Mustafa Nazıroğlu

Suleyman Demirel University, Almaty, Almaty Qalasy, Kazakhstan

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Publications (71)151.71 Total impact

  • Ishak Suat Ovey, Mustafa Nazıroğlu
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    ABSTRACT: Oxidative stress and apoptosis were induced in neuronal cultures by inhibition of glutathione (GSH) biosynthesis with D,L-buthionine-S,R-sulfoximine (BSO). TRPM2 and TRPV1 cation channels are gated by oxidative stress. The oxidant effects of homocysteine (Hcy) may induce activation of TRPV1 and TRPM2 channels in aged mice as a model of Alzheimer's disease (AD). We tested the effects of Hcy, BSO and GSH on oxidative stress, apoptosis and Ca(2+) and influx via TRPM2 and TRPV1 channels in hippocampus of mice. Native mice hippocampus neurons were divided into 5 groups as follows; control, Hcy, BSO, Hcy+BSO and Hcy+BSO+GSH groups. The neurons in TRPM2 and TRPV1 experiments were stimulated by hydrogen peroxide and capsaicin, respectively. BSO and Hcy incubations increased intracellular free Ca(2+) concentrations, reactive oxygen species, apoptosis, mitochondrial depolarization, and levels of caspase 3 and 9. All of these increases were reduced by GSH treatments. Treatment with 2-aminoethyldiphenyl borate (2-APB) and N-(p-amylcinnamoyl)anthranilic acid (ACA) as potent inhibitors of TRPM2, capsazepine as a potent inhibitor of TRPV1, verapamil+diltiazem (V+D) as inhibitors of the voltage-gated Ca(2+) channels (VGCC) and MK-801 as a NMDA channel antagonist indicated that GSH depletion and Hcy elevation activated Ca(2+) entry into the neurons through TRPM2, TRPV1, VGCC and NMDA channels., Inhibitor roles of 2-APB and capsazepine on the Ca(2+) entry higher than in V+D and MK-801 antagonists. In conclusion, these findings support the idea that GSH depletion and Hcy elevation can have damaging effects on hippocampal neurons by perturbing calcium homeostasis, mainly through TRPM2 and TRPV1 channels. GSH treatment can partially reverse these effects.
    Neuroscience 10/2014; · 3.12 Impact Factor
  • Mehmet Cemal Kahya, Mustafa Nazıroğlu, Bilal Ciğ
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    ABSTRACT: Exposure to mobile phone-induced electromagnetic radiation (EMR) may affect biological systems by increasing free oxygen radicals, apoptosis, and mitochondrial depolarization levels although selenium may modulate the values in cancer. The present study was designed to investigate the effects of 900 MHz radiation on the antioxidant redox system, apoptosis, and mitochondrial depolarization levels in MDA-MB-231 breast cancer cell line. Cultures of the cancer cells were divided into four main groups as controls, selenium, EMR, and EMR + selenium. In EMR groups, the cells were exposed to 900 MHz EMR for 1 h (SAR value of the EMR was 0.36 ± 0.02 W/kg). In selenium groups, the cells were also incubated with sodium selenite for 1 h before EMR exposure. Then, the following values were analyzed: (a) cell viability, (b) intracellular ROS production, (c) mitochondrial membrane depolarization, (d) cell apoptosis, and (e) caspase-3 and caspase-9 values. Selenium suppressed EMR-induced oxidative cell damage and cell viability (MTT) through a reduction of oxidative stress and restoring mitochondrial membrane potential. Additionally, selenium indicated anti-apoptotic effects, as demonstrated by plate reader analyses of apoptosis levels and caspase-3 and caspase-9 values. In conclusion, 900 MHz EMR appears to induce apoptosis effects through oxidative stress and mitochondrial depolarization although incubation of selenium seems to counteract the effects on apoptosis and oxidative stress.
