Aysegul Cort

Kafkas University, Cars, Kars, Turkey

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Publications (15)38.55 Total impact

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    ABSTRACT: PURPOSE: Copeptin, the C-terminal fragment of antidiuretic hormone (ADH), is a new biomarker that has been found to be elevated in several cardiovascular disorders and is related with prognosis. Patients with obstructive sleep apnea demonstrate a tendency to develop coronary and cerebral atherosclerotic disease. Our aim was to investigate copeptin levels in untreated new diagnosed obstructive sleep apnea patients without manifest cardiovascular disorders in order to determine whether copeptin could be used as a biomarker in this group. METHODS: A total of 60 patients with obstructive sleep apnea, diagnosed with polysomnography, and 23 healthy volunteers were enrolled into this study. Blood samples were collected after overnight fasting, and copeptin level was measured with an enzyme immunoassay method. RESULTS: Patients with obstructive sleep apnea had a higher incidence of hypertension and body mass index but lower serum copeptin level (0.48 ± 0.24. vs. 0.64 ± 0.28 ng/ml, p = 0.007) compared with the healthy controls. There was no significant difference regarding to serum copeptin levels between the moderate (n = 13) and severe (n = 47) obstructive sleep apnea patients (0.42 ± 0.18 vs. 0.49 ± 0.26 ng/ml, p = 0.409). CONCLUSIONS: Rather than reflecting a reduced risk for cardiovascular disorders, we consider that reduced copeptin level is related with disturbed ADH secretion in obstructive sleep apnea patients. Therefore, it would not be advisable to measure copeptin levels in obstructive sleep apnea patients to determine cardiovascular risk, while this marker could be valuable to demonstrate impairment in ADH regulation in this patient group.
    Sleep And Breathing 02/2013; · 2.26 Impact Factor
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    ABSTRACT: Antioxidants may prevent apoptosis of cancer cells via inhibiting reactive oxygen species (ROS). However, to date no study has been carried out to elucidate the effects of strong antioxidant N-acetylcysteine (NAC) on Bleomycin induced apoptosis in human testicular cancer (NTERA-2, NT2) cells. For this reason, we studied the effects of Bleomycin and NAC alone and in combination on apoptotic signalling pathways in NT2 cell line. We determined the cytotoxic effect of bleomycin on NT2 cells and measured apoptosis markers such as Caspase-3, -8, -9 activities and Bcl-2, Bax, Cyt-c, Annexin V-FTIC and PI levels in NT2 cells incubated with different agents for 24 h. Early apoptosis was determined using FACS assay. We found half of the lethal dose (LD(50) ) of Bleomycin on NT2 cell viability as 400; 100; and 20 µg/ml after incubations for 24 h; 48 h; and 72 h, respectively. Incubation with bleomycin (LD(50) ) and H(2) O(2) for 24 h increased Caspase-3, -8, -9 activities, Cyt-c and Bax levels and decreased Bcl-2 levels. The concurrent incubation of NT2 cells with bleomycin/H(2) O(2) and NAC (5 mM) for 24 h abolished bleomycin/H(2) O(2) -dependent increases in Caspase-3,-8,-9 activities, Bax and Cyt-c levels and bleomycin/H(2) O(2) -dependent decrease in Bcl-2 level. Our results indicate that bleomycin/H(2) O(2) induce apoptosis in NT2 cells by activating mitochondrial pathway of apoptosis, while NAC diminishes bleomycin/H(2) O(2) induced apoptosis. We conclude that NAC has antagonistic effects on Bleomycin-induced apoptosis in NT2 cells and causes resistance to apoptosis which is not a desired effect in eliminating cancer cells. J. Cell. Biochem. © 2013 Wiley Periodicals, Inc.
    Journal of Cellular Biochemistry 02/2013; · 3.06 Impact Factor
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    ABSTRACT: Testicular cancer is the most common cancer among young men of reproductive age. Bleomycin is a frequently used drug for the treatment of several malignancies and is part of the chemotherapy protocols in testicular cancer. Bleomycin causes an increase in oxidative stress which has been shown to induce apoptosis in cancer cells. Curcumin (diferuloylmethane), an active component of the spice turmeric, has attracted interest because of its anti-inflammatory and chemopreventive activities. However, no study has been carried out so far to elucidate its interaction with bleomycin in testicular cancer cells. In this study, we investigated the effects of curcumin and bleomycin on apoptosis signalling pathways and compared the effects of bleomycin with H2O2 which directly produces reactive oxygen species. We measured apoptosis markers such as caspase-3, caspase-8, and caspase-9 activities and Bcl-2, Bax, and Cyt-c levels in NCCIT cells incubated with curcumin (5 μM), bleomycin (120 μg/ml), bleomycin + curcumin, H2O2 (35 μM), and H2O2 + curcumin for 72 h. Curcumin, bleomycin, and H2O2 caused apoptosis indicated as increases in caspase-3, caspase-8, and caspase-9 activities and Bax and cytoplasmic Cyt-c levels and a decrease in Bcl-2 level. Concurrent use of curcumin with bleomycin decreased caspase activities and Bax and Cyt-c levels compared to their separate effects in NCCIT cells. Our findings suggest that concurrent use of curcumin during chemotherapy in testis cancer should be avoided due to the inhibitory effect of curcumin on bleomycin-induced apoptosis.
