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Öğe Attenuation of bleomycin-induced lung fibrosis by oral sulfhydryl containing antioxidants in rats(Academic Press Ltd Elsevier Science Ltd, 2005) Yidirim, Z; Kotuk, M; Iraz, M; Kuku, I; Ulu, R; Armutcu, F; Ozen, SAntioxidant therapy may be useful in diseases with impaired oxidant antioxidant balance such as lung fibrosis. The effects of sulfhydryl-containing antioxidant agents N-acetylcysteine (NAC) and erdosteine on the bleomycin-induced lung fibrosis were compared in rats. The animals were divided into four groups: Vehicle + vehicle, vehicle + bleomycin (2.5 U/kg), bleomycin + erdosteine (10 mg/kg), and bleomycin + NAC (3 mmol/kg). Bleomycin administration resulted in prominent lung fibrosis as measured by lung hydroxylproline content and lung histology which is almost completely prevented by erdosteine and NAC. Hydroxyproline content was 18.7 +/- 3.5 and 11.2 +/- 0.6 mg/g dried tissue in bleomycin and saline treated rats, respectively (P < 0.001), and this level was 11.3 +/- 1.2 and 13.8 +/- 1.2 mg/g dried tissue in erdosteine and NAC pretreated, respectively. Erdosteine and NAC significantly reduced depletion of glutathione peroxidase, and prevented increases in myeloperoxidase activities, nitric oxide, and malondialdehyde levels in lung tissue produced by bleomycin. Data presented here indicate that erdosteine and NAC similarly prevented bleomycin-induced lung fibrosis and their antioxidant effects were also similar in this experiment. (c) 2005 Elsevier Ltd. 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 Effects of aminoguanidine and antioxidant erdosteine on bleomycin-induced lung fibrosis in rats(Academic Press Inc Elsevier Science, 2004) Yildirim, Z; Turkoz, Y; Kotuk, M; Armutcu, F; Gurel, A; Iraz, M; Ozen, SReactive oxygen and nitrogen species have been implicated in the pathogenesis of bleomycin -induced lung fibrosis. The effects of aminoguanidine and erdosteine on the bleomycin-induced lung fibrosis were evaluated in rats. The animals were placed into five groups: Vehicle + vehicle, vehicle + bleomycin (2.5U/kg), bleomycin + aminoguanidine (200mg/kg), bleomycin + erdosteine (10mg/kg), and bleomycin + erdosteine + aminoguanidine. Bleomycin administration resulted in prominent lung fibrosis as measured by lung hydroxyproline content and lung histology, which is completely prevented by erdosteine and aminoguanidine. A strong staining for nitro tyrosine antibody in lung tissue and increased levels of lung NO were found in bleomycin group, that were significantly reduced by aminoguanidine and erdosteine. Aminoguanidine and erdosteine significantly prevented depletion of superoxide dismutase and glutathione peroxidase and elevated myeloperoxidase activities, malondialdehyde level in lung tissue produced by bleomycin. Data presented here indicate that aminoguanidine and erdosteine prevented bleomycin-induced lung fibrosis and that nitric oxide mediated tyrosine nitration of proteins plays a significant role in the pathogenesis of bleomycin-induced lung fibrosis. Also our data suggest that antifibrotic affect of antioxidants may be due to their inhibitory effect on nitric oxide generation in this model. (C) 2004 Elsevier Inc. All rights reserved.Öğe Effects of Ginkgo biloba on plasma oxidant injury induced by bleomycin in rats(Sage Publications Inc, 2006) Erdogan, H; Fadillioglu, E; Kotuk, M; Iraz, M; Tasdemir, S; Oztas, Y; Yildirim, ZBleomycin is an anti-neoplastic agent and its clinical usage is limited by its toxicity, which is mostly induced by oxygen radicals. The aim of this study was to investigate the effect of Ginkgo biloba on plasma indices of oxidants induced by bleomycin in rats. Male Sprague-Dawley rats were divided into five groups: none medicated or 0.9% NaCl injected or only Ginkgo biloba (orally, 100 mg/kg per day for 14 days) or only a single dose of bleomycin (intratracheal, 2.5 U/kg) or Gingko biloba and bleomycin-treated groups. After 14 days, blood was taken before the rats were sacrificed. The plasma was removed and stored at -85 degrees C until the study day. Plasma superoxide dismutase ( SOD), glutathione peroxidase (GSH-Px) and xanthine oxidase (XO) enzyme activities with malondialdehyde and nitric oxide ( NO) levels were studied. The levels of malondialdehyde and NO with activity of XO were higher in plasma of bleomycin group than the other groups (P < 0.05). The activities of SOD and GSH-Px were increased in the bleomycin plus Gingko biloba group in comparison with the bleomycin group (P < 0.05). There was a positive correlation between malondialdehyde and NO levels in the bleomycin group (r = 0.859, P < 0.05). There were positive correlations between SOD and GSH-Px activities (r < 0.760, P < 0.05) and between XO activity and malondialdehyde level (r < 0.822, P < 0.05) in the bleomycin plus Gingko biloba group. In conclusion, it was thought that bleomycin induced oxidative stress can be prevented by Gingko biloba treatment via high anti-oxidant enzyme activity together with decreased radical production from XO.