Effects of 3.5-GHz radiofrequency radiation on energy-regulatory hormone levels in the blood and adipose tissue.

In recent years exposure of living beings to radiofrequency radiation (RFR) emitted from wireless equipment has increased. In this study, we investigated the effects of 3.5-GHz RFR on hormones that regulate energy metabolism in the body. Twenty-eight rats were divided into four groups: healthy sham (n = 7), healthy RFR (n = 7), diabetic sham (n = 7), and diabetic RFR (n = 7). Over a month, each group spent 2 h/day in a Plexiglas carousel. The rats in the experimental group were exposed to RFR, but the sham groups were not. At the end of the experiment, blood and adipose tissues were collected from euthanized rats. Total antioxidant, total oxidant, hydrogen peroxide, ghrelin, nesfatin-1, and irisin were determined. Insulin expression in pancreatic tissues was examined by immunohistochemical analysis. Whole body specific absorption rate was 37 mW/kg. For the parameters analyzed in blood and fat, the estimated effect size varied within the ranges of 0.215-0.929 and 0.503-0.839, respectively. The blood and adipose nesfatin-1 (p = 0.002), blood and pancreatic insulin are decreased, (p = 0.001), gherelin (p = 0.020), irisin (p = 0.020), and blood glucose (p = 0.040) are increased in healthy and diabetic rats exposed to RFR. While nesfatin-1 are negatively correlated with oxidative stress, hyperglycemia and insulin, ghrelin and irisin are positively correlated with oxidative stress and hyperglycemia. Thus, RFR may have deleterious effects on energy metabolism, particularly in the presence of diabetes.

Adverse effects of 900, 1800 and 2100 MHz radiofrequency radiation emitted from mobile phones on bone and skeletal muscle.

The goal of this study was to biomechanically and morphologically research both the impact of mobile phone like radiofrequency radiations (RFR) on the tibia and the effects on skeletal muscle through oxidative stress parameters. Fifty-six rats (200-250 g) were put into groups: healthy sham (n = 7), healthy RFR (900, 1800, 2100 MHz) (n = 21), diabetic sham (n = 7) and diabetic RFR (900, 1800, 2100 MHz) (n = 21). Over a month, each group spent two hours/day in a Plexiglas carousel. The rats in the experimental group were exposed to RFR, but the sham groups were not. At the end of the experiment, the right tibia bones and skeletal muscle tissue were removed. The three-point bending test and radiological evaluations were performed on the bones, and CAT, GSH, MDA, and IMA in muscles were measured. There were differences in biomechanics properties and radiological evaluations between the groups (p < .05). In the measurements in the muscle tissues, significant differences were statistically found (p < .05). The average whole-body SAR values for GSM 900, 1800 and 2100 MHz were 0.026, 0.164, and 0.173 W/kg. RFRs emitted from mobile phone may cause adverse effects on tibia and skeletal muscle health, though further studies are needed.

Effects of 3.5 GHz radiofrequency radiation on ghrelin, nesfatin-1, and irisin level in diabetic and healthy brains.

Diabetes, mobile phone use, and obesity have increased simultaneously in recent years. The radiofrequency radiation (RFR) emitted from mobile phones is largely absorbed in the heads of users. With 5 G, which has started to be used in some countries without the necessary precautions being taken, the amount of RFR to which living things are exposed will increase. In this study, the changes in energy homeostasis and redox balance caused by 5 G (3.5 GHz, GSM-modulated) were explored. The effects of RFR on the brains of diabetic and healthy rats were investigated and histopathological analysis was performed. Twenty-eight Wistar albino rats weighing 200-250 g were divided into 4 groups as sham, RFR, diabetes, and RFR+diabetes groups (n = 7). The rats in each group were kept in a plexiglass carousel for 2 h a day for 30 days. While the rats in the experimental groups were exposed to RFR for 2 h a day, the rats in the sham group were kept under the same experimental conditions but with the radiofrequency generator turned off. At the end of the experiment, brain tissues were collected from euthanized rats. Total antioxidant (TAS), total oxidant (TOS), hydrogen peroxide (H2O2), ghrelin, nesfatin-1, and irisin levels were determined. In addition, histopathological analyses of the brain tissues were performed. The specific absorption rate in the gray matter of the brain was calculated as 323 mW/kg and 195 mW/kg for 1 g and 10 g averaging, respectively. After RFR exposure among diabetic and healthy rats, decreased TAS levels and increased TOS and H2O2 levels were observed in brain tissues. RFR caused increases in ghrelin and irisin and a decrease in nesfatin-1 in the brain. It was also observed that RFR increased the number of degenerated neurons in the hippocampus. Our results indicate that 3.5 GHz RFR causes changes in the energy metabolism and appetite of both healthy and diabetic rats. Thus, 5 G may not be innocent in terms of its biological effects, especially in the presence of diabetes.

