Evaluation of multidrug resistance-1 gene C>T polymorphism frequency in patients with asthma.

OBJECTIVES: Asthma is a chronic inflammatory lung disease characterized by bronchial hyperresponsiveness and airflow obstruction. Genetic and oxidative stress factors, in addition to pulmonary and systemic inflammatory processes, play a pivotal role in the pathogenesis of asthma. The products of the multidrug resistance-1 gene protect lung tissue from oxidative stress. Here, we aimed to evaluate the association between the multidrug resistance-1 gene C>T polymorphism and asthma with regard to oxidative stress-related parameters of asthmatic patients. METHODS: Forty-five patients with asthma and 27 healthy age-matched controls were included in this study. Blood samples were collected in tubes with ethylenediaminetetraacetic acid. DNA was extracted from the blood samples. The multidrug resistance-1 gene polymorphism was detected by polymerase chain reaction and a subsequent enzyme digestion technique. The serum levels of total oxidant status and total antioxidant status were determined by the colorimetric measurement method. RESULTS: The heterozygous polymorphic genotype was the most frequent in both groups. A significant difference in the multidrug resistance-1 genotype frequencies between groups indicated an association of asthma with the TT genotype. A significant difference between groups was found for wild type homozygous participants and carriers of polymorphic allele participants. The frequency of the T allele was significantly higher in asthmatic patients. The increase in the oxidative stress index parameter was significant in the asthma group compared with the control group. CONCLUSIONS: The multidrug resistance-1 gene C/T polymorphism may be an underlying genetic risk factor for the development of asthma via oxidant-antioxidant imbalance, leading to increased oxidative stress.

The effect of ozone on blood pressure in DOCA-salt-induced hypertensive rats.

BACKGROUND: Hypertension is a risk factor for the cardiovascular diseases. Ozone as a therapeutic agent for the treatment of several disorders. We aimed to observe the effects of ozone on the blood pressure in DOCA-salt hypertensive rats. METHODS: Twenty three young Sprague Dawley male rats were divided into three groups; Control (C), Hypertension (H) and Hypertension + Ozone (HO). Hypertension was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly, 4 weeks, whereas intraperitoneal ozone was administered (1.1 mg/kg) for 10 days. Serum endothelin-1, nitric oxide and renin levels were measured with ELISA. Blood pressures were monitored using a tail cuff system. Endothelin-1, ET receptor A and ET receptor B mRNA expression in heart and vascular tissue were assessed by quantitative reverse transcription polymerase chain reaction. RESULTS: Blood pressure, serum endothelin-1 and ET receptor A mRNA expression levels were increased in H group, whereas serum renin, nitric oxide and ET receptor B mRNA expression levels in the heart and vascular tissue decreased compared with C and HO groups, which were counteracted by ozone treatment. CONCLUSION: Ozone treatment decreases blood pressure and is effective in preventing the progression of hypertensive disease, the mechanisms of which are associated with anti-vasoconstrictor effects through reducing the levels of serum endothelin-1 and ET receptor A mRNA expression in the heart and vascular tissue.

Different dose-dependent effects of ebselen in sciatic nerve ischemia-reperfusion injury in rats.