    Journal of physiology and biochemistry 09/2012; 69(2). · 1.65 Impact Factor
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    ABSTRACT: Polyunsaturated fatty acids (PUFA) are major components of phospholipids, the principal structural unit of biological membranes. Unsaturated fatty acids have one or more double-bonds in a cis or trans configuration. Trans isomers are able to perturb both cell membrane arrangement and lipid enzymatic cascades. Endogenous trans fatty acid isomers are formed by the isomerization of fatty acids in cell membranes due to an endogenous free radical process. Reactive oxygen species (ROS) lead to the oxidative degradation of lipids in cell membranes, resulting in cell damage. Cell membranes, which are structurally made up of large amounts of PUFA, are highly susceptible to oxidative attack and, consequent changes result in altered membrane fluidity, permeability, and cellular metabolic dysfunction. N-acetyl cysteine (NAC) is a potent anti-oxidant, can react directly with ROS and a source of cysteine for glutathione synthesis and increases levels of glutathione which is the major antioxidant of body. NAC has been shown to have protective effects towards DNA damage and carcinogenesis. In this study, we identified the fatty acid profile of human testicular cancer cell membranes and examined the effect of NAC on the membrane fatty acid profile of these cells. The membrane fatty acid profile analysis in control and NAC treated samples were performed using gas chromatography (GC) with external reference standards. Membrane lipid were extracted and transesterification was performed to obtain the fatty acid residues as the corresponding methyl esters. Incubation of cells with 10 mM NAC for 24 hour, caused an increase in trans fatty acid concentration and saturated fatty acid percentage. Unlike to these findings, incubation with NAC decreased PUFA and monounsaturated fatty acids percentage in testicular cancer cell membranes.
    FEBS Journal 09/2012; 279(SI(1)):125. · 4.25 Impact Factor
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    ABSTRACT: Testicular cancer is a very common cancer in males aged 15-44 years. Bleomycin is used in chemotherapy regimens in the treatment of patients having testicular germ-cell tumor. Bleomycin generates oxygen radicals, induces oxidative cleavage of DNA strand and induces apoptosis in cancer cells. There is no study in the literature investigating effects of N-Acetyl-l-Cysteine (NAC) on bleomycin-induced oxidative stress in testicular germ cell tumors. For this reason, we studied effects of NAC on oxidative stress produced in wild-type NTera-2 and p53-mutant NCCIT testis cancer cells incubated with bleomycin and compared the results with H(2)O(2) which directly produces oxidative stress. We determined protein carbonyl content, thiobarbituric acid reactive substances (TBARS), glutathione (GSH), 8-isoprostane, lipid hydroperoxide levels and total antioxidant capacity in both testicular cancer cells. Bleomycin and H(2)O(2) significantly increased 8-isoprostane, TBARS, protein carbonyl and lipid hydroperoxide levels in NTera-2 and NCCIT cells. Bleomycin and H(2)O(2) significantly decreased antioxidant capacity and GSH levels in both cell lines. Co-incubation with NAC significantly decreased lipid hydroperoxide, 8-isoprostane, protein carbonyl content and TBARS levels increased by bleomycin and H(2)O(2). NAC enhanced GSH levels and antioxidant capacity in the NTera-2 and NCCIT cells. It can be concluded that NAC diminishes oxidative stress in human testicular cancer cells induced by bleomycin and H(2)O(2).
