC against contrast nephropathy. METHODS: Forty-two adult male rats were divided into six experimental groups, which were control, injected with intravenous (i.v.) CM, injected with i.p. CAPE, injected with i.p. NAC, injected with i.v. CM pretreated with i.p. CAPE, injected with i.v. CM pretreated with i.p. NAC. CAPE and NAC were given daily throughout the study. All rats were deprived of water for 24h at the third day of the study and then contrast medium was administered to CM, CAPECM and NACCM groups. The rats were sacrificed at the fifth day. Oxidant-antioxidant status was determined in renal tissues. The severity of injury was scored with a light microscope in renal tissue. Plasma creatinine levels were measured. RESULTS: Renal injury scores were higher in CAPECM and NACCM groups than in control, CAPE and NAC groups, but lower than the CM group. Likewise, creatinine levels of CAPECM and NACCM groups were higher than the control groups but they were significantly lower than the level of the CM group. Creatinine levels of the NACCM group were significantly higher than the CAPECM group. Malondialdehyde levels were significantly lower in CAPECM and NACCM groups than the CM group. CONCLUSION: CAPE might protect renal structure and functions as well as NAC against CM injury.

The protective effect of fish n-3 fatty acids on cerebral ischemia in rat prefrontal cortex.

This study presents neuroprotective effects of fish n-3 EFA on the prefrontal cortex after cerebral ischemia and reperfusion. Eighteen rats divided into three groups. Group A rats were used as control. Cerebral ischemia and reperfusion was produced in rats either on a standard diet (Group B) or a standard diet plus fish n-3 EFA for 14 days (Group C). The malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD) and catalase (CAT) were measured and the number of apoptotic neurons was counted. The levels of MDA and activities of SOD increased in Group B rats as compared to Group A rats, and decreased in Group C rats as compared to Group B rats. The activities of CAT increased in Group C as compared to Group B rats. The number of apoptotic neurons in the prefrontal cortex was lower in Group C as compared to Group B rats.

The influence of dexmedetomidine on ischemic rat hippocampus.

In our study, we evaluated the neuroprotective effects of dexmedetomidine on oxidant-antioxidant systems, pro-inflammatory cytokine TNF-alpha and number of apoptotic neurons on hippocampus and dentate gyrus after transient global cerebral I/R injury. Eighteen rats divided into 3 groups, equally. Group I rats were used as shams. For group II and III rats, they were prepared for transient global cerebral ischemia using a four-vessel-occlusion model. 5 mL/kg/h 0.9% sodium chloride was infused to the Group II and 3 microg/kg/h/5 ml dexmedetomidine was infused to the Group III for 2 h after I/R injury. The levels of MDA and NO and activities of SOD and CAT were measured in the left hippocampus tissue. The levels of TNF-alpha concentration were measured in the plasma. The number of apoptotic neurons was counted by TUNNEL method in histological samples of right hippocampus tissue. MDA and NO levels increased in Group II compared with Group I rats (p=0.002, p=0.002, respectively). In group III, MDA and NO levels decreased as compared to Group II (p=0.015, p=0.002, respectively). SOD and CAT activities increased in Group III as compared to Group II rats (p=0.002, p=0.002, respectively). The decrease in TNF-alpha levels of group III was significant as compared to group II (p=0.016). The number of apoptotic neurons in group III was lower than Group II rats. Our study showed that dexmedetomidine has a neuroprotective effect on hippocampus and dentate gyrus of rats after transient global cerebral I/R injury.

The neuroprotective effects of caffeic acid phenethyl ester (CAPE) in the hippocampal formation of cigarette smoke exposed rabbits.