Ebselen is an organoselenium compound which has strong antioxidant and anti-inflammatory effects. We investigated the neuroprotective role of ebselen pretreatment in rats with experimental sciatic nerve ischemia-reperfusion (I/R) injury. Adult male Sprague Dawley rats were divided into four groups (N = 7 in each group). Before sciatic nerve I/R was induced, ebselen was injected intraperitoneally at doses of 15 and 30 mg/kg. After a 2 h ischemia and a 3 h reperfusion period, sciatic nerve tissues were excised. Tissue levels of malondialdehyde (MDA) and nitric oxide (NO), and activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were measured. Sciatic nerve tissues were also examined histopathologically. The 15 mg/kg dose of ebselen reduced sciatic nerve damage and apoptosis (p<0.01), levels of MDA, NO, and inducible nitric oxide synthase (iNOS) positive cells (p<0.01, p<0.05, respectively), and increased SOD, GPx, and CAT activities (p<0.001, p<0.01, p<0.05, respectively) compared with the I/R group that did not receive ebselen. Conversely, the 30 mg/kg dose of ebselen increased sciatic nerve damage, apoptosis, iNOS positive cells (p<0.01, p<0.05, p<0.001) and MDA and NO levels (p<0.05, p<0.01) and decreased SOD, GPx, and CAT activities (p<0.05) compared with the sham group. The results of this study suggest that ebselen may cause different effects depending on the dose employed. Ebselen may be protective against sciatic nerve I/R injury via antioxidant and antiapoptotic activities at a 15 mg/kg dose, conversely higher doses may cause detrimental effects.

Evaluation of multidrug resistance-1 gene C>T polymorphism frequency in patients with asthma

OBJECTIVES:Asthma is a chronic inflammatory lung disease characterized by bronchial hyperresponsiveness and airflow obstruction. Genetic and oxidative stress factors, in addition to pulmonary and systemic inflammatory processes, play a pivotal role in the pathogenesis of asthma. The products of the multidrug resistance-1 gene protect lung tissue from oxidative stress. Here, we aimed to evaluate the association between the multidrug resistance-1 gene C>T polymorphism and asthma with regard to oxidative stress-related parameters of asthmatic patients.METHODS:Forty-five patients with asthma and 27 healthy age-matched controls were included in this study. Blood samples were collected in tubes with ethylenediaminetetraacetic acid. DNA was extracted from the blood samples. The multidrug resistance-1 gene polymorphism was detected by polymerase chain reaction and a subsequent enzyme digestion technique. The serum levels of total oxidant status and total antioxidant status were determined by the colorimetric measurement method.RESULTS:The heterozygous polymorphic genotype was the most frequent in both groups. A significant difference in the multidrug resistance-1 genotype frequencies between groups indicated an association of asthma with the TT genotype. A significant difference between groups was found for wild type homozygous participants and carriers of polymorphic allele participants. The frequency of the T allele was significantly higher in asthmatic patients. The increase in the oxidative stress index parameter was significant in the asthma group compared with the control group.CONCLUSIONS:The multidrug resistance-1 gene C/T polymorphism may be an underlying genetic risk factor for the development of asthma via oxidant-antioxidant imbalance, leading to increased oxidative stress.

Visfatin and ghrelin: can they be forthcoming biomarkers or new drug targets for asthma?

BACKGROUND & AIM: Asthma represents chronic inflammation of the airways and is associated with bronchial hyperresponsiveness and reversible airway obstruction. A novel adipokine visfatin and an appetite-modulating hormone ghrelin play a role in several diseases related with inflammation. Although visfatin is a pro-inflammatory adipokine, ghrelin mainly exerts anti-inflammatory effects. However, very little is known about the role of visfatin and ghrelin in asthma. In the present study, we aimed to investigate the role of visfatin and ghrelin in asthma by evaluating their serum levels in asthmatic patients. MATERIALS AND METHODS: This study was performed on 27 asthma and 23 healthy controls. Blood samples were collected in tubes without EDTA. Serum levels of visfatin and ghrelin were measured by human ELISA assay kits. Statistical analyses were performed by SPSS 16.0 package program and differences were considered statistically significant at p < 0.05. RESULTS: Serum levels of visfatin and ghrelin were significantly higher in asthma group (respectively; p = 0.001, p = 0.002). CONCLUSION: While visfatin has a pro-inflammatory role, ghrelin exerts an anti-inflammatory effect in asthma. Therefore, visfatin can be a forthcoming biomarker and ghrelin may be a new anti-inflammatory drug target to diagnose and treat asthmatic patients.

Protective effects of simvastatin administered in the experimental hepatic ischemia-reperfusion injury rat model.

