Yazar "Gulec, M" seçeneğine göre listele
Listeleniyor 1 - 10 / 10
Sayfa Başına Sonuç
Sıralama seçenekleri
Öğe Antioxidant enzyme activities and oxidative stress in affective disorders(Lippincott Williams & Wilkins, 2004) Ozcan, ME; Gulec, M; Ozerol, E; Polat, R; Akyol, ORecent data from several reports indicate that free radicals are involved in the biochemical mechanisms underlying neuropsychiatric disorders in human. The results of several reports suggest that lower antioxidant defences against lipid peroxidation exist in patients with depression and that there is a therapeutic benefit from antioxidant supplementation in unstable manic-depressive patients. We investigated the antioxidant enzyme status and the indices of oxidative stress and lipid peroxidation end products in erythrocytes from patients with affective disorder. For this purpose, we measured superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities, as well as malondialdehyde (MDA) and nitric oxide (NO) levels in patients with affective disorders (n=30) in both pre- and post-treatment periods, and in a control group (n = 21). CAT activities were significantly decreased in both pre-, and post-treatment periods in patients compared to the control group. GSH-Px activity in the pre-treatment period in the patients was significantly lower than both post-treatment patient and control groups. MDA levels were increased in both pre-, and post-treatment patient groups compared to the control group. NO level was lower in the pre-treatment patient group than in the control group. There were statistically significant correlations between SOD and MDA, and SOD and NO in the pre-treatment patient and control groups. Because the overall study sample was small, and the post-treatment patient group was even smaller, it can tentatively be suggested that the antioxidant system is impaired during a mood episode in patients with affective disorders, normalizing at the end of the episode. (C) 2004 Lippincott Williams Wilkins.Öğe Antioxidant properties of propofol and erythropoietin after closed head injury in rats(Pergamon-Elsevier Science Ltd, 2005) Ozturk, E; Demirbilek, S; But, AK; Saricicek, V; Gulec, M; Akyol, O; Ersoy, MOReactive oxygen species play a role during brain injury due to closed head trauma. Enzymatic or nonenzymatic antioxidants may protect brain tissue against oxidative damage. The present study was performed to assess the changes of endogenous indices of oxidative stress in serum from rats subjected to head trauma and whether treatment with propofol and/or erythropoietin (EPO) modifies the levels of endogenous indices of oxidative stress. For these purposes, female Wistar Albino rats were divided into five groups: nontraumatic sham group, trauma performed control, trauma with propofol (i.p.), trauma with EPO (i.p.) and trauma with propofol and EPO performed study groups. At the end of the experimental procedure, blood was taken by cardiac puncture to determine superoxide dismutase (SOD) and xanthine oxidase (XO) activities as well as malondialdehyde (MDA) and nitric oxide (NO) levels in serum. Serum NIDA level of control traumatic brain injury (TBI) group was significantly higher than sham operation group (p < 0.012). Serum NIDA levels in propofol, EPO and propofol+EPO groups were found to be decreased in comparison with control group (p < 0.039, p < 0.030 and p < 0.018, respectively). Serum NO level was found to be increased in TBI group, but difference was not statistically significant when compared to sham-operated group (p=0.092). Propofol, EPO and propofol+EPO administration efficiently reduced serum NO levels to reach sham-operated group (p < 0.002, p < 0.001 and p < 0.015, respectively). These results suggested that acute administration of both propofol and EPO altered the indices of oxidative stress similarly against brain injury due to trauma. (c) 2005 Elsevier Inc. All rights reserved.