BACKGROUND: In this study, the neuroprotective effects of caffeic acid phenethyl ester (CAPE) in the hippocampus of cigarette smoke exposed rabbits were investigated. MATERIALS AND METHODS: Eighteen rabbits were used as experimental subjects and divided into three equal groups. The control group (Group A) was exposed to clean air. Rabbits in the cigarette smoke (CS) group (Group B) were exposed to cigarette smoke 1 hour daily in a room within a glass chamber for 4 weeks. Animals in the CS+CAPE group (Group C) were exposed to cigarette smoke as in Group B and administered CAPE (10 micromol/kg/day) intraperitoneally for 4 weeks just before the exposure to cigarette smoke. Rabbits in all three groups were sacrificed with intraperitoneal administration of 100 mg/kg sodium pentothal and their brains were removed immediately. In the hippocampal formation samples of left hemispheres, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured and the number of apoptotic neurons was counted by 'terminal transferase dUTP nick end labelling' (TUNEL) assay in the right hippocampal formation. RESULTS: We found that MDA levels increased significantly in the Group B rabbits compared with the control group (Group A; p = 0.001). In contrast, SOD activities decreased significantly in Group B rabbits compared with the control group (p = 0.001). In the CAPE treated rabbits (Group C), MDA levels decreased and SOD activities increased significantly as compared with Group B rabbits (p = 0.002, p = 0.002, respectively). The number of apoptotic neurons (TUNEL+) in the CA1, CA2, CA3 and dentate gyrus areas of rabbits' hippocampal formation were significantly increased in Group B rabbits compared with the control group. On the other hand, the number of apoptotic neurons in the hippocampus areas was decreased significantly in Group C rabbits compared with Group B rabbits. CONCLUSION: These findings suggest that cigarette smoking induces apoptosis in the hippocampal formation of rabbits and CAPE has a protective role against this induction.

Oral administration of avocado soybean unsaponifiables (ASU) reduces ischemic damage in the rat hippocampus.

BACKGROUND: The beneficial effects of avocado/soybean unsaponifiables (ASU) are known as an antiarthritic agent. This experimental study presents the effects of ASU on oxidant/antioxidant systems and the number of apoptotic neurons of hippocampal formation after ischemia and reperfusion. METHODS: Eighteen rats were divided into three equal groups: group I rats were used as controls; group II rats were fed with standard diet and group III rats were fed with standard diet plus ASU pills for 10 days. One day after electrocauterization of bilateral vertebral arteries for groups II and III, bilateral common carotid arteries were occluded for 30 min and then reperfused for 30 min. After these procedures, rats of all groups were sacrificed. The levels of malondialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in the left hippocampus. The number of apoptotic neurons was counted by Tunel method in histological samples of right hippocampus. RESULTS: MDA and NO levels increased in group II compared with group I rats (p = 0.002, p = 0.015). In group III, MDA and NO levels decreased as compared to group II (p = 0.041, p = 0.002). SOD and CAT activities increased in group III as compared to group II rats (p = 0.002, p = 0.002). The number of apoptotic neurons was lower in group III as compared to group II rats. CONCLUSIONS: The present findings suggest that ASU could decrease oxidative stress and apoptotic changes in ischemic rat hippocampus. Dietary supplementation of ASU may be beneficial to prevent or ameliorate ischemic cerebral vascular disease.

Protective effects of erdosteine on doxorubicin-induced hepatotoxicity in rats.

BACKGROUND: Oxidative stress has an important role in the pathogenesis of doxorubicin-induced hepatotoxicity. The aim of this study was to investigate the hepatoprotective effects of erdosteine, an antioxidant agent, on doxorubicin-induced hepatotoxicity. METHODS: Rats were divided into control, doxorubicin alone (20 mg/kg, i.p.) and doxorubicin plus erdosteine (50 mg/kg/day, oral) groups. At the end of the 10(th) day, liver tissues were removed for light microscopy and analysis. The levels of tissue protein carbonyl content, malondialdehyde and nitric oxide, as well as the activities of superoxide dismutase, catalase, were determined. RESULTS: The tissue of the doxorubicin group showed some histopathological changes such as necrosis, hepatocyte degeneration, sinusoidal dilatation, hemorrhage and vascular congestion and dilatation. In the doxorubicin plus erdosteine group, histopathological evidence of hepatic damage was markedly reduced. Biochemical parameters were consistent with histological parameters. CONCLUSIONS: Doxorubicin caused hepatotoxicity, and erdosteine treatment prevented lipid peroxidation and protein oxidant in liver tissue.

Lung toxicity of nitrogen mustard may be mediated by nitric oxide and peroxynitrite in rats.

