Does Cardiovascular Disease Risk Decrease after Smoking Cessation in Occupational Risk Groups?

Objectives: Smoking cessation is very important for workers due to the possibility of exposure to additional environmental risks in the workplace environment. This study was performed to determine the changes in the Framingham Risk Score (FRS) and 10-year risk of cardiovascular disease (CVD) of employees before smoking cessation and after 6 months. Materials and Methods: Five hundred and sixty-two employees who want to quit smoking were included in the study. In this prospective study, the baseline and 6-month FRS, and 10-year risk of CVD of workers were calculated. Furthermore, the Hospital Anxiety and Depression Scale was used for assessments of employees' anxiety and depression symptoms. Results: After 6 months, 37% of the participants quit smoking. It was determined that 11.9% of employees have a high CVD risk and 10.6% moderate CVD risk. After 6 months, there was a statistically significant reduction in FRS who quit smoking (P < 0.001). In addition, within the 6 months after smoking cessation, 10-year coronary heart disease risk reduction was higher in quitters than those who cannot quit smoking (47.6% decrease in quitters and 14.9% in nonquitters, P < 0.001). Significant decreases in fasting blood glucose levels were determined after smoking cessation (P = 0.003). Conclusions: The FRS and CVD risk of smoker employees were decreased 6 months after smoking cessation. In 6 months, CVD risk is reduced in almost half of those who quit smoking. Even in the short term, it is possible to reduce the CVD risk of a worker who quits smoking.

Effect of MDR C3435T polymorphism on Varenicline treatment in quit smoking

Despite so many global efforts, smoking still remains to be one of the most common addictions worldwide. Even though most smokers wish to quit smoking, many of them fail. In this respect, genetic variants are thought to be remarkable factors in nicotine dependence and in treatment of smoking cessation. This is a paper investigating a single variant p-glycoprotein (P-gp) polymorphisms and its effect on Varenicline efficacy in the smoking cessation. 158 smokers and 52 non-smoker healthy volunteers were included. We determined the P-gp C3435T gene polymorphisms in all subjects. Face to face interviews with smokers were performed for smoking cessation and Varenicline was given for smoking cessation. Cessation success was evaluated in the 6th month and success rates were compared according to the P-gp genotype distributions. In our study, smoking cessation rate by Varenicline was 57.0%. This rate was 55.0% in females, and 57.2% in males (p=0.85). The P-gp C3435T gene distribution was similar in control, quitters and not-quitter groups. Cessation rate was at highest point in genotype CT (62.2%) and at the lowest in TT (47.6%). It was 53.8% in genotype CC and there was no statistically significant difference (p=0.27). Our results suggest that genetic variants of P-gp C3435T did not significantly affect Varenicline treatment for smoking cessation.

Effect of acute and chronic exercise on plasma matrix metalloproteinase and total antioxidant levels.

The relationship between acute and chronic exercise and expression of matrix metalloproteinases (MMPs) in muscles is unknown. There happen some alterations in the oxidant-antioxidant balance due to exercise. This study aimed to investigate the levels of MMP-1, tissue inhibitors of metalloproteinases (TIMP-1), hyaluronic acid (HA), total antioxidant status (TAS), and total oxidant status (TOS) following acute and chronic exercising in rats. Twenty-six Wistar Albino male rats were divided in to three groups: control, acute, and chronic groups. In acute group, treadmill exercise was performed 3 days/wk, 10 min/day for 1 week. In chronic group, exercise performed 7 days/wk, 60 min/day for 4 weeks. At the end of the experiment, plasma MMP-1, TIMP-1, HA, TAS, and TOS levels were measured. In current study, the MMP-1, TIMP-1, HA, and TOS levels not observed statistically significant difference among all groups, but in chronic group, there was a significantly difference (P<0.05) between the control and experimental groups in terms of TAS and oxidative stress index (OSI) levels. TAS, TOS, and OSI levels were significantly different between control and chronic exercise group (P<0.01, P<0.05, and P<0.01, respectively). According to these results, we can say acute and chronic exercise does not effect on plasma MMP-1, TIMP-1, and HA levels.

Examination of levels pentraxin-3, interleukin-6, and C-reactive protein in rat model acute and chronic exercise.