    Biological Trace Element Research 06/2014; · 1.31 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate the potentially beneficial effects of apple cider vinegar (ACV) supplementation on serum triglycerides, total cholesterol, liver and kidney membrane lipid peroxidation, and antioxidant levels in ovariectomized (OVX) mice fed high cholesterol. Four groups of ten female mice were treated as follows: Group I received no treatment and was used as control. Group II was OVX mice. Group III received ACV intragastrically (0.6 % of feed), and group IV was OVX and was treated with ACV as described for group III. The treatment was continued for 28 days, during which the mice were fed a high-cholesterol diet. The lipid peroxidation levels in erythrocyte, liver and kidney, triglycerides, total, and VLDL cholesterol levels in serum were higher in the OVX group than in groups III and IV. The levels of vitamin E in liver, the kidney and erythrocyte glutathione peroxidase (GSH-Px), and erythrocyte-reduced glutathione (GSH) were decreased in group II. The GSH-Px, vitamin C, E, and β-carotene, and the erythrocyte GSH and GSH-Px values were higher in kidney of groups III and IV, but in liver the vitamin E and β-carotene concentrations were decreased. In conclusion, ACV induced a protective effect against erythrocyte, kidney, and liver oxidative injury, and lowered the serum lipid levels in mice fed high cholesterol, suggesting that it possesses oxidative stress scavenging effects, inhibits lipid peroxidation, and increases the levels of antioxidant enzymes and vitamin.
    Journal of Membrane Biology 06/2014; · 2.48 Impact Factor
  • Nilgün Senol, Mustafa Nazıroğlu
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    ABSTRACT: Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We investigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex β-carotene, vitamin C, vitamin E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain injury-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system.
    Neural Regeneration Research 06/2014; 9(11):1112-6. · 0.14 Impact Factor
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    ABSTRACT: Neurodegeneration associated with acute central nervous system injuries and diseases such as spinal cord injury and traumatic brain injury (TBI) are reported to be mediated by the regulation of apoptosis and oxidative stress through Ca(2+) influx. The thiol redox system antioxidants, such as N-acetylcysteine (NAC) and selenium (Se), display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties. However, there are no reports on hippocampal apoptosis, cytosolic reactive oxygen species (ROS), or Ca(2+) values in rats with an induced TBI. Therefore, we tested the effects of Se and NAC administration on apoptosis, oxidative stress, and Ca(2+) influx through TRPV1 channel activations in the hippocampus of TBI-induced rats. The 32 rats were divided into four groups: control, TBI, TBI + NAC, and TBI + Se groups. Intraperitoneal administrations of NAC and Se were performed at 1, 24, 48, and 72 h after TBI induction. After 3 days, the hippocampal neurons were freshly isolated from the rats. In cytosolic-free Ca(2+) analyses, the neurons were stimulated with the TRPV1 channel agonist capsaicin, a pungent compound found in hot chili peppers. Cytosolic-free Ca(2+), apoptosis, cytosolic ROS levels, and caspase-3 and -9 activities were higher in the TBI group than control. The values in the hippocampus were decreased by Se and NAC administrations. In conclusion, we observed that NAC and Se have protective effects on oxidative stress, apoptosis, and Ca(2+) entry via TRPV1 channel activation in the hippocampus of this TBI model, but the effect of NAC appears to be much greater than that of Se. They are both interesting candidates for studying the amelioration of TBIs.