Öğe Caffeic acid phenethyl ester ameliorated ototoxicity induced by cisplatin in rats(E I F T Srl, 2004) Kizilay, A; Kalcioglu, MT; Ozerol, E; Iraz, M; Gulec, M; Akyol, O; Ozturan, OCaffeic acid phenethyl ester (CAPE), an active component of propolis, exhibits antioxidant properties. This experimental study was designed to determine the effect of CAPE on ototoxicity induced with cisplatin. Twenty-four adult Wistar albino rats were divided into four groups: cisplatin (n=6), saline (n=6), CAPE (n=6), and cisplatin plus CAPE (n=6). Rats were tested before and 5 days after cisplatin treatment with or without chemo protection. The Distortion Product Otoacoustic Emissions (DPOAEs) were elicited from the control and experimental animals utilizing the standard commercial Otoacoustic Emission (OAEs) apparatus. The animals in all groups were sacrificed under general anesthesia on the fifth day following last OAE measurements. For biochemical investigations, the blood samples were drawn from inferior vena cava. On day 0, the initial baseline DPOAEs measurement results presented similar values while comparing the groups in drug free phase (p>0.05). On day 5, intrasubject measurement parameters of DPgrams and I/O functions of cisplatin group were significantly deteriorated (p<0.05). The second measurements of the other groups revealed no significant differences between their DPgrams and I/O functions in all frequencies (p>0.05). Among the biochemical parameters, plasma xanthine oxidase (XO) activity was found to be more elevated in the cisplatin group than the saline group (p<0.05). CAPE led to more decreased XO activity than cisplatin (p<0.05). The results of this study show that prophylactic administration of CAPE for cisplatin ototoxicity ameliorated hearing deterioration in rats.Öğe The effect of long-term therapy with sodium valproate on oxidant/antioxidant status in epileptic children(Wiley, 2003) Ozerol, E; Aslan, M; Cakmak, EA; Gulec, M; Yakinci, C; Akyol, OAntiepileptic drugs may cause the changes in the oxidant/antioxidant status of the body. Reactive oxygen species have been suggested to be an important factor in the pathogenesis of various diseases as well as drug interactions and/or adverse effects. The aim of this study, therefore, is to investigate the status of major antioxidant enzyme activities as well as the end products of lipid peroxidation in erythrocyte and plasma from epileptic children after therapy with sodium valproate (VPA). Superoxide dismutase (SOD), catalase (CAT) activities and malondialdehyde (MDA) levels in erythrocyte and plasma were analyzed in 41 epileptic patients under long-term antiepileptic therapy with VPA and 32 healthy controls. Erythrocyte SOD activity was found to be increased (p=0.024) whereas erythrocyte CAT activity decreased (p=0.016) in patients with epilepsy under VPA treatment compared to the controls. MDA levels in erythrocyte were found to be markedly decreased in epileptic children compared to controls (p<0.001). In conclusion, decreased CAT activity seems to be compensated with increased SOD activity in erythrocytes protecting erythrocyte membranes from lipid peroxidation in patients with epilepsy under VPA treatment.Öğe Effects of caffeic acid phenethyl ester and alpha-tocopherol on reperfusion injury in rat brain(Wiley, 2003) Irmak, MK; Fadillioglu, E; Sogut, S; Erdogan, H; Gulec, M; Ozer, M; Yagmurca, MOxygen-derived free radicals have been implicated in the pathogenesis of cerebral injury after ischaemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. The purpose of the present study was to investigate the effects of ischaemia and subsequent reperfusion on rat brain and to investigate the effects of two free radical scavengers, CAPE and alpha-tocopherol, on this in vivo model of cerebral injury. Ischaemia was induced by bilateral occlusion of the carotid arteries for 20 min and reperfusion was achieved by releasing the occlusion to restore the circulation for 20 min. Control rats underwent a sham operation. CAPE at 10 mumol kg(-1) or alpha-tocopherol at 25 mumol kg(-1) was administered intraperitoneally before reperfusion. Reperfusion led to significant increase in the activity of xanthine oxidase and higher malondialdehyde levels in the brain. Acute administration of both CAPE and alpha-tocopherol suppressed ischaemia-reperfusion-induced cerebral lipid peroxidation and injury, but CAPE seems to offer a better therapeutic advantage over alpha-tocopherol. Copyright (C) 2003 John Wiley Sons, Ltd.