Different types of exercise occurs damage at the cellular level in the muscles. Muscle damage caused by exercise is determined creatine kinase, myoglobin, and increase in levels of acute phase protein and interleukin in blood. The purpose of this study was investigated the levels of pentraxin-3 (PTX-3), interleukin-6 (IL-6), and C-reactive protein (CRP) following acute and chronic exercising in rats. Twenty-six Wistar Albino male rats were divided in to three groups. A treadmill exercise was performed 3 days/week, 10 min/day for 1 week in acute groups. In chronic group, exercise performed 7 days/week, 60 min/day for 4 weeks. At the end of the experiment, plasma PTX-3, IL-6, and CRP levels were measured. In current study, the PTX-3, IL-6, and CRP levels not observed statistically significant difference among control, acute, and chronic groups. The levels IL-6 and CRP were not significantly different between acute and chronic exercise groups (P>0.05). However, the level of PTX-3 was found to be higher in the chronic group compared to the acute group (P<0.05). The PTX-3 level increase on chronic exercise-induced muscle damage. Accorting to our results, we think that PTX-3 may have a protect role on muscle damage during chronic exercises.

Leptin Receptor Gene Polymorphism may Affect Subclinical Atherosclerosis in Patients with Acromegaly.

BACKGROUND: Acromegaly is associated with increased morbidity and mortality related to cardiovascular diseases. Leptin (LEP) and Leptin Receptor (LEPR) gene polymorphisms can increase cardiovascular risks. The aim of this study was to investigate association between the frequencies of LEP and LEPR gene polymorphisms and subclinical atherosclerosis in acromegalic patients. METHODS: Forty-four acromegalic patients and 30 controls were admitted to study. The polymorphisms were identified by using polymerase chain reaction from peripheral blood samples. The levels of systolic and diastolic blood pressure, BMI, fasting plasma glucose, fasting insulin, IGF-I, GH, IGFBP3, leptin, triglyceride, carotid Intima Media Thickness (cIMT) and HDL and LDL cholesterol concentrations were evaluated. RESULTS: There was statistically significant difference between the LEPR genotypes of acromegalic patients (GG 11.4%, GA 52.3%, and AA 36.4%) and controls (GG 33.3%, GA 50%, and AA 16.7%) although their LEP genotype distribution was similar. In addition, the prevalence of the LEPR gene G and A alleles was significantly different between patients and controls. No significant difference was found among the G(-2548) A leptin genotypes of groups in terms of the clinical parameters. cIMT significantly increased homozygote LEPR GG genotype group compared to AA subjects in patients. But the other parameters were not different between LEPR genotypes groups of patients and controls. CONCLUSION: It can be said that the LEPR gene polymorphism may affect cIMT in patients. The reason is that LEPR GG genotype carriers may have more risk than other genotypes in the development of subclinical atherosclerosis in acromegaly.

Vitamin-D Receptor (VDR) Gene Polymorphisms (TaqI, FokI) in Turkish Patients with Hashimoto's Thyroiditis: Relationship to the Levels of Vit-D and Cytokines.

BACKGROUND: Hashimoto's thyroiditis (HT) is a common autoimmune disease. Vitamin D is an important regulator of immune system. It has been shown in several studies that vitamin D prevents the development of lots of autoimmune diseases. There are some studies that prove vitamin D receptor (VDR) gene polymorphism increases the risk of Hashimoto's thyroiditis. In this study, we aimed to investigate the association between HT and level of 25(OH)D3, IL-2, IL-4, IL-5, TNF-α and IFN-γ and VDR FokI and TaqI gene polymorphism. Moreover, to find out whether low levels of vitamin D affect HT pathogenesis over inflammatory parameters. METHODS: We performed a case-control study that included 136 cases with HT (49 euthyroid, 49 subclinical hypothyroid, 38 hypothyroid patients) and 50 healthy control. Serum levels of 25(OH)D3, glucose, insulin, parathyroid hormone, calcium, phosphorus, alkaline phosphatase were measured and IL-4, IL-5, TNF-α, IFN-γ analysis were performed with ELISA kits in all 186 subjects. Genetic analysis for VDR FokI and TaqI gene polymorphisms were done by RFLP in all subjects. RESULTS: Mean serum 25(OH)D levels were 14.88±8.23 ng/ml in patient with HT and 15.52±1.34 ng/ml in healthy controls. There were no statically significant differences between the groups in terms of vitamin D levels (P=0.977). Prevalence of vitamin D insufficiency in HT cases was significantly higher than controls (p=0.02). Although serum IL-2, IL-4, TNF-α and IFN-γ were significantly higher in HT patients, there were no significant differences regarding IL-5 levels. Significant differences were observed between the groups regarding the genotype of TaqI but no differences regarding FokI genotype. CONCLUSION: Vitamin D insufficiency is associated with HT. There is a relationship between VDR TaqI gene polymorphism and HT. Although vitamin D levels are low in both patient and control group, detection of high level of inflammatory parameters in HT group makes us think that low level of vitamin D does not affect HT pathogenesis over these parameters.