BACKGROUND: Hepatic ischemia-reperfusion (I/R) injury is a major complication in clinical practice. Previous studies suggest that statins have pleiotropic effects in addition to cholesterol-lowering effects. In this study, we aimed to investigate the hepatoprotective role of two different doses of simvastatin (SV) pretreatment in rats with experimental hepatic I/R injury. METHODS: Adult male Sprague-Dawley rats were divided into four groups (n = 7 in each group) :control, I/R, I/R with 2.5-mg/kg SV, and I/R with 5.0-mg/kg SV. Before hepatic I/R was induced, SV was injected intraperitoneally at doses of 2.5 and 5.0 mg/kg. After 45-min ischemia and a 60-min reperfusion period, the animals were euthanized, and liver tissues were excised. Tissue levels of malondialdehyde and nitric oxide, and activities of superoxide dismutase, glutathione peroxidase, and catalase were measured. Liver tissues were also evaluated histopathologically and immunohistochemically. RESULTS: Histopathologic evaluation showed that 5.0-mg/kg SV reduced hepatic damage and apoptosis. Pretreatment with 5.0-mg/kg SV reduced malondialdehyde and nitric oxide levels (P < 0.01) and increased superoxide dismutase, glutathione peroxidase, and catalase activities significantly (P < 0.001, P < 0.01) in I/R with 2.5-mg/kg SV compared with I/R group. In addition, SV decreased Kupffer cell activation, and hypoxia-inducible factor-1α and vascular endothelial growth factor protein levels. CONCLUSIONS: The results of this study suggest that 5.0-mg/kg SV pretreatment may be protective against hepatic I/R injury. This effect can be achieved by antioxidant and antiapoptotic activities.

Balanced oxidative status by nesfatin-1 in intestinal ischemia-reperfusion.

OBJECTIVE: Ischemia causes reversible or irreversible cell or tissue damage and reperfusion can exaggerate cellular damage. Microvascular dysfunction is induced and causes enhanced fluid filtration in capillaries. At the acute phase of reperfusion more oxygen radicals are activated. Nesfatin-1 protects brain against oxidative damage and heart against ischemia/reperfusion damage. In our study, we aimed to investigate the acute effect of chronic peripheral nesfatin-1 administration in intestinal ischemia/reperfusion created rats. METHOD: Two-months-old, 28 Wistar Albino male rats, weighing an average of 200-250 g, were used and randomly divided into four experimental groups (n=7) as; Laparotomy, Ischemia/Reperfusion, Nesfatin-1+Laparotomy, Nesfatin-1+Ischemia/Reperfusion. Serum levels of total oxidant status (TOS) and total antioxidant status (TAS) were determined by colorimetric measurement method. The plasma levels of endotelin-1 and endothelial nitric oxide syntheses (eNOS) were analyzed by rat ELISA assay kits. RESULTS: Plasma levels of endothelin-1 significantly increased, plasma level of eNOS, serum levels of TOS and TAS significantly decreased in nesfatin-1 applied groups. Additionally, The oxidative stress index (OSI) parameters decreased significantly in three groups compared to laparotomy. CONCLUSION: Chronic peripheral nesfatin-1 administration can decrease eNOS level and OSI at the acute phase of ischemia/reperfusion. We suppose that it can be protective for ischemia/reperfusion injury by balancing oxidant capacity. On the other hand, this effect of nesfatin-1 is not related with micro-circular compensation and increases anti-oxidant capacity.