Effects of mobile phone exposure on biochemical parameters of cord blood: A preliminary study.

The purpose of this study is to investigate foetal impact of radiofrequencies (RFs) emitted from mobile phones in postnatal cord blood. The study carried on 149 pregnant women divided into four groups such as nonusers of mobile phone (n: 37; control group), 2-15 min/d (n: 39; group 1), 15-60 min/d (n: 37; group 2) and participants using mobile phone for more than 60 min/d (n: 36; group 3). Cord blood of the infants was taken in all groups for biochemical analyses immediately after birth. The results of the study showed that the biggest foetal impact was observed in the third study group which was pregnant exposed RFRs (RF radiation) more than 1 h/d (1 hour per day). AST (aspartat aminotransferaz), ALT (alanine aminotransferase), LDH (lactate dehydrogenase), CK (creatine kinase), CK-MB (creatine kinase-miyocardial band), CRP (c-reactive protein), PCT (procalcitonin), TnT (troponin T), uric acid and lactate levels of third group were found higher than the other groups (p < 0.001). However, Mean platelet volume values of third group were found lower than the other groups (p < 0.001). Finally, this is the first human study which was performed on pregnant and infants because there is no previous work in this area. However, the results of this study revealed that long-term RFR exposure of pregnant may result in some biochemical changes in the infants. Therefore, our suggestion to pregnant is to avoid from RFR exposure emitted from mobile phones at least during pregnancy.

Effects of shock waves on oxidative stress in parotid gland of rat.

This study was designed to investigate whether extracorporeal shock wave lithotripsy (ESWL) exposure to parotid gland produces an oxidative stress in parotid glands of rats. Twelve male Wistar-albino rats, 6 months of age with an average body weight of 250-300 g, were divided randomly into two groups, each consisting of six rats. The animals in the first group did not receive any treatment and served as control. The left parotid glands of animals in group 2 (ESWL treated) received a thousand 18 kV shock waves after anesthetizing the rats with 50 mg/kg of ketamine. The animals in both groups were killed 72 hours after the ESWL treatment, and the parotid glands were harvested for the determination of lipid peroxidation product malondialdehyde (MDA), antioxidant glutathione (GSH) levels and the activities of antioxidant enzymes such as superoxide dismutase (SOD), GSH-Px and catalase (CAT). It was found that MDA level increased in parotid glands of rats after the ESWL treatment. The SOD, GSH-Px and CAT enzyme activities, and the level of antioxidant GSH decreased in parotid gland of rats after the ESWL treatment. It was concluded that short-term ESWL treatment caused an increase in the free radical production and a decrease in the antioxidant enzyme activity in parotid glands of ESWL-treated rats.

Effect of short-term treatment with levosimendan on oxidative stress in renal tissues of rats.

The aim of this study is to evaluate the influences of short-term treatment with levosimendan (chemical formula: C14H12N6O) on oxidative stress and some trace element levels in renal tissues of healthy rats. A total of 20 male Wistar-albino rats were randomly divided into two groups, each consisting of 10 rats. Animals in the first group were not treated with levosimendan and served as control. Animals in the second group were injected intraperitoneally with 12 µg/kg levosimendan and served as levosimendan group. Animals in both the groups were killed 3 days after the treatment, and their kidneys were harvested for the determination of tissue oxidant/antioxidant statues and trace element levels in renal tissues. The tissue malondialdehyde level was significantly (p < 0.001) lower in levosimendan group than in controls. The protective enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase and antioxidant glutathione level were significantly (p < 0.001) higher in levosimendan group than in controls. It was concluded that levosimendan reduced oxidative stress by avoiding lipid peroxidation and production of reactive oxygen species, and overactivating and/or increasing the protective antioxidant enzyme levels in renal tissues of rats. It is supposed that this experimental study provides beneficial data for clinicians in the management of renal tissue damage related to obstruction and/or ischemia.

The effects of levosimendan exposure on oxidant/antioxidant status and trace element levels in the pulmonary artery of rats.