    Cellular and Molecular Neurobiology 05/2014; · 2.29 Impact Factor
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    ABSTRACT: Abstract Background: Despite the importance of oxidative stress and apoptosis through mitochondrial depolarization in neurodegenerative diseases, their roles in etiology of glaucoma are poorly understood. We aimed to investigate whether oxidative stress and apoptosis formation are altered in rat pheochromocytoma-derived cell line-12 (PC12) neuronal cell cultures exposed to elevated different hydrostatic pressures as a cell culture model of glaucoma. Materials: Cultured PC12 cells were subjected to 0, 15 and 70 mmHg hydrostatic pressure for 1 and 24 h. Then, the following values were analyzed: (a) cell viability; (b) lipid peroxidation and intracellular reactive oxygen species production; (c) mitochondrial membrane depolarization; (d) cell apoptosis; (e) caspase-3 and caspase-9 activities; (f) reduced glutathione (GSH) and glutathione peroxidase (GSH-Px). Results: The hydrostatic pressures (15 and 70 mmHg) increased oxidative cell damage through a decrease of GSH and GSH-Px values, and increasing mitochondrial membrane potential. Additionally, 70 mmHg hydrostatic pressure for 24 h indicated highest apoptotic effects, as demonstrated by plate reader analyses of apoptosis, caspase-3 and -9 values. Conclusion: The present data indicated oxidative stress, apoptosis and mitochondrial changes in PC12 cell line during different hydrostatic pressure as a cell culture model of glaucoma. This findings support the view that mitochondrial oxidative injury contributes early to glaucomatous optic neuropathy.
    Journal of Receptor and Signal Transduction Research 05/2014; · 1.63 Impact Factor
  • Vahid Ghazizadeh, Mustafa Nazıroğlu
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    ABSTRACT: Incidence rates of epilepsy and use of Wi-Fi worldwide have been increasing. TRPV1 is a Ca(2+) permeable and non-selective channel, gated by noxious heat, oxidative stress and capsaicin (CAP). The hyperthermia and oxidant effects of Wi-Fi may induce apoptosis and Ca(2+) entry through activation of TRPV1 channel in epilepsy. Therefore, we tested the effects of Wi-Fi (2.45 GHz) exposure on Ca(2+) influx, oxidative stress and apoptosis through TRPV1 channel in the murine dorsal root ganglion (DRG) and hippocampus of pentylentetrazol (PTZ)-induced epileptic rats. Rats in the present study were divided into two groups as controls and PTZ. The PTZ groups were divided into two subgroups namely PTZ + Wi-Fi and PTZ + Wi-Fi + capsazepine (CPZ). The hippocampal and DRG neurons were freshly isolated from the rats. The DRG and hippocampus in PTZ + Wi-Fi and PTZ + Wi-Fi + CPZ groups were exposed to Wi-Fi for 1 hour before CAP stimulation. The cytosolic free Ca(2+), reactive oxygen species production, apoptosis, mitochondrial membrane depolarization, caspase-3 and -9 values in hippocampus were higher in the PTZ group than in the control although cell viability values decreased. The Wi-Fi exposure induced additional effects on the cytosolic Ca(2+) increase. However, pretreatment of the neurons with CPZ, results in a protection against epilepsy-induced Ca(2+) influx, apoptosis and oxidative damages. In results of whole cell patch-clamp experiments, treatment of DRG with Ca(2+) channel antagonists [thapsigargin, verapamil + diltiazem, 2-APB, MK-801] indicated that Wi-Fi exposure induced Ca(2+) influx via the TRPV1 channels. In conclusion, epilepsy and Wi-Fi in our experimental model is involved in Ca(2+) influx and oxidative stress-induced hippocampal and DRG death through activation of TRPV1 channels, and negative modulation of this channel activity by CPZ pretreatment may account for the neuroprotective activity against oxidative stress.