Angiotensinogen gene M235T and angiotensin II-type 1 receptor gene A/C1166 polymorphisms in chronic obtructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) occurs irreversibly and is characterized by progressive airflow obstruction. Renin angiotensin system (RAS) has many different key enzymes and receptors that have a role for different systemic processes. We aimed to determine genotype and allele frequencies of angiotensinogen (AGT) M235T and angiotensin II-type 1 receptor (AT1-R) A/C1166 polymorphisms in patients with COPD. This study was performed on 56 unrelated COPD patients and 29 healthy subjects. DNA samples for each individual were isolated from peripheral blood by phenol/chloroform method, analyzed by polymerase chain reaction and enzymatic digestion methodologies. The distribution for each of AGT genotypes were 23.2% for MM (13), 75.0% for MT (42) and 1.8% for TT (1) in the COPD group; 37.9% for MM (11), 34.5% for MT (10) and 27.6% for TT (8) in the control group. The distribution of AGT genotypes was found significantly different between groups (X(2) = 18.604; df = 2; P = 0.000). The frequencies for each of the AT1-R genotypes were found as 53.6% for AA (30), 42.9% for AC (24), 3.6% for CC (2) in the COPD group; 55.2% for AA (16), 41.4% for AC (12) and 3.4% for CC (1) in the control group. The distribution of AT1-R genotypes did not change significantly between groups. Allele frequencies of interested genes were not significantly different between groups. We suggest that AGT polymorphism may play a role for the development of COPD. We believe these data can be served for large scale population genetics research, considering the frequency of AGT and AT1-R genes and alleles in COPD patients in the Turkish population.

Nephrotoxic effects of varenicline as the most effective drug used for smoking cessation: a preliminary experimental study.

PURPOSE: Varenicline is a new most effective drug for smoking cessation. Its effect on kidney functions remains unclear. This study purposed to investigate whether varenicline causes nephrotoxicity in rats. METHODS: Fifteen rats were randomly assigned to three groups: control, 0.0125 mg kg(-1) varenicline and 0.025 mg kg(-1) varenicline (single dose for 3 days, i.p.). Before and after experimental period, serum neutrophil gelatinase-associated lipocalin, creatinine and urea levels were measured. Total oxidant and antioxidant status were measured in kidney homogenates. Histological examination was performed in kidney. RESULTS: The nephrotoxic effects of varenicline were detected by histopathological and biochemical examinations in the varenicline treatment groups. No change was observed in the control group. CONCLUSIONS: These findings firstly indicate that a 3-day varenicline treatment causes nephrotoxic effects in rats.

Effects of ukrain in rats with intestinal ischemia and reperfusion.

BACKGROUND: The purpose of this study is to investigate the potential protective effect of the ukrain on ischemia-reperfusion (IR) injury in rat intestine, which has not previously been studied. METHODS: Thirty-one male Sprague-Dawley rats were randomly assigned to four groups, each consisting of eight rats as follows: (1) a sham group (S) (laparotomy, but no IR injury); (2) ukrain group (U) (no IR, and ukrain was administered intraperitoneally 1 h before laparotomy); (3) intestinal ischemia-reperfusion (II/R) group (30-min occlusion of the superior mesenteric artery then 2-h reperfusion); and (4) ukrain + II/R group (U + II/R) (30-min occlusion of the superior mesenteric artery then 2-h reperfusion; ukrain was administered intraperitoneally 1 h before IR). RESULTS: Serum total oxidant status (TOS) and total antioxidant status (TAS) were measured using Erel method. Oxidative stress index was calculated using the TOS/TAS ratio. TAS levels increased and TOS serum levels were also significantly decreased in the ukrain + IR group compared with the IR group (P = 0.000 and P = 0.015). CONCLUSIONS: In this study, we demonstrated for the first time in literature that ukrain helps to prevent intestinal tissue breakdown against II/R injury and that this effect can be achieved by antioxidant activities.

Characterization of the apelin -1860T>C polymorphism in Turkish coronary artery disease patients and healthy individuals.

