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Öğe Caffeic acid phenethyl ester as a protective agent against doxorubicin nephrotoxicity in rats(Elsevier, 2004) Yagmurca, M; Erdogan, H; Iraz, M; Songur, A; Ucar, M; Fadillioglu, EBackground: Nephrotoxicity is one of the important side effects of antracycline antibiotics. The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, against nephrotoxicity induced by doxorubicin (DXR). Methods: The rats were divided into control, CAPE alone, doxorubicin (20 mg/kg, i.p.) and doxorubicin plus CAPE (10 mumol/kg/day, i.p.) groups. At the end of the 10th day, kidney tissues were removed for light microscopy and analysis. The levels of tissues protein carbonyl content (PC), malondialdehyde (MDA) and nitric oxide (NO) as well as the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) were determined. Plasma oxidants and antioxidants were also measured. Results: The activities of CAT and GSH-Px were decreased as well as myeloperoxidase, NO, MDA and PC were increased in renal tissue of doxorubicin group compared with the other groups. Plasma GSH-Px activity was higher in doxorubicin plus CAPE group than the others and plasma MDA level was higher in doxorubicin group than the other groups. There were glomerular vacuolization, tubular desquamation, loss of brush border, and adhesion to Bowman's in the light microscopy in the kidneys of doxorubicin group. The tubules and brush border were almost normal and some of the glomerulus was filled with fine vacuoles in CAPE treated rats. Conclusion: Doxorubicin caused renal injury and CAPE treatment prevented lipid peroxidation and protein oxidation in renal tissue and partially preserved glomerulus and tubules. (C) 2004 Elsevier B.V. All rights reserved.Öğe Cisplatin-induced acute renal failure is ameliorated by erdosteine in a dose-dependent manner(Wiley, 2004) Özyurt, H; Yildirim, Z; Kotuk, M; Yilmaz, HR; Yagmurca, M; Iraz, M; Sögüt, SThe aim of this study was to investigate the optimum dosage of erdosteine to ameliorate cisplatin-induced nephrotoxicity. Three different doses of erdosteine at 25, 50 and 75 mg kg(-1) were studied in rats. Intraperitoneal administration of 7 mg kg(-1) cisplatin led to acute renal failure, as indicated by kidney histology and increases in plasma creatinine and blood urea nitrogen (BUN) levels. At 5 days after cisplatin injection the BUN level was increased significantly from 15.1 +/- 4.3 to 126.7 +/- 152.6 mg dl(-1) and plasma creatinine levels increased from 0.37 +/- 0.005 to 1.68 +/- 1.9 mg dl(-1). When the rats were administered 50 and 75 mg kg(-1) erdosteine 24 h before cisplatin injection that was continued until sacrifice (total of 6 days), the BUN and creatinine levels remained similar to control levels and the grade of histology was similar. Erdosteine at doses of 50 and 75 mg kg(-1) ameliorates cisplatin-induced renal failure. The optimum dose of erdosteine may be 50 mg kg(-1) in this study. Copyright 2004 John Wiley Sons, Ltd.Öğe The effect of caffeic acid phenethyl ester on ischemia-reperfusion injury in comparison with ?-tocopherol in rat kidneys(Springer-Verlag, 2001) Irmak, MK; Koltuksuz, U; Kutlu, NO; Yagmurca, M; Özyurt, H; Karaman, A; Akyol, ÖOxygen-derived free radicals have been implicated in the pathogenesis of renal injury after ischemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant and anti-inflammatory properties. To determine whether CAPE offers any advantage over alpha -tocopherol, we compared their effects on an in vivo model of renal ischemia-reperfusion injury in rats. CAFE at 10 mu mol/kg or alpha -tocopherol at 10 mg/kg was administered intraperitoneally before reperfusion. Acute administration of CAFE suppressed ischemia-reperfusion induced renal lipid peroxidation and tissue injury more than alpha -tocopherol. CAFE may therefore offer a therapeutic advantage in acute injury settings.