    Biochimie 08/2012; · 3.14 Impact Factor
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    ABSTRACT: Bleomycin is commonly used in the treatment of testicular cancer. Bleomycin generates oxygen radicals, induces the oxidative cleavage of DNA strands and induces cancer cell apoptosis. Curcumin (diferuloylmethane) is a potent antioxidant and chief component of the spice turmeric. No study investigating the effects of curcumin on intrinsic and bleomycin-induced oxidative stress in testicular germ cell tumors has been reported in the literature. For this reason, the present study aimed to examine the effects of curcumin on oxidative stress produced in wild-type NTera-2 and p53-mutant NCCIT testicular cancer cells incubated with bleomycin and the results were compared with cells treated with H2O2 which directly produces oxidative stress. The protein carbonyl content, thiobarbituric acid reactive substances (TBARS), glutathione (GSH), 8-isoprostane, lipid hydroperoxide (LPO) levels and total antioxidant capacity in the two testicular cancer cell lines were determined. Results showed that bleomycin and H2O2 significantly increased protein carbonyl, TBARS, 8-isoprostane and LPO levels in the NTera-2 and NCCIT cell lines. Bleomycin and H2O2 significantly decreased the antioxidant capacity and GSH levels in NTera-2 cells. Curcumin significantly decreased LPO, 8-isoprostane and protein carbonyl content, and TBARS levels increased in cells treated with bleomycin and H2O2. Curcumin enhanced GSH levels and the antioxidant capacity of NTera-2 cells. In conclusion, curcumin inhibits bleomycin and H2O2-induced oxidative stress in human testicular cancer cells.
    Molecular Medicine Reports 07/2012; 6(4):860-6. · 1.17 Impact Factor
  • 22nd Biennial Congress of the European-Association-for-Cancer-Research; 07/2012
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    ABSTRACT: Oxidative stress has been shown to induce apoptosis in cancer cells. Therefore, one might suspect that antioxidants may inhibit reactive oxygen species (ROS) and prevent apoptosis of cancer cells. No study has been carried out so far to elucidate the effects of N-acetylcysteine (NAC) on bleomycin-induced apoptosis in human testicular cancer (NCCIT) cells. We investigated the molecular mechanisms of apoptosis induced by bleomycin and the effect of NAC in NCCIT cells. We compared the effects of bleomycin on apoptosis with H(2)O(2) which directly produces ROS. Strong antioxidant NAC was evaluated alone and in combination with bleomycin or H(2)O(2) in germ cell tumor-derived NCCIT cell line (embryonal carcinoma, being the nonseminomatous stem cell component). We determined the cytotoxic effect of bleomycin and H(2)O(2) on NCCIT cells and measured apoptosis markers such as caspase-3, caspase-8, and caspase-9 activities and Bcl-2, Bax, and cytochrome c (Cyt-c) levels in NCCIT cells incubated with bleomycin, H(2)O(2), and/or NAC. We found half of the lethal dose (LD(50)) of bleomycin on NCCIT cell viability as 120 μg/ml after incubation for 72 h. Incubation with bleomycin (LD(50)) induced increases in caspase-3, caspase-8, and caspase-9 activities and Cyt-c and Bax protein levels and a decrease in Bcl-2 level. Co-incubation of NCCIT cells with bleomycin and 10 mM NAC abolished bleomycin-induced increases in caspase-3 and caspase-9 activities, Bax, and Cyt-c levels and bleomycin-induced decrease in Bcl-2 level. Our results indicate that bleomycin induces apoptosis in NICCT cells and that NAC diminishes bleomycin-induced apoptosis via inhibiting the mitochondrial pathway. We conclude that NAC has negative effects on bleomycin-induced apoptosis in NICCT cells and causes resistance to apoptosis, which is not a desirable effect in the fight against cancer.
    Journal of physiology and biochemistry 05/2012; · 1.65 Impact Factor
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    ABSTRACT: Testicular cancer is the most common cancer among young men of reproductive age. Bleomycin is a frequently used drug for the treatment of several malignancies and is part of the chemotherapy protocols used for testicular cancer; however, side-effects are common. Bleomycin causes an increase in oxidative stress which has been shown to induce apoptosis in cancer cells. Curcumin (diferuloylmethane), an active component of the spice turmeric, has been demonstrated to induce apoptosis in a number of malignancies. However, to date no study has been carried out to elucidate its anticancer activity and interaction with bleomycin in testicular cancer cells. In this study, we investigated and compared the effects of curcumin, bleomycin and hydrogen peroxide (H2O2) on apoptotic signaling pathways. Curcumin (20 µM), bleomycin (400 µg/ml) and H2O2 (400 µM) incubation for 24 h decreased the viability of NTera-2 cells, and increased caspase-3, -8 and -9 activities, Bax and cytoplasmic cytochrome c levels and decreased Bcl-2 levels. The concurrent use of curcumin with bleomycin induced caspase-3, -8 and -9 activities to a greater extent in NTera-2 cells than the use of each drug alone. Our observations suggest that the effects of curcumin and bleomycin on apoptotic signaling pathways are synergistic. Therefore, we propose to use curcumin together with bleomycin to decrease its therapeutic dose and, therefore, its side-effects.