To evaluate the association between the apelin -1860T>C polymorphism and plasma apelin levels in Turkish patients with coronary artery disease (CAD). A total of 276 individuals were enrolled in the present study, including 158 patients with CAD and 118 individuals without CAD as controls. The presence of the apelin -1860T>C gene polymorphism and plasma apelin levels were determined using polymerase chain reaction/restriction fragment length polymorphism and enzyme-linked immunosorbent assay, respectively. Significance was set at p≤0.05 for all statistical analyses. The genotype and allele frequencies of interested genes were significantly different between groups (χ(2)=10.2; df=2; p=0.006 and χ(2)=13.4; df=1; p=0.000, respectively). Frequency of CC genotype and the C allele of -1860T>C site was significantly higher in CAD patients compared to healthy controls. We found that individuals with the TC and CC genotypes were associated with an increased risk of CAD when compared with the TT genotype in CAD patients, and the adjusted ORs (95% CI) were 6.50 (1.27-33.0) and 6.39 (1.77-23.0), respectively. Plasma apelin levels were significantly lower in CAD patients compared to control group. Apelin level of CAD patient group having CC genotype of -1860T>C site was significantly lower compared to those having TT genotypes, but it was not statistically significant (p > 0.05). The homozygous CC genotype of apelin gene is associated with high risk of CAD. Apelin gene polymorphism -1860T>C is a significant predictor of predisposition to CAD in in Turkish population.

APJ receptor A445C gene polymorphism in Turkish patients with coronary artery disease.

Coronary artery disease (CAD) is a disease in which a waxy substance called plaque builds up inside the coronary arteries. Apelin is a novel endogenous peptide with inotropic and vasodilatory properties and is the ligand for the angiotensin receptor-like 1 (APJ) receptor. We aimed to determine genotype and allele frequencies of APJ receptor A445C gene polymorphism in Turkish patients with CAD and healthy controls by RFLP-PCR. This study was performed on 159 unrelated CAD patients and 62 healthy controls. We obtained AA, AC and CC genotype frequencies in CAD patients as 41.5%, 49.1% and 9.4%, respectively. In the control group, frequencies of genotypes were found as 35.5% for AA, 48.4% for AC and 16.1% for CC. We did not observe difference in APJ receptor A445C polymorphism between CAD patients and healthy controls (χ(2) = 2.178; df = 2; P = 0.336). The A allele was encountered in 66% (210) of the CAD and 59.7% (74) of the controls. The C allele was seen in 34% (108) of the CAD and 40.3% (50) of the controls. Allele frequencies of interested genes were not significantly different between groups (χ(2) = 1.57; df = 1; p = 0.225). The frequencies of APJ receptor A445C genotype were not significantly different between control and patients. None of the three APJ receptor A445C genotypes, AA, AC and CC displayed significant difference in CAD patients. We did not find any difference in the clinical parameters except for weight and diastolic blood pressure levels in the AA, AC and CC genotypes of patients. Individuals with CC genotypes had significantly higher weight, systolic and diastolic blood pressure levels and systolic blood pressure than other genotypes, P ≤ 0.05. In addition, HDL-C level was found decreased, but this reduction was not statistically significant. Contrarily, the low levels of weight, SBP, DBP and TC were statistically significant in the subjects with AA genotype in CAD. In conclusion, CC genotype carriers may have more risk than other genotypes in the development of hypertension in CAD, but not AAgenotype carriers. We suggest that this polymorphism may not be a marker of CAD, but it may cause useful in function of the apelin/APJ system and may be a genetic predisposing factor for diagnostic processes and can be helpfull in finding new treatment strategies. We think that it is required to further comprehensive studies in order to make clear this situation in CAD.

MDR-1 gene C/T polymorphism in COPD: data from Aegean part of Turkey.