Öğe Effects of caffeic acid phenethyl ester against doxorubicin-induced neuronal oxidant injury(Wiley, 2003) Fadillioglu, E; Erdogan, H; Iraz, M; Yagmurca, MOxygen-derived free radicals have been implicated in the pathogenesis of doxorubicin-induced toxicities. The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on doxorubicin-induced neuronal oxidative injury in rats. The rats were treated with CAPE (10 mumol/kg/day i.p.) or saline starting 2 days before a single dose of doxorubicin (20 mg/kg i.p.) or saline. Ten days after the first experiments, the brain was excised to analyze the activities of antioxidant enzymes and levels of malondialdehyde (MDA) and nitric oxide (NO). Doxorubicin alone resulted in higher MDA level in brain tissue than the other groups. The activity of catalase was higher in doxorubicin plus CAPE group than doxorubicin group. There were no significant differences in NO level, glutathione peroxidase (GSH-Px) and superoxide dismutase activities between the groups. There were negative correlations between GSH-Px activity and MDA level in both doxorubicin and doxorubicin plus CAPE groups. It can be concluded that doxorubicin induced oxidant injury can be prevented by CAPE treatment through its antioxidant properties in rat brain.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 Effects of electromagnetic radiation from a cellular telephone on epidermal Merkel cells(Blackwell Munksgaard, 2003) Irmak, MK; Oztas, E; Yagmurca, M; Fadillioglu, E; Bakir, BThe number of reports on the effects induced by electromagnetic radiation (EMR) from cellular telephones in various cellular systems is still increasing. Until now, no satisfactory mechanism has been proposed to explain the biological effects of this radiation except a role suggested for mast cells. Merkel cells may also play a role in the mechanisms of biological effects of EMR. This study was undertaken to investigate the influence of EMR from a cellular telephone (900 MHz) on Merkel cells in rats. A group of rats was exposed to a cellular telephone in speech position for 30 min. Another group of rats was sham-exposed under the same environmental conditions for 30 min. Exposure led to significantly higher exocytotic activity in Merkel cells compared with the sham exposure group. This finding may indicate the possible role of Merkel cells in the pathophysiology of the effects of EMR.Öğe Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant levels in rabbits(Wiley, 2002) Irmak, MK; Fadilloglu, E; Güleç, M; Erdogan, H; Yagmurca, M; Akyol, ÖThe number of reports on the effects induced by electromagnetic radiation (EMR) in various cellular systems is still increasing. Until now no satisfactory mechanism has been proposed to explain the biological effects of this radiation. Oxygen free radicals may play a role in mechanisms of adverse effects of EMR. This study was undertaken to investigate the influence of electromagnetic radiation of a digital GSM mobile telephone (900 MHz) on oxidant and antioxidant levels in rabbits. Adenosine deaminase, xanthine oxidase, catalase, myeloperoxidase, superoxide dismutase (SOD) and glutathione peroxidase activities as well as nitric oxide (NO) and malondialdehyde levels were measured in sera and brains of EMR-exposed and sham-exposed rabbits. Serum SOD activity increased, and serum NO levels decreased in EMR-exposed animals compared to the sham group. Other parameters were not changed in either group. This finding may indicate the possible role of increased oxidative stress in the pathophysiology of adverse effect of EMR. Decreased NO levels may also suggest a probable role of NO in the adverse effect. Copyright (C) 2002 John Wiley Sons, Ltd.Öğe Erdosteine prevents doxorubicin-induced cardiotoxicity in rats(Academic Press Ltd- Elsevier Science Ltd, 2003) Yagmurca, M; Fadillioglu, E; Erdogan, H; Ucar, M; Sogut, S; Irmak, MKThe clinical use of doxorubicin (Dxr) is limited by its cardiotoxic effects which are mediated by oxygen radicals. The purpose of this study was to investigate in vivo protective effects of erdosteine, an antioxidant agent because of its secondary active metabolites in vivo, against the cardiotoxicity induced by Dxr in rats. Three groups of male Sprague-Dawley rats (60 days old) were used. Group I was untreated group used as control; the other groups were treated with Dxr (single i.p. dosage of 20 mg kg(-1) b.wt.) or Dxr plus erdosteine (10 mg kg(-1) day(-1), orally), respectively. Erdosteine or oral saline treatment was done starting 2 days before Dxr for 12 