Nitric oxide (NO) has previously been shown to be responsible for nitrogen mustard (NM)-induced tissue toxicity. Excessive amounts of NO are known to be able to produce peroxynitrite, an important reactive nitrogen compound, by reacting with superoxide. Previous studies reported that NO synthase inhibitors are able to prevent NM toxicity. The aim of this study was to evaluate whether peroxynitrite is also responsible for NM-induced lung tissue damage in rats. Wistar rats were divided into four groups. NM was injected intratracheally and was treated with the selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG) (intraperitoneal) or the peroxynitrite scavenger ebselen (intragastric). Control animals were exposed to saline only. NM injection caused both oxidative and nitrosative stress, reflected by dramatically increased levels of the lipid peroxidation end product malondialdehyde (MDA), iNOS activation and urine nitrite-nitrate (NOx) values. Histopathological evaluation demonstrated lung damage with NM exposure. AG blocked iNOS activation and decreased urine NOx levels, and resulted in less histopathological changes in the lung. Although the histopathological outcome was found to be similar to AG, ebselen did not change urinary NOx or lung iNOS levels. Furthermore, ebselen was more able than AG to protect against MDA accumulation. In conclusion, the ability of ebselen to prevent against lung damage without blocking NO synthesis suggests that peroxynitrites may have an important role in the pathogenesis of NM toxicity in addition to NO.

Antioxidant effects of melatonin in rats during chronic exposure to hyperbaric oxygen.

In addition to its beneficial effects, hyperbaric oxygen (HBO) exposure causes some detrimental effects via oxidative stress. Previous experimental studies showed that melatonin is a useful agent to block single session HBO-induced oxidative stress. In the present study, we investigated the antioxidant effect of exogenously administered as well as endogenously produced melatonin in lung and brain tissues of rats exposed to long term HBO. The HBO procedure was set as daily exposures to 2.5 ATA of oxygen for 1 hr and a total of 10 sessions. Twenty-eight male Sprague-Dawley rats were divided into four groups as follows: control, daytime HBO, daytime HBO plus melatonin (5 mg/kg), nighttime HBO. Tissue oxidative/antioxidant status was examined by determining the protein carbonyl content as a criteria for oxidative stress and the activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). HBO exposure for 10 days caused significant increases in protein carbonyl content and SOD levels of lung and brain, but GSH-Px activities remained unaffected. The increases in protein carbonyls were blocked by exogenously administered melatonin and in part by nighttime exposure to darkness whereas the increase of SOD activity was only impeded by endogenously produced melatonin in brain tissue. Lung SOD activity was augmented by endogenous melatonin. In conclusion, melatonin blocks long-term HBO-induced cumulative oxidative stress as indicated changes in protein carbonyls. Both exogenously injected and physiologically secreted melatonin has this potential. The effects of HBO-exposure and melatonin on the activities of the antioxidative enzymes are less clear.

The protective effect of fish n-3 fatty acids on cerebral ischemia in rat hippocampus.

Reactive oxygen species (ROS) have been implicated in the pathogenesis of cerebral injury after ischemia-reperfusion (I/R). Fish n-3 essential fatty acids (EFA), contain eicosapentaenoic acids (EPA) and docosahexoenoic acids (DHA), exhibit antioxidant properties. DHA is an important component of brain membrane phospholipids and is necessary for the continuity of neuronal functions. EPA prevents platelet aggregation and inhibits the conversion of arachidonic acid into thromboxane A(2) and prostaglandins. They have been suggested to be protective agents against neurological and neuropsychiatric disorders. In this study, the neuroprotective effects of fish n-3 EFA on oxidant-antioxidant systems and number of apoptotic neurons of the hippocampal formation (HF) subjected to cerebral I/R injury was investigated in Sprague-Dawley rats. Six rats were used as control (Group I). Cerebral ischemia was produced by occlusion of both the common carotid arteries combined with hypotension for 45 min, followed by reperfusion for 30 min, in rats either on a standard diet (Group II) or a standard diet plus fish n-3 EFA (Marincap((R)), 0.4 g/kg/day, by gavage) for 14 days (Group III). At the end of procedures, the rats were sacrificed and their brains were removed immediately. The levels of malonedialdehyde (MDA) and nitric oxide (NO) and activities of superoxide dismutase (SOD) and catalase (CAT) were measured in left HF. In addition, the number of apoptotic neurons was counted by terminal transferase dUTP nick end labelling (TUNEL) assay in histological samples of the right HF. We found that SOD activities and MDA levels increased in Group III rats compared with Group II rats. On the other hand, CAT activities and NO levels were found to be decreased in Group III rats compared with Group II rats. Additionally, the number of apoptotic neurons was lower in Group III in comparison with Group II rats. The present findings suggest that fish n-3 EFA could decrease the oxidative status and apoptotic changes in ischemic rat hippocampal formation. Dietary supplementation of n-3 EFA may be beneficial to preserve or ameliorate ischemic cerebral vascular disease.