We investigated both the effect of levosimendan and the role of oxidant/antioxidant status and trace element levels in the pulmonary artery of rats. Fourteen male Wistar albino rats were randomly divided into two groups of seven animals each. Group 1 was not exposed to levosimendan and served as a control. Levosimendan (12 µg/kg) diluted in 10 ml 0.9 % NaCl was administered intraperitoneally to group 2. Animals of both groups were killed after 3 days, and their pulmonary arteries were harvested to determine changes in tissue oxidant/antioxidant status and trace element levels. The animals in both groups were killed 72 h after the levosimendan exposure treatment, and pulmonary arteries were harvested to determine levels of the lipid peroxidation product MDA and the antioxidant GSH as well as the decreased activity of antioxidant enzymes such as SOD, GSH-Px and CAT. It was found that MDA levels increased in pulmonary artery tissues of rats after levosimendan administration. The GSH level decreased in the pulmonary artery of rats after levosimendan treatment. Co, Mn, Fe, Cd and Pb levels were significantly higher (P < 0.001) and Mg, Zn and Cu levels significantly lower (P < 0.001) in the levosimendan group compared to the control group. These results suggest that levosimendan treatment caused an increase in free radical production and a decrease in antioxidant enzyme activity in the pulmonary artery of levosimendan-treated rats. It also caused a decrease or increase in the levels of many minerals in the pulmonary artery, which is an undesirable condition for normal pharmacological function.

Effect of levosimendan injection on oxidative stress of rat myocardium.

This experiment was designed to investigate the effect of levosimendan injection on lipid peroxidation product malondialdehyde (MDA) and antioxidant glutathione (GSH) levels, and activities of antioxidant enzymes in myocardium of rats. Twenty male Wistar-albino rats were divided randomly into 2 study groups, each consisting of 10 rats. The animals in the first group were not treated with drug and served as control. It was found that the MDA and GSH levels decreased in levosimendan injected group. Superoxide dismutase, glutathione peroxidase, catalase and carbonic anhydrase enzyme activities were lower in levosimendan injected group than controls. It was concluded that lower tissue free radical level caused by levosimendan injection led to a lower antioxidant enzymes synthesis in the body and a decrease in the antioxidant enzyme activity and free radical scavenger level in myocardium of rat.

Investigation of the hepatoprotective effects of Sesame (Sesamum indicum L.) in carbon tetrachloride-induced liver toxicity.

More than 600 chemicals can cause damage in liver, one of which is carbon tetrachloride (CCl4). Hepatoprotective agents could prevent tissue damage and reduce morbidity and mortality rates; such agents may include alternative or folkloric treatments. We investigated sesame (Sesamum indicum L.) for its hepatoprotective effect in CCl4-induced experimental liver damage. To this end, 0.8 mg/kg of sesame fixed oil was provided intraperitoneally to rats whose livers were damaged by CCl4. Tissue and blood samples were taken at the end of the experiments and evaluated histologically and biochemically. Ballooning degenerations and an increase in lipid droplets in liver parenchyma and increases in serum alanine transaminase, aspartate transaminase, and bilirubin were found in the CCl4 group. Biochemical and histopathological findings in the sesame fixed oil treated group were not significantly different from the CCl4 group. Sesame did not show a hepatoprotective effect in CCl4-induced liver toxicity.

Analysis of the influences of short-term levosimendan exposure on oxidant/antioxidant status and trace-element levels in the physiological status of the thoracic aorta of rats.

The objective of this study was to evaluate the effect of levosimendan (chemical formula C14H12N6O) exposure on oxidant/antioxidant status and trace-element levels in the thoracic aorta of rats. Eighteen male Wistar albino rats were randomly divided into two groups of eight animals each. Group 1 was not exposed to levosimendan and served as a control. Levosimendan (12 µg/kg) diluted in 10 ml 0.5 % dextrose was administered intraperitoneally to group 2. Animals of both groups were killed after 3 days, and their thoracic aortae were harvested for determination of changes in tissue oxidant/antioxidant status and trace-element levels. The animals in both groups were killed 72 h after levosimendan exposure, and thoracic aortae were harvested for determination of the lipid peroxidation product MDA and antioxidant GSH levels and the activities of antioxidant enzymes such as SOD, GSH-Px and CAT. It was found that MDA, GSH and CAT enzyme levels increased in thoracic aortae of rats after levosimendan administration. SOD and CA enzyme activities and the level of antioxidant GSH decreased in thoracic aortae of rats after levosimendan treatment. Pb, Cd and Fe levels of thoracic aortae were significantly higher (P < 0.001) and Mg, Mn, Zn and Cu were significantly lower (P < 0.001) in the levosimendan group compared to the control group. These results suggest that short-term levosimendan treatment caused an increase in free radical production and a decrease in antioxidant enzyme activity in thoracic aortae of levosimendan-treated rats. It also causes a decrease or increase in many mineral levels of the thoracic aorta, which is an undesirable condition for normal pharmacological function.