days. The analyses were done at the 10th day of Dxr treatment. The protein carbonyl content, the activities of myeloperoxidase, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine kinase (CK) as well as heart rate and blood pressures were significantly increased in Dxr group in comparison with the other groups. However, pulse pressure was decreased in Dxr group. The body and heart weights were decreased in both Dxr administered groups in comparison with control group. Disorganization of myocardial histology, picnotic nuclei, edema, and increase in collagen content around vessels were seen in the slides of Dxr group, whereas normal myocardial microscopy was preserved in Dxr plus erdosteine group. Collectively, these in vivo hemodynamic, enzymatic and morphologic studies provide an evidence for a possible prevention of cardiac toxicity in Dxr-treated patients. (C) 2003 Elsevier Ltd. All rights reserved.Öğe Ginkgo biloba inhibits bleomycin-induced lung fibrosis in rats(Academic Press Ltd- Elsevier Science Ltd, 2006) Iraz, M; Erdogan, H; Kotuk, M; Yagmurca, M; Kilic, T; Ermis, H; Fadillioglu, EOxidative stress has been implicated in the pathogenesis of bleomycin-induced lung fibrosis and many antioxidant agents have been studied for prevention and treatment of the disease in animals and humans. We therefore examined whether Ginkgo biloba (Gb), a flavonoid-rich antioxidant, inhibits bleomycin-induced lung fibrosis in rats. Male Spraque-Dawley rats were given a single dose of bleomycin (2.5 mg/kg, intratracheally) in pulmonary fibrosis groups and saline in controls. First dose of Gb was given a day before the bleomycin injection and continued until sacrifice. At day 14, fibrotic changes in lung were estimated to occur by Aschoft's criteria and lung hydroxyproline content. Bleomycin challenge provoked severe pulmonary fibrosis with marked increase in hydroxyproline content of lung tissue and typical histological findings, which is prevented by Gb. Hydroxyproline level was significantly higher (13.51 +/- 0.87 mg/g dried tissue) in bleomycin treated rats than controls (9.2 +/- 1.33), and its level was remained to the control levels (7.38 +/- 0.76) in rats treated with prophylactic Gb. On the other hand, bleomycin injection significantly reduced activities of glutathione peroxidase, superoxide dismutase and catalase in lung tissue which is prevented by Gb. Also, bleomycin injection resulted in a marked increase of malondialdehyde and nirite level which is attenuated by Gb. The data suggest that Gb has a potent antioxidant activity in the model of bleomycin-induced lung fibrosis in rats, and therefore has a potent antifibrotic activity against bleomycin-induced lung fibrosis model in rats. (c) 2006 Elsevier Ltd. All rights reserved.Öğe Preventive effect of melatonin on bleomycin-induced lung fibrosis in rats(Wiley, 2006) Yildirim, Z; Kotuk, M; Erdogan, H; Iraz, M; Yagmurca, M; Kuku, I; Fadillioglu, EOxidative stress has an important role in the pathogenesis of idiopathic pulmonary fibrosis. Melatonin has direct and indirect free radical-detoxifying activity. The present study investigated whether melatonin treatment attenuates bleomycin-induced lung fibrosis in rats. A group of rats was given one dose of bleomycin while the control animals were given saline. The first dose of melatonin (4 mg/kg/day) was given 2 days before the bleomycin injection. At day 14, fibrotic changes were evaluated using Aschoft's criteria and lung hydroxyproline content. Bleomycin produced a 2.7-fold rise in the fibrosis score that was decreased 65% by melatonin (P < 0.05) and a 1.4-fold increase in hydroxyproline content which was completely prevented by melatonin. Protein carbonyl and thiobarbituric acid reactive substances levels, which were significantly elevated in the bleomycin treated rats, were significantly attenuated by melatonin. Bleomycin administration significantly reduced the activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in lung tissue. The reduction in CAT activity was prevented by melatonin but SOD and GSH-Px were not influenced. These results revealed that melatonin may prevent the development of bleomycin-induced lung fibrosis via the repression of protein and lipid peroxidation.