Melatonin modulates 900 Mhz microwave-induced lipid peroxidation changes in rat brain.

Microwaves (MW) from cellular phones may affect biological systems by increasing free radicals, which may enhance lipid peroxidation levels of the brain, thus leading to oxidative damage. Melatonin is synthesized in and secreted by the pineal gland at night and exhibits anti-oxidant properties. Several studies suggest that supplementation with anti-oxidant can influence MW-induced brain damage. The present study was designed to determine the effects of MW on the brain lipid peroxidation system, and the possible protective effects of melatonin on brain degeneration induced by MW. Twenty-eight Sprague-Dawley male rats were randomly divided into three groups as follows: (1) sham-operated control group (N = 8); (2) study 900-MHz MW-exposed group (N = 8); and (3) 900-MHz MW-exposed+melatonin (100 microg/kg sc before daily MW exposure treated group) (N = 10). Cortex brain and hippocampus tissues were removed to study the levels of lipid peroxidation as malonyl dialdehyde. The levels of lipid peroxidation in the brain cortex and hippocampus increased in the MW group compared with the control group, although the levels in the hippocampus were decreased by MW+melatonin administration. The brain cortex lipid peroxidation levels were unaffected by melatonin treatment. We conclude that melatonin may prevent MW-induced oxidative changes in the hippocampus by strengthening the anti-oxidant defense system, by reducing oxidative stress products.

Caffeic acid phenethyl ester prevents cadmium-induced cardiac impairment in rat.

Caffeic acid phenethyl ester (CAPE), a flavonoid like compound, is one of the major components of honeybee propolis. It was found to be a potent free radical scavenger and antioxidant recently. The aim of this study was to examine the effect of CAPE on cadmium (Cd)-induced hypertension and cardiomyopathy in rats. In particular, nitric oxide (NO) may contribute to the pathophysiology of Cd induced cardiac impairment. Malondialdehyde (MDA, an index of lipid peroxidation) levels and nitric oxide (NO, a vasodilator) levels were used as markers Cd-induced cardiac impairment and the success of CAPE treatment. Also, the findings have been supported by the histopathologic evidences. The rats were randomly divided into three experimental groups each (12), as follows: the control group, Cd-treated group (Cd) and Cd plus CAPE-treated group (Cd+CAPE). CdCl(2) in 0.9% NaCl was administrated intraperitoneally (i.p.) with a dose of 1mg/kg/day. CAPE was co-administered i.p. a dose of 10 microM/kg for 15 days. Hypertension was found to be induced by intraperitoneal administration of Cd in a dose of 1mg/kg/day on the measurements taken 15 days later. MDA levels were increased (p<0.001) in cardiac tissue and NO levels were decreased (p<0.05) in serum in the Cd group than those of the control group had. On the other hand, there was a slight difference (increase) in MDA levels in the Cd+CAPE group than the ones in the control group (p<0.003). In addition, MDA levels were decreased and NO levels were increased in the Cd+CAPE group compared with the Cd group (p<0.001, p<0.0001, respectively). As a result, treatment with CAPE significantly reversed the increased lipid peroxidation (LPO) product, MDA, and decreased NO levels in Cd treated animals. In the histopathologic examination, a significant hypertrophy in atrial and ventricular myofibrils was observed in only Cd administered group, in comparison with the control group. There was no statistically significant difference between the CAPE given and control groups by means of atrial and ventricular myofibril diameters. In conclusion, the underlying mechanism of the myocardial hypertrophy may be related to hypertension due to inhibition of NO production in the vessels, and CAPE has a protective effect on Cd-induced hypertension mediated cardiac impairment in the rats.