Öğe The effects of ginkgo biloba extract on tissue adenosine deaminase, xanthine oxidase, myeloperoxidase, malondialdehyde, and nitric oxide in cisplatin-induced nephrotoxicity(Sage Publications Inc, 2006) Gulec, M; Iraz, M; Yilmaz, HR; Ozyurt, H; Temel, IThis study was carried out to determine if Ginkgo Biloba Extract (GBE or Egb 761) exerts a beneficial effect against cisplatin-induced renal failure in rats. Sprague Dawley rats were divided into four groups. The first group (control) received orally 1 mL/kg/day of 0.9% saline by an oral carrier vehicle on days 1 to 10. The second group was injected with 7 mg/kg cisplatin intraperitoneally (i.p.) on the fourth day, once only. The third group (vit E + cisplatin) was administered 10 mg/kg/day i.p. vit E on 1 to 10 days with one dose of i.p. cisplatin (7 mg/kg) injection on the fourth day. The fourth group (GBE + cisplatin) was given GBE orally at 100 mg/mL/kg started on the first day up to the tenth day with one dose of cisplatin (7 mg/kg) injection on the fourth day. Cisplatin was found to lead a statistically significant increase in plasma BUN and creatinine levels, as well as urine micro total protein (MTP) levels, leading to acute renal failure (ARF) in rats. Renal xanthine oxidase (XO) activities increased in all groups (statistically significant in cisplatin + GBE-treated rats; P < 0.001). Adenosine deaminase (AD) activities were increased in cisplatin-treated rats, and decreased in cisplatin + GBE-treated (P < 0.041) and cisplatin + vit E-treated (P < 0.005) rats, compared to controls. Malondialdehyde (MDA), nitric oxide (NO) levels and myeloperoxidase (MPO) activities were increased in the kidney tissue of cisplatin-treated rats. Vit E improved plasma creatinine and urine MTP levels, together with tissue MDA, NO levels, and MPO activities. But GBE had no statistically significant effect on those parameters. These results indicate that increased XO, AD and MPO activities, as well as MDA and NO levels play a critical role in cisplatin nephrotoxicity. GBE has been shown to protect against cisplatin-induced nephrotoxicity.Öğe The effects of single-dose dexamethasone on wound healing in rats(Lippincott Williams & Wilkins, 2003) Durmus, M; Karaaslan, E; Ozturk, E; Gulec, M; Iraz, M; Edali, N; Ersoy, MODexamethasone effectively decreases the incidence of nausea and vomiting among pediatric and adult patients. In this study, we evaluated the effects of single-dose dexamethasone on wound healing in a prospective, randomized, experimental animal model. Anesthesia was induced with thiopental 100 mg/kg intraperitoneally. Dexamethasone 1 mg/kg was administered intraperitoneally in a dexamethasone group, and physiological saline was administered in a control group. Collagenization, epithelization, and fibroblast content were significantly less in the dexamethasone group compared with the control group (P values of 0.002, 0.041, and 0.023, respectively). The vascularity and the degree of inflammatory cells were more intense in the dexamethasone group compared with the control group (P values of 0.023 and 0.002, respectively). The white blood cell count was similar in the control (7.84 +/- 2.09) and dexamethasone (6.98 +/- 2.12) groups. The mean hydroxyproline level was 0.72 +/- 0.13 mg/g in the dexamethasone and 1.03 +/- 0.19 mg/g in the control group. Hydroxyproline levels were significantly less in the dexamethasone group (P = 0.001). We conclude that dexamethasone at I mg/kg may have negative effects on wound healing.Öğe The protective effect of erdosteine against ototoxicity induced by cisplatin in rats(Springer, 2005) Kalcioglu, MT; Kizilay, A; Gulec, M; Karatas, E; Iraz, M; Akyol, O; Egri, MThe elimination of cisplatin ototoxicity is an ongoing concern. This experimental study was undertaken to investigate the effect of oral erdosteine in ameliorating cisplatin-induced ototoxicity. Twenty-eight adult female Wistar albino rats were randomly divided into four equal groups. Group A received an oral carrier vehicle of the drug erdosteine with 0.2 ml of 0.9% saline. Group B was administered only erdosteine (per oral 10 mg/kg twice a day) for 6 days. Group C was injected with cisplatin intraperitoneally (i.p.) on day 0 (16 mg/kg body weight), once only. Group D was given erdosteine (per oral 10 mg/kg/day) 1 day before and for 5 days consecutively after cisplatin injection (16 mg/kg, i.p.). Distortion product otoacoustic emissions (DPOAEs) were elicited in different frequency regions, ranging from 1,001 to 6,299 Hz as DPgram and input/output (I/O) functions from the control and experimental animals. All experimental animals were killed under general anesthesia on day 5, following the last otoacoustic emission