OBJECTIVE: Genetic factors, in addition to oxidative stress factors, have been implicated in the development of chronic obstructive pulmonary disease (COPD). Multi-drug resistant-1 (MDR-1) is a gene located on chromosome 7 and the products of this gene protect lung tissue from oxidative stress. We searched the frequency of MDR-1 gene C/T polymorphism in patients with COPD and aimed to explain the association between MDR-1 gene and COPD development. METHODS: 47 patients with COPD and 64 healthy control participants were placed in this study. DNAs were extracted from blood samples and MDR-1 amplification of DNA was performed using polymerase chain reaction and enzyme digestion techniques. RESULTS: The frequencies of MDR-1 genotypes were found 17.0% for CC, 51.1% for CT and 31.9% for TT in the COPD group and 39.1% for CC, 53.1% for CT and 7.8% for TT in the control group. The distribution of MDR-1 gene C alleles were found 32.3% in COPD group and 67.7% in control group; T alleles were found 55.1% in COPD group and 44.9% in control group. There was statistically significant difference between the groups for genotype and allele frequency of MDR-1 gene (P = 0.001). CONCLUSION: TT genotype of MDR-1 gene was significantly more frequent in COPD patients. MDR-1 gene C/T polymorphism may play a role in COPD development.

Single dose varenicline may trigger epileptic activity.

Varenicline is a new drug for smoking cessation, and its effect on epilepsy is not clear. The aim of this study was to investigate whether different doses of varenicline cause epileptic activity. Forty rats were randomly assigned to the following eight groups: control, saline, and 0.025, 0.04, 0.1, 0.5, 1, and 2 mg kg(-1) varenicline (single dose, i.p.). EEGs were recorded before the varenicline injection and during the following 240 min. While epileptic discharges were observed on the EEGs of the rats in all of the varenicline-treated groups, motor findings of epileptic seizure were not observed in some rats in these groups except the 1 and 2 mg kg(-1) groups. These findings indicate that different single doses of varenicline cause epileptic activity in rats.

Anticancer agent ukrain and bortezomib combination is synergistic in 4T1 breast cancer cells.

The identification and in-depth understanding of intracellular signalling pathways led to the synthesis and discovery of many agents targeting cancer cells. In this study, we investigated for the first time the effect of anticancer agent ukrain as a single agent or in combination with cisplatin, etoposide, 5-fluorouracil, quercetin and bortezomib in 4T1 breast cancer and B16F10 melanoma cells. It was found that ukrain is cytotoxic and apoptotic in 4T1 breast carcinoma and B16F10 melanoma cells when given alone. The IC50 value of ukrain in 4T1 cells was found as 40 ± 6.8 µM and that in B16F10 cells as 76 ± 10 µM. It was then found that apoptosis can be induced in 4T1 breast cancer cells in a dose-dependent manner in response to ukrain treatment, based on DNA fragmentation evidence. The induction of apoptosis was corroborated by the analysis of cleavage products of caspase-3 in 4T1 cells using Western blot technique. When ukrain was tested in combination with cisplatin and etoposide, no significant enhancement of cytotoxicity was detected as compared with single agent treatments. Similarly, 5-fluorouracil and quercetin also did not potentiate the cytotoxic effects of ukrain in 4T1 cells. Finally, we examined the effect of various concentrations of ukrain in combination with 10 nM bortezomib in 4T1 cells. Determination of combination index values showed that bortezomib potentiated the effect of ukrain. And the combination was found to cause synergistic cell death. The lowest combination index detected was 0.57 which was obtained when the cells were treated with 10 nM bortezomib + 100 µM ukrain. Likewise, when cells were treated with different doses of bortezomib in the presence of 25 µM ukrain, synergism was similarly detected between the two drugs in a dose-dependent manner. Altogether, the results presented here suggest that the combination of ukrain + bortezomib may be further evaluated and tested in clinical settings.

Blood pressure measurement in freely moving rats by the tail cuff method.

Inconsistency in consecutive blood pressure values is one of the most frequently observed problems in tail cuff method. The aim of this study was to measure blood pressure using the tail cuff method in rats without heating, anesthesia, and movement restriction. In this study, it has been shown that blood pressure measurement could be obtained without problem using the tail cuff method in freely moving rats in their cage environment. Also, the reliability of consecutive blood pressure values obtained from freely moving rats was higher than ether anesthesia and restricted groups.