Erythrocyte oxidant/antioxidant status in essential hyperhidrosis.

Essential hyperhidrosis is a disorder of excessive, bilateral, and relatively symmetric sweating occurring in the axillae, palms, soles, or craniofacial region without obvious etiology. Nitric oxide may play a physiological part in the production and/or excretion of sweat in skin eccrine glands. Tempol, a SOD mimetic, increases the half-life of NO and results in vasodilatation, hypotension, and reflex activation of sympathetic nervous system. Reactive oxygen species (ROS) may directly activate both central and peripheral sympathetic nervous system activity. We assessed the levels of malondialdehyde (MDA), the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) of red blood cells in patients with essential hyperhidrosis (n = 31) compared to age-and sex-matched healthy controls (n = 28). Erythrocyte activities of SOD and level of MDA were detected significantly higher (p = 0.020, p = 0.004 and respectively) and activities of CAT and GSH-Px were significantly lower (p = 0.0001, p = 0.0001 respectively) in patients than controls. Our results support the hypothesis that oxidative damage resulting from increased ROS production along with insufficient capacity of antioxidant mechanisms may be involved in pathogenesis of EH.

No effects of 900 MHz and 1800 MHz electromagnetic field emitted from cellular phone on nocturnal serum melatonin levels in rats.

In this study, the effects of exposure to a 900 MHz and 1800 MHz electromagnetic field (EMF) on serum nocturnal melatonin levels of adult male Sprague-Dawley rats were studied. Thirty rats were used in three independent groups, 10 of which were exposed to 900 MHz, 10 of which were exposed to 1800 MHz and 10 of which were sham-exposed (control). The exposures were performed 30 min/day, for five days/week for four weeks to 900 MHz or 1800 MHz EMF Control animals were kept under the same environmental conditions as the study groups except with no EMF exposure. The concentration of nocturnal melatonin in the rat serum was measured by using a radioimmunoassay method. There were no statistically significant differences in serum melatonin concentrations between the 900 MHz EMF group and the sham-exposed group (P > 0.05). The values at 12:00 pm were 39.11 +/- 6.5 pg/mL in the sham-exposed group and 34.97 +/- 5.1 pg/mL in the 900 MHz EMF-exposed group. Also, there were no statistically significant differences in serum melatonin concentrations between the sham-exposed group and the 1800 MHz EMF-exposed group (P > 0.05). The values at 12:00 pm were 39.11 +/- 6.5 pg/mL in the sham-exposed group and 37.96 +/- 7.4 pg/mL in the exposed group. These results indicate that mobile phones, emitting 900 and 1800 MHz EMF, have no effect on nocturnal serum melatonin levels in rats.

Oxidative damage in the kidney induced by 900-MHz-emitted mobile phone: protection by melatonin.

BACKGROUND: The mobile phones emitting 900-MHz electromagnetic radiation (EMR) may be mainly absorbed by kidneys because they are often carried in belts. Melatonin, the chief secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. The aim of this study was to examine 900-MHz mobile phone-induced oxidative stress that promotes production of reactive oxygen species (ROS) on renal tubular damage and the role of melatonin on kidney tissue against possible oxidative damage in rats. METHODS: The animals were randomly grouped as follows: 1) sham-operated control group and 2) study groups: i) 900-MHz EMR exposed (30 min/day for 10 days) group and ii) 900-MHz EMR exposed+melatonin (100 microg kg(-1) s.c. before the daily EMR exposure) treated group. Malondialdehyde (MDA), an index of lipid peroxidation), and urine N-acetyl-beta-d-glucosaminidase (NAG), a marker of renal tubular damage were used as markers of oxidative stress-induced renal impairment. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status. RESULTS: In the EMR-exposed group, while tissue MDA and urine NAG levels increased, SOD, CAT, and GSH-Px activities were reduced. Melatonin treatment reversed these effects as well. In this study, the increase in MDA levels of renal tissue and in urine NAG and also the decrease in renal SOD, CAT, GSH-Px activities demonstrated the role of oxidative mechanism induced by 900-MHz mobile phone exposure, and melatonin, via its free radical scavenging and antioxidant properties, ameliorated oxidative tissue injury in rat kidney. CONCLUSIONS: These results show that melatonin may exhibit a protective effect on mobile phone-induced renal impairment in rats.