    Metabolic Brain Disease 05/2014; · 2.33 Impact Factor
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    ABSTRACT: Calcium ion (Ca(2+)) is one of the universal second messengers, which acts in a wide range of cellular processes. Results of recent studies indicated that ROS generated by depression leads to loss of endoplasmic reticulum-Ca(2+) homeostasis, oxidative stress, and apoptosis. Agomelatine and duloxetine are novel antidepressant and antioxidant drugs and may reduce oxidative stress, apoptosis, and Ca(2+) entry through TRPM2 and voltage-gated calcium channels. We tested the effects of agomelatine, duloxetine, and their combination on oxidative stress, Ca(2+) influx, mitochondrial depolarization, apoptosis, and caspase values in the PC-12 neuronal cells. PC-12 neuronal cells were exposed in cell culture and exposed to appropriate non-toxic concentrations and incubation times for agomelatine were determined in the neurons by assessing cell viability. Then PC-12 cells were incubated with agomelatine and duloxetine for 24 h. Treatment of cultured PC-12 cells with agomelatine, duloxetine, and their combination results in a protection on apoptosis, caspase-3, caspase-9, mitochondrial membrane depolarization, cytosolic ROS production, glutathione peroxidase, reduced glutathione, and lipid peroxidation, values. Ca(2+) entry through non-specific TRPM2 channel blocker (2-APB) and voltage-gated Ca(2+) channel blockers (verapamil and diltiazem) was modulated by agomelatine and duloxetine. However, effects of duloxetine on the Ca(2+) entry through TRPM2 channels were higher than in agomelatine. Results of current study suggest that the agomelatine and duloxetine are useful against apoptotic cell death and oxidative stress in PC-12 cells, which seem to be dependent on mitochondrial damage and increased levels of intracellular Ca(2+) through activation of TRPM2 and voltage-gated Ca(2+) channels.
    Journal of Membrane Biology 03/2014; · 2.48 Impact Factor
  • Seyit Ali Köse, Mustafa Nazıroğlu
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    ABSTRACT: Polycystic ovary syndrome (PCOS) is a common inflammatory disease with an uncertain pathogenesis, although one consistent finding is increased neutrophil activity. It has been recently reported that the essential antioxidant element selenium has protective effects on oxidative stress and cytosolic Ca(2+) concentrations in human neutrophil. We aimed to investigate the effects of selenium on oxidative stress and Ca(2+) levels through TRPV1 channels in neutrophils from patients with PCOS. Blood samples were obtained for neutrophil isolation from ten female patients with PCOS and ten healthy female subjects. Neutrophils isolated from PCOS group were investigated in four settings: (1) PCOS, (2) after incubation with TRPV1 channel blocker capsazepine (CPZ), (3) after incubation with selenium (sodium selenite), and (4) with combination (CPZ + selenium) exposure. Intracellular free Ca(2+) concentrations were higher in the patients than those in the controls, although their levels were reduced after CPZ and selenium incubations. The cytosolic Ca(2+) concentrations in neutrophils obtained from PCOS group were further decreased after incubation with CPZ + selenium, as compared with those exposed to neither agent. Lipid peroxidation levels were higher in the PCOS group than those in the control although neutrophil glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) values were decreased. The lipid peroxidation level was lower in the CPZ and selenium groups than that in the PCOS group although GSH and GSH-Px values were higher in the treatment with selenium and CPZ. In conclusion, we observed the importance of Ca(2+) influx into the neutrophils through TRPV1 channels in the pathogenesis of the patients with PCOS. The selenium appeared to provide a protective effect against oxidative stress and Ca(2+) entry through modulation of neutrophil TRPV1 calcium channels.
    Biological trace element research 03/2014; · 1.92 Impact Factor
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    ABSTRACT: Abstract Objectives: The present study determined the effects of mobile phone (900 and 1800 MHz)-induced electromagnetic radiation (EMR) exposure on oxidative stress in the brain and liver as well as the element levels in growing rats from pregnancy to 6 weeks of age. Methods: Thirty-two rats and their offspring were equally divided into 3 different groups: the control, 900 MHz, and 1800 MHz groups. The 900 MHz and 1800 MHz groups were exposed to EMR for 60 min/day during pregnancy and neonatal development. At the 4th, 5th, and 6th weeks of the experiment, brain samples were obtained. Results: Brain and liver glutathione peroxidase (GSH-Px) activities, as well as liver vitamin A and β-carotene concentrations decreased in the EMR groups, although brain iron, vitamin A, and β-carotene concentrations increased in the EMR groups. In the 6th week, selenium concentrations in the brain decreased in the EMR groups. There were no statistically significant differences in glutathione, vitamin E, chromium, copper, magnesium, manganese, and zinc concentrations between the 3 groups. Conclusion: EMR-induced oxidative stress in the brain and liver was reduced during the development of offspring. Mobile phone-induced EMR could be considered as a cause of oxidative brain and liver injury in growing rats.