Effect of Erythropoietin and Stem Cells on Traumatic Brain Injury.

OBJECTIVE: To investigate the healing effects of erythropoietin (EPO) and stem cells (SCs) in traumatic brain injury (TBI). METHODS: Twenty-nine Wistar albino rats were used and separated into the following groups: control (C), EPO, SC, and SC+EPO. Group C received a TBI only, with no treatment. In the EPO group, 1000 U/kg EPO was given intraperitoneally at 30 minutes after TBI. In SC group, immediately after formation of TBI, 3 × 10,000 CD34(+) stem cells were injected into the affected area. In the SC+EPO group, half an hour after TBI and the injection of stem cells, 1000 U/kg EPO was injected. Before and after injury, trauma coordination performance was measured by the rotarod and inclined plane tests. RESULTS: Seven weeks after trauma, rat brains were examined by radiology and histology. Rotarod performance test did not change remarkably, even after the injury. Compared with group C, the SC+EPO group was found to have significant differences in the inclined plane test results. CONCLUSIONS: Separately given, SCs and EPO have a positive effect on TBI, and our findings suggest that their coadministration is even more powerful.

Association of Adipokines, Insulin Resistance, Hypertension and Dyslipidemia in Patients with Psoriasis Vulgaris.

BACKGROUND: Systemic inflammation in psoriasis causes insulin resistance and cardiovascular diseases. Adipokines are adipose-tissue-derived factors that are involved in metabolic processes. It is thought that these adipokines are associated with the development of psoriasis. OBJECTIVE: The purpose of this study was to determine the changes in adipokine levels, insulin resistance, hypertension, and dyslipidemia over a 12-week period. METHODS: The study comprised 35 psoriasis patients and 50 controls. Blood samples were obtained twice from the patients, one sample at the start and one at the end of a 12-week follow-up period. The following parameters were assessed in both groups: serum fasting glucose, fasting insulin, homeostasis model assessment-estimated insulin resistance (HOMA-IR) index, serum lipids, adiponectin, leptin, resistin, chemerin, omentin, vaspin, visfatin, retinol-binding protein 4, and high-sensitivity C-reactive protein (hs-CRP) levels; blood pressure; body mass index; and the psoriasis area severity index (PASI) scores. RESULTS: The patients showed an improvement in the PASI score and a significant decrease in serum hs-CRP, omentin, and chemerin values. Moreover, at the start of the follow-up, the psoriasis patients had significantly lower levels of adiponectin and visfatin and significantly higher levels of vaspin and resistin than those of the control group. Visfatin levels correlated negatively with low-density lipoprotein (LDL) and cholesterol, while vaspin and omentin levels correlated positively with diastolic blood pressure. Decreased adiponectin levels correlated negatively with diastolic blood pressure and LDL. CONCLUSION: Plasma levels of adipokines might be useful for evaluating the disease activity of psoriasis and its comorbidities.

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.

The effects of apelin treatment on a rat model of type 2 diabetes.

PURPOSE: Apelin is an adipokine that plays a role in the regulation of many biological functions in mammals including the neuroendocrine, cardiovascular, immune systems, glucose homeostasis and obesity. It can act via autocrine, paracrine, endocrine, and exocrine signaling. We aimed to identify the role of apelin pathophysiology of diabetes. MATERIAL/METHODS: 37 male Wistar Albino rats aged 8-10 weeks were divided in four experimental groups as: control group (C) control+apelin group (C+A), diabetic group (D) diabetic+apelin group (D+A). Apelin and apelin receptor mRNA gene expressions in heart and aorta tissue were determined by real-time polymerase chain reaction. The plasma levels of insulin and plasma apelin were determined by ELISA. RESULTS: Plasma levels of insulin, glucose, blood pressure levels were significantly lower in D+A group. There was no statistically significant difference for level of apelin between diabetic groups. On the other hand, differences for apelin and APJ mRNA expression in heart and vascular tissue were found significant between groups. CONCLUSIONS: Apelin can be used as a therapeutic agent in the treatment of type II diabetes in the future.