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 In vivo evidence suggesting a role for purine-catabolizing enzymes in the pathogenesis of cisplatin-induced nephrotoxicity in rats and effect of erdosteine against this toxicity(Wiley, 2004) Sögüt, S; Kotuk, M; Yilmaz, HR; Ulu, R; Özyurt, H; Yildirim, ZThe aim of this experimental study was to investigate the possible role of adenosine deaminase (AD) and xanthine oxidase (XO) in the pathogenesis of cisplatin-induced nephrotoxicity and the effect of erdosteine in decreasing the toxicity. The intraperitoneal injection of cisplatin (7m kg(-1) body weight) induced a significant increase in plasma creatinine level and blood urea nitrogen (BUN), and plasma and damaged renal tissue activities of AD and XO in rats. Co-treatment with erdosteine (10 mg kg(-1) day(-1)) attenuated the increase in the plasma creatinine and BUN levels, and significantly prevented the increase in tissue and plasma AD and XO activities (P < 0.05). The results of this study revealed that XO and AD may play an important role in the pathogenesis of cisplatin-induced nephrotoxicity. The potent free radical scavenger erdosteine may have protective potential in this process and it will become a promising drug in the prevention of this undesired side-effect of cisplatin. but further studies are needed to illuminate the exact protection mechanism of erdosteine against cisptatin-induced nephrotoxicity. Copyright (C) 2004 John Wiley Sons, Ltd.Öğe Oral erdosteine administration attenuates cisplatin-induced renal tubular damage in rats(Academic Press Ltd- Elsevier Science Ltd, 2003) Yildirim, Z; Sogut, S; Odaci, E; Iraz, M; Ozyurt, H; Kotuk, M; Akyol, OThe effect of oral erdosteine on tissue malondialdehyde (MDA) and nitric oxide (NO) levels, and catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities are investigated in the cisplatin model of acute renal failure in rats. A single dose of cisplatin caused kidney damage manifested by kidney histology as well as increases in plasma creatinine and blood urea nitrogen (BUN) levels. Treatment with free radical scavenger erdosteine attenuated increases in plasma creatinine and BUN, and tissue MDA and NO levels, and provided a histologically-proven protection against cisplatin-induced acute renal failure. Erdosteine also reduced depletion in the tissue CAT, GSH-Px, and SOD activities. These results show that erdosteine may be a promising drug for protection against cisplatin-induced nephrotoxicity. However, further studies with different doses of erdosteine are warranted for clarifying the issue. (C) 2002 Published by Elsevier Science Ltd.Öğe Preventive effect of lacrimal occlusion on topical timolol-induced bronchoconstriction in asthmatics(Wiley, 2004) Hepsen, IF; Yildirim, Z; Yilmaz, H; Kotuk, MAim: To evaluate the potential preventive role of lacrimal occlusion on the topical timolol-induced bronchoconstriction in asthmatics. Methods: This was a prospective and single-masked study. Fourteen volunteer subjects with asthma were included. Collagen plugs were inserted into both canaliculi on one side to inhibit lacrimal drainage. The effect of lacrimal occlusion on lung function tests was measured before and 60 min after the instillation of a timolol drop in unplugged and plugged eyes. The spirometric measurements include forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, and mid expiratory flow-rate (FEF25-75). Results: The timolol (0.5%) drop administration into the eye caused a significant decrease in pulmonary functions in patients with asthma in whom the lacrimal punctae had not been occluded by collagen plug. P values were 0.008 for FVC and 0.001 for FEV1 and FEF25-75. The occlusion of the lacrimal duct by intracanalicular plugs significantly reduced this decrease in pulmonary function. P values were 0.6 for FVC, 0.8 for FEV1, and 0.5 for FEF25-75. The lacrimal occlusion did not affect heart rate and blood pressures. Three subjects complained of epiphora. Conclusions: Lacrimal occlusion with intracanalicular collagen plugs may almost completely prevent the bronchoconstriction caused by topical timolol in asthmatics by inhibiting or decreasing systemic absorption of the medication.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 effect of ipratropium bromide on bronchoconstriction induced by sulfur dioxide exposure during apricot sufurization processes that causes asthma-like syndrome in agricultural environment(Academic Press Ltd- Elsevier Science Ltd, 2005) Yildirim, Z; Kilic, T; Koksal, N; Kotuk, MWe previously showed that apricot sulfurization workers are exposed to high concentrations of sulfur dioxide (SO2) resulting in an asthmalike syndrome. The aim of this study was to investigate whether pre-treatment of ipratropium bromide protects bronchoconstriction induced by SO2 exposure during apricot sulfurization processes that causes asthma-like syndrome. Firstly, pulmonary function tests were measured before and immediately after SO2 exposure due to processes of apricot sulfurization in 21 healthy volunteer apricot sulfurization workers who did not use any medication in apricot farms. One week later, same measurements were repeated in the same workers when they were working in same farm but they were administered two puffs of ipratropium bromide (20 mu g per dose) before 30 min second SO2 exposure for protection Of SO2-induced bronchoconstriction. Occupational SO2 exposure caused significant decrement in forced vital capacity (FVC), forced expiratory volume (FEVI) and forced mid-expiratory flow rate (FEF25-75%) in the worker and these decrements were prevented by ipratropium bromide given 30 min before SO2 exposure. This result suggests that pre-treatment of ipratropium bromide protects SO2-induced bronchoconstriction in healthy worker during apricot sulfurization processes that causes asthma-like syndrome in agricultural environment. (c) 2005 Elsevier Ltd. All rights reserved.