    The journal of maternal-fetal & neonatal medicine: the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 03/2014; · 1.36 Impact Factor
  • Nilgün Senol, Mustafa Nazıroğlu, Vehbi Yürüker
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    ABSTRACT: It has been suggested that oxidative stress plays an important role in the pathophysiology of traumatic brain injury (TBI). N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1β and IL-4 levels in brain and blood of TBI-induced rats. We investigated effects of NAC and Se administration on physical injury-induced brain toxicity in rats. Thirty-six male Sprague-Dawley rats were equally divided into four groups. First and second groups were used as control and TBI groups, respectively. NAC and Se were administrated to rats constituting third and forth groups at 1, 24, 48 and 72 h after TBI induction, respectively. At the end of 72 h, plasma, erythrocytes and brain cortex samples were taken. TBI resulted in significant increase in brain cortex, erythrocytes and plasma lipid peroxidation, total oxidant status (TOS) in brain cortex, and plasma IL-1β values although brain cortex vitamin A, β-carotene, vitamin C, vitamin E, reduced glutathione (GSH) and total antioxidant status (TAS) values, and plasma vitamin E concentrations, plasma IL-4 level and brain cortex and erythrocyte glutathione peroxidase (GSH-Px) activities decreased by TBI. The lipid peroxidation and IL-1β values were decreased by NAC and Se treatments. Plasma IL-4, brain cortex GSH, TAS, vitamin C and vitamin E values were increased by NAC and Se treatments although the brain cortex vitamin A and erythrocyte GSH-Px values were increased through NAC only. In conclusion, NAC and Se caused protective effects on the TBI-induced oxidative brain injury and interleukin production by inhibiting free radical production, regulation of cytokine-dependent processes and supporting antioxidant redox system.
    Neurochemical Research 02/2014; · 2.13 Impact Factor
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    ABSTRACT: Behcet's disease (BD) is a chronic, inflammatory, and multisystemic condition although its pathogenesis is uncertain. Main component of St. John's wort (Hypericum perforatum, HP) is hyperforin and induces antiinflammatory and antioxidant properties. We aimed to investigate effects of HP on oxidative stress, apoptosis, and cytosolic-free Ca(2+) [Ca(2+)]i concentration in neutrophil of BD patients. Nine new-diagnosed active patients with BD and nine control subjects were included in the study. Disease activity was considered by clinical findings. Neutrophil samples were obtained from the patients and controls. The neutrophils from patients were divided into three subgroups and were incubated with HP, voltage-gated calcium channel (VGCC) blockers, (verapamil+dilitiazem) and non-specific TRPM2 channel blocker (2-aminoethyl diphenylborinate, 2-APB), respectively. The neutrophils were stimulated by fMLP as a Ca(2+)-concentration agonist and oxidative stress former. Caspase-3, caspase-9, apoptosis, lipid peroxidation, and [Ca(2+)]i values were high in the patient groups, although cell viability, glutathione (GSH), and glutathione peroxidase (GSH-Px) values were low in patient group. However, the [Ca(2+)]i, caspase-3, and caspase-9 values decreased markedly in patient+HP group although GSH and GSH-Px values increased in the group. The [Ca(2+)]i concentration was also decreased in the patient group by V+D, 2-APB, and HP incubations. In conclusion, we observed the importance of neutrophil Ca(2+) entry, apoptosis, and oxidative stress through gating VGCC and TRPM2 channels in the neutrophils in the pathogenesis and activation of the patients with BD. HP induced protective effects on oxidative stress by modulating Ca(2+) influx in BD patients.