Effects of 900 MHz electromagnetic field on TSH and thyroid hormones in rats.

In this study, the effects of exposure to a 900 megahertz (MHz) electromagnetic field (EMF) on serum thyroid stimulating hormone (TSH) and triiodothronine-thyroxin (T3-T4) hormones levels of adult male Sprague-Dawley rats were studied. Thirty rats were used in three independent groups, 10 of which were control (without stress and EMF), 10 of which were exposed to 900 MHz EMF and 10 of which were sham-exposed. The exposures were performed 30 min/day, for 5 days/week for 4 weeks to 900 MHz EMF. Sham-exposed animals were kept under the same environmental conditions as the study groups except with no EMF exposure. The concentration of TSH and T3-T4 hormones in the rat serum was measured by using an immunoradiometric assay (IRMA) method for TSH and a radio-immunoassay (RIA) method for T3 and T4 hormones. TSH values and T3-T4 at the 900 MHz EMF group were significantly lower than the sham-exposed group (p<0.01). There were no statistically significant differences in serum TSH values and T3-T4 hormone concentrations between the control and the sham-exposed group (p>0.05). These results indicate that 900 MHz EMF emitted by cellular telephones decrease serum TSH and T3-T4 levels.

Oxidative stress-mediated skin damage in an experimental mobile phone model can be prevented by melatonin.

Most mobile phones emit 900 MHz of radiation that is mainly absorbed by the external organs. The effects of 900 MHz of radiation on fibrosis, lipid peroxidation, and anti-oxidant enzymes and the ameliorating effects of melatonin (Mel) were evaluated in rat skin. Thirty Wistar-Albino rats were used in the study. The experimental groups were the control group, the irradiated group (IR), and the irradiated+Mel treated group (IR+Mel). A dose of 900 MHz, 2 W radiation was applied to the IR group every day for 10 days (30 min/day). The IR+Mel group received 10 mg/kg/day melatonin in tap water for 10 days before the irradiation. At the end of the 10th day, a skin specimen was excised from the thoracoabdominal area. The levels of malondialdehyde (MDA) and hydroxypyroline and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were studied in the skin samples. MDA and hydroxyproline levels and activities of CAT and GSH-Px were increased significantly in the IR group compared to the control group (p<0.05) and decreased significantly in the IR+Mel group (p<0.05). SOD activity was decreased significantly in the IR group and this decrease was not prevented by the Mel treatment. These results suggest that rats irradiated with 900 MHz suffer from increased fibrosis and lipid peroxidation (LPO). Mel treatment can reduce the fibrosis and LPO caused by radiation.

Prevention of mobile phone induced skin tissue changes by melatonin in rat: an experimental study.

Most of the mobile phones in Turkey emit 900 MHz radiation which is mainly absorbed by the skin and, to a lesser extent, muscle. The aim of this study was to investigate the effects the 900 MHz electromagnetic irradiation emitted by these devices on the induction of histopathologic changes in skin and the effect of melatonin (Mel) on any of these changes. Thirty male Wistar-Albino rats were used in the study. The experimental groups were composed of: a nontreated control group, an irradiated group (IR) without Mel and an irradiated with Mel treatment group (IR + Mel). 900 MHz radiation was applied to IR group for 10 days (30 min/day). The IR + Mel group received 10 mg/kg per day melatonin in tap water for 10 days before irradiation. At the end of the tenth day, the skin graft was excized from the thoraco-abdominal area. Histopathologic changes in skin were analyzed. In the IR group, increased thickness of stratum corneum, atrophy of epidermis, papillamatosis, basal cell proliferation, increased granular cell layer (hypergranulosis) in epidermis and capillary proliferation, impairment in collagen tissue distribution and separation of collagen bundles in dermis were all observed compared to the control group. Most of these changes, except hypergranulosis, were prevented with melatonin treatment. In conclusion, exposure to 900 MHz radiation emitted by mobile phones caused mild skin changes. Furthermore, melatonin treatment can reduce these changes and may have a beneficial effect to prevent 900 MHz mobile phone-induced rat skin changes.