    Molecular Medicine Reports 03/2012; 5(6):1481-6. · 1.17 Impact Factor
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    ABSTRACT: This study aimed to determine plasma and neutrophil oxidase activities that may contribute to vascular inflammation in Behçet's disease (BD) patients. Cyclooxygenase (COX), NADPH oxidase and myeloperoxidase (MPO) activity was determined in neutrophils isolated from BD patients and healthy controls. Functional assay of NADPH oxidase was significantly increased in BD patients, both at basal conditions and in response to fMLP stimulation. There was a significant increase in plasma MPO activity in the disease group as compared to controls. Total COX activity was significantly increased in BD neutrophils. The increase in total COX activity was accompanied with enhanced activity of COX-2, differentiated by using the COX-1 isoform-specific inhibitor SC-560. Neutrophil nitrate/nitrite levels showed no significant difference in BD; however, plasma nitrate/nitrite contents in BD patients were significantly greater compared to controls. In conclusion, increased plasma MPO, neutrophil NADPH and COX activities may contribute to intravascular inflammation documented in BD patients.
    Journal of Enzyme Inhibition and Medicinal Chemistry 06/2011; 27(1):12-7. · 1.50 Impact Factor
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    ABSTRACT: This study aimed to clarify the possible therapeutic benefit of preferential nitric oxide synthase (NOS) inhibition and catalytic antioxidant Mn (III) meso-tetrakis (N-n-hexylpyridinium-2-yl) porphyrin (MnTnHex-2-PyP(5+)) treatment in a rat model of elevated intraocular pressure (EIOP). Rats were randomly divided into different experimental groups which received either intraperitoneal MnTnHex-2-PyP(5+) (0.1 mg/kg/day), intragastric NOS inhibitor (S-methylthiourea: SMT; 5 mg/kg/day) or both agents for a period of 6 weeks. Ocular hypertension was induced by unilaterally cauterizing three episcleral vessels and the unoperated eye served as control. Neuroprotective effects of given treatments were determined via electrophysiological measurements of visual evoked potentials (VEP) while retina and vitreous levels of MnTnHex-2-PyP(5+) were measured via LC-MS/MS. Latencies of all VEP components (P(1), N(1), P(2), N(2), P(3)) were significantly prolonged (p < 0.05) in EIOP and returned to control levels following all three treatment protocols. Ocular hypertension significantly increased retinal protein nitration (p < 0.001) which returned to baseline levels in all treated groups. NOS-2 expression and nitrate/nitrite levels were significantly greater in non-treated rats with EIOP. Retinal TUNEL staining showed apoptosis in all ocular hypertensive rats. The presented data confirm the role of oxidative injury in EIOP and highlight the protective effect of MnTnHex-2-PyP(5+) treatment and NOS inhibition in ocular hypertension.
    Experimental Eye Research 06/2011; 93(4):387-96. · 3.03 Impact Factor
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    ABSTRACT: Polyunsaturated fatty acids are major components of phospholipids, the principal structural unit of biological membranes. Unsaturated fatty acids have one or more double-bonds in a cis or trans configuration. Trans isomers are able to perturb both cell membrane arrangement and lipid enzymatic cascades. Endogenous trans fatty acid isomers are relative to the isomerization of fatty acids in cell membranes due to an endogenous free radical process. Reactive oxygen species (ROS) lead to the oxidative degradation of lipids in cell membranes, resulting in cell damage. Cell membranes, which are structurally made up of large amounts of PUFA, are highly susceptible to oxidative attack and, consequent changes result in altered membrane fluidity, permeability, and cellular metabolic dysfunction. Some chemotherapeutic agents and all radiation therapy induce oxidative stress by generation of ROS which might be an alternative mechanism for their cytotoxic effect via inducing cell death. Bleomycin is used commonly in the treatment of testicular cancer. Bleomycin is an antibiotic which affects nucleic acids and generates high level of ROS. In this study, we aimed to compare the fatty acid profile of human testicular cancer cell membranes during normal culturing and bleomycin treatment. The evaluation of fatty acid concentration in control and bleomycin treated samples was carried out by using standards as the external reference in the gas chromatography (GC) analysis. Lipid extraction and transesterification to obtain the fatty acid residues as the corresponding methyl esters were performed. Incubation of cells with 100 ug/ml bleomycin for 24 hours, caused an increase in trans lipid concentration. Our results indicated that bleomycin induced ROS generation results in trans lipid isomerization in testicular cancer cell membrane.