    Journal of Membrane Biology 01/2014; · 2.48 Impact Factor
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    Mustafa Nazıroğlu, Bilal Ciğ, Cemil Ozgül
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    ABSTRACT: A main component of St. John's Wort (Hypericum Perforatum, HP) is hyperforin which has antioxidant properties in dorsal root ganglion (DRG) neurons, due to its ability to modulate NADPH oxidase and protein kinase C. Recent reports indicate that oxidative stress through NADPH oxidase activates TRPM2 channels. HP may be a useful treatment for Ca(2+) entry and oxidative stress through modulation of TRPM2 channels in the DRG. We aimed to investigate the protective role of HP on Ca(2+) entry and oxidative stress through TRPM2 channels in DRG neurons of rats. The native rat DRG neurons were used in whole-cell patch clamp, Fura-2 and antioxidant experiments. Appropriate, nontoxic concentrations and incubation times for HP were determined in the DRG neurons by assessing cell viability. The H2O2-induced TRPM2 currents were inhibited by 2-aminoethyldiphenyl borate (2-APB) and N-(p-amylcinnamoyl)anthranilic acid (ACA). TRPM2 current densities and cytosolic free Ca(2+) concentration in the neurons were also reduced by HP (2 and 24 hours). In Fura-2 experiments, cytosolic Ca(2+) mobilization was reduced by voltage-gated calcium channel blockers (verapamil+diltiazem, V+D) and HP. Glutathione peroxidase activity and GSH values in the DRG were high in HP, 2-APB and V+D groups although lipid peroxidation level was low in the groups. In conclusion, we observed a protective role for HP on Ca(2+) entry through a TRPM2 channel in the DRG neurons. Since over-production of oxidative stress and Ca(2+) entry are implicated in the pathophysiology of neuropathic pain and neuronal inflammation, our findings may be relevant to the etiology and treatment of neuropathology in DRG neurons.
    Neuroscience 01/2014; · 3.12 Impact Factor
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    ABSTRACT: Introduction: Melatonin has been considered a potent antioxidant that detoxifies a variety of reactive oxygen species in many pathophysiological states of eye. The present study was designed to determine the effects of Wi-Fi exposure on the lens oxidant, antioxidant redox systems, as well as the possible protective effects of melatonin on the lens injury induced by electromagnetic radiation (EMR). Materials and Methods: Thirty-two rats were used in the current study and they were randomly divided into four equal groups as follows: First and second groups were cage-control and sham-control rats. Rats in third group were exposed to Wi-Fi (2.45 GHz) for duration of 60 min/day for 30 days. As in the third group, the fourth group was treated with melatonin. The one-hour exposure to irradiation in second, third and fourth took place at noon each day. Results: Lipid peroxidation levels in the lens were slightly higher in third (Wi-Fi) group than in cage and sham control groups although their concentrations were significantly (P < 0.05) decreased by melatonin supplementation. Glutathione peroxidase (GSH-Px) activity was significantly (P < 0.05) lower in Wi-Fi group than in cage and sham control groups although GSH-Px (P < 0.01) and reduced glutathione (P < 0.05) values were significantly higher in Wi-Fi + melatonin group than in Wi-Fi group. Conclusions: There are poor oxidative toxic effects of one hour of Wi-Fi exposure on the lens in the animals. However, melatonin supplementation in the lens seems to have protective effects on the oxidant system by modulation of GSH-Px activity.
    Indian Journal of Ophthalmology 01/2014; 62(1):12-5. · 1.02 Impact Factor
  • M. Nazıroğlu, B. Çiğ, C. Özgül
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    ABSTRACT: Possible modulator role of Hypericum perforatum (HP) through protein kinase C (PKC) modulators and antioxidant properties of HP on Ca2+ signaling and oxidative stress through TRPM2 channels in the DRG neurons. ADP-ribose pyrophosphate enzyme of TRPM2 channels in the Nudix domain are activated by ADP-ribose and oxidative stress.