The effect of chronic peripheral nesfatin-1 application on blood pressure in normal and chronic restraint stressed rats: related with circulating level of blood pressure regulators.

Nesfatin is a peptide secreted by peripheral tissues, central and peripheral nervous system. It is involved in the regulation of homeostasis. Although the effects of nesfatin-1 on nutrition have been studied widely in the literature, the mechanisms of nesfatin-1 action and also relations with other physiological parameters are still not clarified well. We aimed to investigate the effect of peripheral chronic nesfatin-1 application on blood pressure regulation in normal and in rats exposed to restraint immobilization stress. In our study, three month-old male Wistar rats were used. Rats were divided into 4 groups as Control, Stress, Control+Nesfatin-1, Nesfatin-1+Stress. Angiotensinogen, angiotensin converting enzyme 2, angiotensin II, endothelin-1, endothelial nitric oxide synthase, aldosterone, cortisol, nesfatin-1 levels were determined in plasma samples by ELISA. Our results have shown that chronic peripheral nesfatin-1 administration increases blood pressure in normal and in rats exposed to chronic restraint stress. Effect of nesfatin-1 on circulating level of angiotensinogen, angiotensin converting enzyme 2, angiotensin II, endothelin-1, endothelial nitric oxide synthase, aldosterone and cortisol has been identified. We can conclude that elevated high blood pressure after chronic peripheral nesfatin-1 administration in rats exposed to chronic restraint stress may be related to decreased plasma level of endothelial nitric oxide synthase concentration.

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.

Apelin-induced hemorheological alterations in DOCA-salt hypertensive rats.

Apelin is a hypotensive peptide. Red blood cell (RBC) deformability and aggregation were previously demonstrated to be altered in various hypertension (HT) models. In the present study, we investigated possible alterations in RBC deformability and aggregation in response to apelin in DOCA-salt hypertensive rats. Rats were randomly divided into 4 groups: Control (C), Hypertension (HT), Apelin, and Apelin + Hypertension (Apelin + HT). HT was induced by injection of DOCA-salt (25 mg/kg, s.c.) twice weekly for 4 weeks, whereas apelin was administered (200 µg/kg i.p.) for 17 days. RBC deformability and aggregation were determined using an ektacytometer. Blood pressure was monitored using a tail cuff system. Systolic blood pressure was decreased in the Apelin and Apelin + HT groups and increased in the HT group. RBC deformability was not significantly altered in the HT group. Apelin administration induced a statistically significant increase in RBC deformability in control animals, whereas erythrocytic deformability in the Apelin + HT group was decreased compared to the Apelin group. RBC aggregation of hypertensive animals was reduced compared to controls. Apelin administration induced increased RBC aggregation in hypertensive rats. Our results showed favorable effects of apelin on RBC deformability in control animals, but not in hypertensive rats.

Apelin effects on blood pressure and RAS in DOCA-salt-induced hypertensive rats.

Apelin, a novel multifunctional peptide implicated in the regulation of the cardiovascular system, including blood pressure and cardiac function control, has been postulated to be involved in the pathophysiology of hypertension and hypertensive heart disease. The aim of this study was to investigate, for the first time, whether the effects of apelin's chronic application might be involved in deoxycorticosterone acetate-salt-induced hypertensive rats (DOCA-salt rats). In this study, 8-10-week-old male Wistar rats were divided into four groups: control, control + apelin, DOCA-salt rats, DOCA-salt rats + apelin. Deoxycorticosterone Acetate (25 mg/kg of body weight) was injected subcutaneously, twice a week for 4 weeks. These rats received NaCl 1% instead of tap water for drinking during the experimental period. Later, rats were randomly treated with pyroglutamylated apelin-13 (200 µg. kg(-1). day(-1) intraperitonealy) for 17 days. The concentrations of apelin, endothelin-1, angiotensin-converting enzyme, angiotensinogen, and angiotensin II were analyzed in the plasma. The mRNA level of apelin and apelin receptor were determined in the heart and aorta tissue by real-time polymerase chain reaction, respectively. It was found that apelin reduces blood pressure in DOCA-salt rats. Apelin can be used as a therapeutic agent in the treatment of hypertension in the future.