Öğe Protective effects of caffeic acid phenethyl ester on doxorubicin-induced cardiotoxicity in rats(Wiley, 2004) Fadillioglu, E; Oztas, E; Erdogan, H; Yagmurca, M; Sogut, S; Ucar, M; Irmak, MKThe prevention of doxorubicin (DXR)-induced cardiotoxicity may be helpful to improve future DXR therapy. The aim of this study was to investigate the cardio-protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on DXR-induced cardiotoxicity. Rats were divided into three groups and treated with saline, DXR and DXR + CAPE. Rats were treated with CAPE (10 gmol kg(-1) day(-1) i.p.) or saline starting 2 days before a single dose of DXR (20 mg kg(-1) i.p.). Ten days later, haemodynamic measurements were performed and the hearts were excised for biochemical analyses and microscopic examination. The heart rate and mean blood pressure were higher and the pulse pressure was lower in the DXR group than in the other two groups. The administration of DXR alone resulted in higher myeloperoxidase activity, lipid peroxidation and protein carbonyl content than in the other groups. The activities of superoxide dismutase and catalase were higher in DXR and DXR + CAPE groups than in the saline group. Rats in the DXR + CAPE group had increased catalase activity in comparison with the DXR group and high glutathione peroxidase activity in comparison with the other two groups. There was severe disruption of mitochondrial fine structure in the electron microscopy of the DXR group. In contrast, myocardial microscopy appeared nearly normal in the DXR + CAPE group (as defined at the electron microscopic level). In light of these in vivo haemodynamic, enzymatic and morphological results, we conclude that CAPE pretreatment significantly attenuated DXR-induced cardiac injury, possibly with its antioxidant effects. Copyright (C) 2004 John Wiley Sons, Ltd.Öğe Protein oxidation and lipid peroxidation after renal ischemia-reperfusion injury(Springer, 2006) Erdogan, H; Fadillioglu, E; Yagmurca, M; Uçar, M; Irmak, MKOxygen radicals have roles in the renal ischemia-reperfusion (IR) injury usually encountered in several conditions such as renal transplantation. The aim of this study was to investigate the effects of erdosteine and N-acetylcysteine (NAC) on the oxidant/antioxidant status and microscopy of renal tissues after IR injury. Male Sprague-Dawley rats were randomly assigned to four groups: control untreated rats, IR (30 min ischemia and 120 min reperfusion), IR + NAC (i.p.; 180 mg/kg) and IR + erdosteine (oral; 50 mg/kg/day for 2 days before experiments) groups. After unilateral renal IR, the right kidney was rapidly excised and sectioned vertically into two pieces for microscopic examination and biochemical analysis. Erdosteine and NAC treatment did not cause any significant change in the activity of superoxide dismutase (SOD) in comparison with the IR group, even if the SOD activity increased in IR groups than in the control group. Catalase (CAT) activity was decreased in the IR group in comparison with control and IR + erdosteine groups (P < 0.05), whereas it was higher in the IR + erdosteine group than in the IR + NAC group (P < 0.05). Xanthine oxidase (XO) activity was higher in all the IR-performed groups than in the control group (P < 0.05). Thiobarbituric acid-reactive substances (TBARS) level and protein carbonyl (PC) content were increased after IR injury (P < 0.05). Erdosteine or NAC treatments ameliorated these increased TBARS and PC contents in comparison with the IR group (P < 0.05). Light microscopy of the IR group showed tubular dilatation, tubular necrosis and vacuole formation in epithelial cells. Erdosteine but not NAC apparently reduced the renal tissue damage. The pathological damage score after IR was significantly reduced after erdosteine treatment (P < 0.05), but not after NAC treatment. In conclusion, renal IR resulted in oxidative damage as seen in biochemical lipid peroxidation and protein oxidation results with aggravated tubular necrosis. Erdosteine and NAC treatments improved the biochemical results of IR injury. However, on microscopic evaulations, animals receiving erdosteine showed a great reduction in renal damage when compared with the NAC group.