    Neuroscience 01/2014; 263:27–35. · 3.12 Impact Factor
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    ABSTRACT: We investigated the effects of bisphosphonate (BP) on oxidative stress levels in blood of patients with cancer. In total, 19 patients with cancer and 21 healthy subjects were included in the study. BP was intravenously administrated to the participants for 6 weeks. The patients had higher lipid peroxidation (LP) levels in the plasma and erythrocyte samples but lower glutathione peroxidase (GSH-Px) and plasma vitamin E values. In patients treated with BP, calcium and LP levels decreased, but GSH-Px and vitamin E values improved. In conclusion, we observed that treatment with BP alleviated oxidative stress induced by cancer.
    Cancer Investigation 12/2013; · 2.24 Impact Factor
  • Onder Kaplan, Mustafa Nazıroğlu, Mehmet Güney, Mehmet Aykur
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    ABSTRACT: Primary dysmenorrhea is a common inflammatory disease with an uncertain pathogenesis, although one consistent finding is increased neutrophil activity. We aimed to investigate the effects of a non-steroidal anti-inflammatory drug (NSAID) on oxidative stress and Ca(2+) levels in neutrophils from patients with primary dysmenorrhea. Blood samples were obtained for neutrophil isolation from six female patients with primary dysmenorrhea (patients) and six healthy female subjects. The NSAID (diclofenac) was taken daily by the patient group for 6 weeks before a second blood sample was taken. Neutrophils isolated after diclofenac treatment were investigated in three settings: (1) after incubation with verapamil and diltiazem (V+D), (2) after incubation with 2-aminoethoxydiphenyl borate (2-APB), and (3) with neither exposure. Neutrophil lipid peroxidation and stimulated intracellular Ca(2+) levels were higher in the patients than in the controls, although their levels were reduced after six weeks of treatment with diclofenac. Ca(2+) levels from neutrophils obtained after diclofenac treatment were further decreased after incubation with V+D or 2-APB, compared with those exposed to neither agent. Neutrophil glutathione peroxidase and total antioxidant status were lower in the patients than in the controls and higher post-treatment with diclofenac. Reduced glutathione levels were similar in the control, patient, and treatment groups. In conclusion, we observed the importance of Ca(2+) influx into the neutrophils and oxidative stress in the pathogenesis of the patients with primary dysmenorrhea. The NSAID diclofenac appeared to provide a protective effect against oxidative stress and Ca(2+) entry through modulation of neutrophil VGCC and TRP calcium channels.
    Journal of Reproductive Immunology 11/2013; · 2.34 Impact Factor
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    ABSTRACT: Environmental exposure to electromagnetic radiation (EMR) has been increasing with the increasing demand for communication devices. The aim of the study was to discuss the mechanisms and risk factors of EMR changes on reproductive functions and membrane oxidative biology in females and males. It was reported that even chronic exposure to EMR did not increase the risk of reproductive functions such as increased levels of neoantigens abort. However, the results of some studies indicate that EMR induced endometriosis and inflammation and decreased the number of follicles in the ovarium or uterus of rats. In studies with male rats, exposure caused degeneration in the seminiferous tubules, reduction in the number of Leydig cells and testosterone production as well as increases in luteinizing hormone levels and apoptotic cells. In some cases of male and female infertility, increased levels of oxidative stress and lipid peroxidation and decreased values of antioxidants such as melatonin, vitamin E and glutathione peroxidase were reported in animals exposed to EMR. In conclusion, the results of current studies indicate that oxidative stress from exposure to Wi-Fi and mobile phone-induced EMR is a significant mechanism affecting female and male reproductive systems. However, there is no evidence to this date to support an increased risk of female and male infertility related to EMR exposure.