    FEBS Journal 06/2011; 278(SI(1)):201. · 4.25 Impact Factor
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    ABSTRACT: The aim of this study was to clarify the possible protective effect of astaxanthin (ASX) on the retina in rats with elevated intraocular pressure (EIOP). Rats were randomly divided into two groups which received olive oil or 5mg/kg/day ASX for a period of 8 weeks. Elevated intraocular pressure was induced by unilaterally cauterizing three episcleral vessels and the unoperated eye served as control. At the end of the experimental period, neuroprotective effect of ASX was determined via electrophysiological measurements of visual evoked potentials (VEP) and rats were subsequently sacrificed to obtain enucleated globes which were divided into four groups including control, ASX treated, EIOP, EIOP+ASX treated. Retinoprotective properties of ASX were determined by evaluating retinal apoptosis, protein carbonyl levels and nitric oxide synthase-2 (NOS-2) expression. Latencies of all VEP components were significantly prolonged in EIOP and returned to control levels following ASX administration. When compared to controls, EIOP significantly increased retinal protein oxidation which returned to baseline levels in ASX treated EIOP group. NOS-2 expression determined by Western blot analysis and immunohistochemical staining was significantly greater in rats with EIOP compared to ASX and control groups. Retinal TUNEL staining showed apoptosis in all EIOP groups; however ASX treatment significantly decreased the percent of apoptotic cells when compared to non treated ocular hypertensive controls. The presented data confirm the role of oxidative injury in EIOP and highlight the protective effect of ASX in ocular hypertension.
    Regulatory Toxicology and Pharmacology 05/2010; 58(1):121-30. · 2.13 Impact Factor
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    ABSTRACT: This study investigated the effect of astaxanthin (ASX; 3,3-dihydroxybeta, beta-carotene-4,4-dione), a water-dispersible synthetic carotenoid, on liver ischemia-reperfusion (IR) injury. Astaxanthin (5 mg/kg/day) or olive oil was administered to rats via intragastric intubation for 14 consecutive days before the induction of hepatic IR. On the 15th day, blood vessels supplying the median and left lateral hepatic lobes were occluded with an arterial clamp for 60 min, followed by 60 min reperfusion. At the end of the experimental period, blood samples were obtained from the right ventricule to determine plasma alanine aminotransferase (ALT) and xanthine oxidase (XO) activities and animals were sacrificed to obtain samples of nonischemic and postischemic liver tissue. The effects of ASX on IR injury were evaluated by assessing hepatic ultrastructure via transmission electron microscopy and by histopathological scoring. Hepatic conversion of xanthine dehygrogenase (XDH) to XO, total GSH and protein carbonyl levels were also measured as markers of oxidative stress. Expression of NOS2 was determined by immunohistochemistry and Western blot analysis while nitrate/nitrite levels were measured via spectral analysis. Total histopathological scoring of cellular damage was significantly decreased in hepatic IR injury following ASX treatment. Electron microscopy of postischemic tissue demonstrated parenchymal cell damage, swelling of mitochondria, disarrangement of rough endoplasmatic reticulum which was also partially reduced by ASX treatment. Astaxanthine treatment significantly decreased hepatic conversion of XDH to XO and tissue protein carbonyl levels following IR injury. The current results suggest that the mechanisms of action by which ASX reduces IR damage may include antioxidant protection against oxidative injury.
    Toxicology 11/2009; 267(1-3):147-53. · 4.02 Impact Factor
  • Mutay Aslan, Aysegul Cort, Iclal Yucel
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    ABSTRACT: Glaucoma is a progressive optic neuropathy and is the leading cause of blindness in the United States and other industrialized countries. Elevated pressure in the eye is a risk factor for glaucoma and indeed experimental studies of induced pressure elevation in nonhuman primate's results in typical glaucomatous optic nerve damage. However, normal intraocular pressure can also lead to loss of vision in glaucoma. Although the initiating causes leading to glaucoma are unknown, oxidative and nitrative stress appears to play a role in the progressive neuronal death that is characteristic of glaucomatous optic nerve damage. Increased markers of oxidative stress that have been reported in glaucoma include protein nitrotyrosine, carbonyls in proteins, lipid oxidation products and oxidized DNA bases. Studies have also highlighted the role of nitric oxide in glaucoma by reporting the presence of inducible nitric oxide synthase in the iris-ciliary body, retina and in the glaucomatous optic nerve head of experimental rat models. This review discusses the role of reactive oxygen and nitrogen species in the pathogenesis of glaucoma and examines the relevance of antioxidants in neurodegeneration associated with the disease. It is concluded that oxidative and nitrative stress have a pathogenic role in glaucoma.
    Free Radical Biology and Medicine 09/2008; 45(4):367-76. · 5.27 Impact Factor