Exercise and DHA prevent the negative effects of hypoxia on EEG and nerve conduction velocity.

It is known that hypoxia has a negative effect on nervous system functions, but exercise and DHA (docosahexaenoic acid) have positive effect. In this study, it was investigated whether exercise and/or DHA can prevent the effects of hypoxia on EEG and nerve conduction velocity (NCV). 35 adult Wistar albino male rats were divided into five groups (n=7): control (C), hypoxia (H), hypoxia and exercise (HE), hypoxia and DHA (HD), and hypoxia and exercise and DHA (HED) groups. During the 28-day hypoxia exposure, the HE and HED groups of rats were exercised (0% incline, 30 m/min speed, 20 min/day, 5 days a week). In addition, DHA (36 mg/kg/day) was given by oral gavage to rats in the HD and HED groups. While EEG records were taken before and after the experimental period, NCV records were taken after the experimental period from anesthetized rats. Data were analyzed by paired t-test, one-way ANOVA, and post hoc Tukey test. In this study, it was shown that exposure to hypoxia decreased theta activity and NCV, but exercise and DHA reduced the delta activity, while theta, alpha, beta activities, and NCV were increased. These results have shown that the effects of hypoxia exposure on EEG and NCV can be prevented by exercise and/or DHA.

Orexins cause epileptic activity.

Orexins have been implicated in the regulation of sleep-wake cycle, energy homeostasis, drinking behavior, analgesia, attention, learning and memory but their effects on epileptic activity are controversial. We investigated whether intracortical injections of orexin A (100 pmol) and B (100 pmol) cause epileptic activity in rats. We observed epileptic seizure findings on these two groups rats. Orexin A and B also significantly increased total EEG power spectrum. Our findings indicate that orexins cause epileptic activity.

Orexins increase penicillin-induced epileptic activity.

Orexins have been implicated with physiological function including sleep-wake cycle, energy homeostasis, drinking behavior, analgesia, attention, learning and memory but their effects on excitability are controversial. We investigated the effects of intracortical injections of orexin A (100 pmol) and B (100 pmol) on the electrophysiological manifestation of epileptic seizures induced by cortical penicillin application in adult male rats. In comparison to saline, orexin A and B enhanced significantly the spike number, spike amplitude and spectral power values induced by cortical penicillin. Our findings indicates that orexins enhances the hyperexcitable and hypersyncronic cortical epileptic activity induced by focal application of penicillin-G.

The Effects of Electromagnetic Fields Generated from 1800 MHz Cell Phones on Erythrocyte Rheological Parameters and Zinc Level in Rats.

OBJECTIVE: The aim of this study was to investigate the effects of the electromagnetic field generated from the 1800 MHz radiofrequency radiation (EF) on erythrocyte rheological parameters and erythrocyte zinc levels. MATERIAL AND METHODS: Twenty-four male Wistar Albino rats were randomly grouped as follows: 1) two control groups and 2) study groups: i) Group A: EF exposed group (2.5 h/day for 30 days, the phone on stand-by), and ii) Group B: EF exposed group (2.5 min/day for 30 days, the phone ringing in silent mode). At the end of the experimental period erythrocyte rheological parameters such as erythrocyte deformability and aggregation were determined by an ectacytometer. Erythrocyte zinc level, which affects hemorheological parameters, was also measured by atomic absorption spectrophotometer. RESULTS: Erythrocyte deformability was decreased in both study groups but the decrease in group A was not statistically significant. Exposure to EF did not have any significant effect on erythrocyte aggregation. On the other hand, erythrocyte zinc level was significantly reduced in both study groups. CONCLUSION: Exposure to EF may have decreased tissue oxygenation due to reduced erythrocyte deformability. Decrease in erythrocyte zinc level may have caused the impairment in erythrocyte deformability.