    Journal of Membrane Biology 10/2013; · 2.48 Impact Factor
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    ABSTRACT: The present study was designed to determine the effects of both Wi-Fi (2.45 GHz)- and mobile phone (900 and 1800 MHz)-induced electromagnetic radiation (EMR) on oxidative stress and trace element levels in the kidney and testis of growing rats from pregnancy to 6 weeks of age. Thirty-two rats and their 96 newborn offspring were equally divided into four different groups, namely, control, 2.45 GHz, 900 MHz, and 1800 MHz groups. The 2.45 GHz, 900 MHz, and 1,800 MHz groups were exposed to EMR for 60 min/day during pregnancy and growth. During the fourth, fifth, and sixth weeks of the experiment, kidney and testis samples were taken from decapitated rats. Results from the fourth week showed that the level of lipid peroxidation in the kidney and testis and the copper, zinc, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), and total antioxidant status (TAS) values in the kidney decreased in the EMR groups, while iron concentrations in the kidney as well as vitamin A and vitamin E concentrations in the testis increased in the EMR groups. Results for fifth-week samples showed that iron, vitamin A, and β-carotene concentrations in the kidney increased in the EMR groups, while the GSH and TAS levels decreased. The sixth week results showed that iron concentrations in the kidney and the extent of lipid peroxidation in the kidney and testis increased in the EMR groups, while copper, TAS, and GSH concentrations decreased. There were no statistically significant differences in kidney chromium, magnesium, and manganese concentrations among the four groups. In conclusion, Wi-Fi- and mobile phone-induced EMR caused oxidative damage by increasing the extent of lipid peroxidation and the iron level, while decreasing total antioxidant status, copper, and GSH values. Wi-Fi- and mobile phone-induced EMR may cause precocious puberty and oxidative kidney and testis injury in growing rats.
    Biological trace element research 10/2013; · 1.92 Impact Factor
  • Murat Koçer, Mustafa Nazıroğlu
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    ABSTRACT: The administration of chemotherapeutic agents for colorectal carcinoma is associated with an increase in oxidative stress and a concomitant decrease in antioxidant and element levels in the blood. This study investigated the effects of 5-fluorouracil (5-FU) chemotherapy on the levels of lipid peroxidation, reduced glutathione (GSH), glutathione peroxidase (GSH-Px), antioxidant vitamins, and elements in colorectal cancer patients. Twelve patients with newly diagnosed colorectal carcinoma and 12 healthy subjects were included in this study. Blood samples were collected from both the healthy controls and patients. 5-FU was intravenously administered to the patients for 6 weeks, and blood samples were collected again from the treatment group. In the patient group, lipid peroxidation levels were increased in both the plasma and erythrocyte samples, whereas GSH-Px activity and concentrations of GSH, vitamin E, and β-carotene in erythrocytes were decreased. The oxidant, antioxidant, and plasma calcium values were lower in 5-FU-treated patients than in the controls. Plasma vitamin A, chloride, sodium, and potassium concentrations did not change with 5-FU treatment. In conclusion, oxidative stress in patients with newly diagnosed colorectal cancer is attributable to the disease and not to 5-FU treatment. Blood vitamin E, β-carotene, GSH, and GSH-Px levels could be useful as early biomarkers of the prognosis of colorectal cancer patients.
    Biological trace element research 08/2013; · 1.92 Impact Factor

Publication Stats

722 Citations
151.71 Total Impact Points

Institutions

  • 2014
    • Suleyman Demirel University
      Almaty, Almaty Qalasy, Kazakhstan
  • 2007–2014
    • T.C. Süleyman Demirel Üniversitesi
      • • Department of Biophysics
      • • Faculty of Medicine
      Hamitabat, Isparta, Turkey
  • 2013
    • Badji Mokhtar - Annaba University
      Bône, Annaba, Algeria
  • 2012
    • Istanbul University
      • Department of Family Medicine (Cerrahpasa Faculty of Medicine)
      İstanbul, Istanbul, Turkey