measurements. Prior to death, blood samples were drawn for measurement of superoxide dismutase, xanthine oxidase (XO), malondialdehyde and nitric oxide. Initial DPgram and I/O function baseline measurements were similar in all groups prior to any drug administration ( P > 0.05). On day 5, intra-subject measurement parameters of DPgrams and I/O functions in the cisplatin group showed significant deterioration ( P < 0.05). The other groups revealed no differences between their pre- and post-test drug administration DPgrams and I/O functions at any test frequency ( P > 0.05). Comparison of the amplitudes of DPgrams and I/O functions between the cisplatin and control groups showed significant changes ( P < 0.05). Biochemical studies noted an increased XO activity following cisplatin administration ( P < 0.007). The other biochemical results did not show significant differences between the study and control groups. This study demonstrates that, in rats, erdosteine is protective for cochlear function against the disruptive effects of cisplatin as measured by DPOAEs.Öğe Protective role of ?-tocopherol and caffeic acid phenethyl ester on ischemia-reperfusion injury via nitric oxide and myeloperoxidase in rat kidneys(Elsevier, 2004) Gurel, A; Armutcu, F; Sahin, S; Sogut, S; Ozyurt, H; Gulec, M; Kutlu, NOBackground: The aim of this study was to determine the acute effects of antioxidant caffeic acid phenethyl ester (CAPE) and alpha-tocopherol (vitamin E) on nitric oxide (NO) production, neutrophil infiltration, and antioxidant enzyme activities on an in vivo model of renal ischemia-reperfusion injury. Methods: Rats were divided into five equal groups each consisting six rats: sham operation, ischemia, ischemia-reperfusion (I/R), I/R plus CAPE, and I/R plus vitamin E groups. CAPE or vitamin E was administered intraperitoneally before reperfusion. After experimental procedure, rats were sacrificed and both ipsilateral and contralateral kidneys were removed and prepared for NO concentrations, myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Acute administration of vitamin E decreased NO concentrations in both ipsilateral and contralateral renal tissues compared to I/R group. SOD activity was increased in I/R and I/R + CAPE groups compared to sham operation group. The most prominent results were encountered in MPO activities, which did not change in contralateral kidneys in both ischemia and I/R groups. There was a significant decrease in ipsilateral MPO activity in ischemia group and a significant increase in I/R group compared to sham operation group. Pretreatment with intraperitoneal CAPE significantly diminished the tissue MPO activity indicating the prevention of the neutrophil sequestration into the kidney. Conclusion: There is a role for CAPE in attenuation in renal damage after I/R injury of the kidney, in part at least by inhibition of neutrophil sequestration. (C) 2003 Elsevier B.V. All rights reserved.Öğe The regulatory role of dietary ?-3 essential fatty acids on oxidant/antioxidant balance in rat hippocampus(John Wiley & Sons Ltd, 2003) Sarsimaz, M; Songur, A; Kus, I; Ozyurt, B; Gulec, M; Sogut, S; Ilhan, AOmega-3 essential fatty acids (omega-3 EFA) contains eicosapentaenoic acid and docosahexaenoic acid (DHA). DHA is one of the building structures of membrane phospholipids of brain and necessary for continuity of neuronal functions. omega-3 EFA has been suggested to be protective against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in superoxide dismutase (SOD), xanthine oxidase (XO), malondialdehyde (MDA), and nitric oxide (NO) in the hippocampus of rats fed with omega-3 EFA diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with omega-3 EFA were decapitated under ether anesthesia, and hippocampus was removed immediately. Rats treated with omega-3 EFA had significantly lower XO activity (p<0.002) and NO level (p<0.0001) whereas higher SOD activity (p<0.002) and MDA levels (p<0.019) than the control rats. These results suggest that the dietary omega-3 EFA may act on the oxidant/antioxidant parameters in hippocampus. On the other hand, although the mechanism is not clear, omega-3 EFA may enhance one of the most important antioxidant enzymes, SOD. Further studies are needed to clarify the molecular mechanism involved and the therapeutic implication of omega-3 EFA in animal psychosis models and clinical studies.