MDR1 single nucleotide polymorphism C3435T in Turkish patients with non-small-cell lung cancer.

We assessed whether single nucleotide polymorphisms (SNPs) in MDR1 gene C3435T predicted the outcome of platinum-based chemotherapies and survival in our non small cell lung cancer (NSCLC) patients. A total of 79 non-small cell lung cancer patients were enrolled to study. We determined the MDR1 C3435T single nucleotide gene polymorphisms. Median age was 60years: 91.7% male, 8.9% female. We found that CC, CT, TT genotype and T, C allele frequencies in lung cancer patients as 24.1%, 62%, 13.9% and 44.3%, 55.7%, respectively. Patients with CT genotype had a higher response rate (11.4%) than the other genotypes. However, this difference is not statistically significant (p=0.743). Cox regression analysis for overall survival showed that ECOG PS status 0 (HR PS 1 vs. 0, 5.68 p=0.002; HR of PS 2 vs. 0 is 21.579, p=0.001; HR of PS 3 vs. 0 is 35.35, p=0.001), stage ≤II (HR of stage III vs. I+II is 17.77; p=0.016, HR of stage IV vs. I+II is 26.97, p=0.006), and albumin level ≥3g/dl (HR of albumin <3g/dl vs. ≥3g/dl is 2.46, p=0.044) were the most important prognostic factors (also, time to progression was related to these factors). There was no significant association between the genotypes and clinicopathologic parameters; however, good performance status, early stage and ≥3g/dl albumin level were found to be the most important prognostic factors for overall survival and progression-free survival.

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.

Insulin-like growth factor I (Igf-1) gene polymorphism in patients with non-metastatic breast cancer.

We aimed to assess the association between IGF-I gene (CA repeats) polymorphism in breast cancer patients and their clinicopathological features, as well as disease recurrence and survival. Seventy-six non-metastatic breast cancer patients were enrolled in the present study. The IGF-I (CA) repeats were studied with polymerase chain reaction by using proper primers belonging to these gene areas from DNA samples. Results show that the non 19- non 19 homozygote were more common in patients without lymph node involvement (p=0.04), with low histological grade (p=0.04), with positive hormone receptor status (p=0.01), and in patients without recurrence (p=0.06). These results suggest that the non 19-non 19 carriers have some favorable prognostic factors, and IGF-I gene polymorphism (CA repeats) may affect disease recurrence and overall survival.

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 growth hormone receptor polymorphism in patients with acromegaly: relationship to BMI and glucose metabolism.

The aim of this study was to investigate association between the frequencies of Growth Hormone receptor (d3GHR) gene polymorphisms and some clinical parameters of acromegalic patients. Total of 35 acromegalic patients were enrolled to study. The d3GHR polymorphism was identified by using polymerase chain reaction from peripheral blood samples. The levels of systolic and diastolic blood pressure, BMI, fasting plasma glucose (FPG), Fasting insulin, HOMA-IR, IGF-I, GH, IGFBP3, triglyceride, HDL and LDL cholesterol concentrations were evaluated. The frequencies of d3GHR genotypes were found as follows; 5 (14.3%) subjects had d3/d3, 11 (31.4%) had d3/fl and 19 (54.3%) had fl/fl in patients. The prevalence of the d3 and fl alleles was 30 and 70%, respectively. Systolic blood pressure, fasting insulin and HOMA-IR was found significantly increased in homozygote d3GHR genotype group compared to d3/fl subjects (P < 0.05). In addition, BMI was observed significantly different among three genotypes (P = 0.007) and in the subjects with d3/d3 genotype, BMI was found significantly higher than d3/fl and fl/fl genotypes groups. As well as, no significant difference was found between the d3 and fl alleles group in terms of the clinical parameters except for BMI (P = 0.002). It can be said that the d3GHR gene polymorphism may affect BMI, systolic blood pressure and insulin regulation. At the same time we can say homozygote d3GHR genotype and d3 allele carriers may have more risk than other genotypes for high BMI.

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.