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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 effects of erdosteine on the activities of some metabolic enzymes during cisplatin-induced nephrotoxicity in rats(Academic Press Ltd- Elsevier Science Ltd, 2004) Yilmaz, HR; Iraz, M; Sogut, S; Ozyurt, H; Yildirim, Z; Akyol, O; Gergerlioglu, SCisplatin is one of the widely used chemothrapeutic agents. One of the major side effects of the drug is renal toxicity. The aims of the presented study was (1) to investigate the effect of cisplatin on some renal metabolic enzyme activities such as hexokinase (HK), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH), and malate dehydrogenase (MDH) in an experimental model of acute renal failure and (2) to examine the protective role of erdosteine, an expectorant agent which has also antioxidant properties on cisplatin-induced nephrotoxicity and the enzyme activities mentioned above. Female Wistar albino rats were divided into three groups: sham operation group (n = 6). cisplatin group (n = 9), erdostein + cisplatin group (n = 8). All the chemicals used were applied intraperitoneally. Hexokinase, G6PD, LDH, and MDH activities were determined in the kidney supernatant at the end of the surgical procedures. Spectrophotometric methods were used to determine the activities of above-mentioned enzymes in the kidney tissue. Hexokinase and G6PD activities were found to be increased in cisplatin group compared to control group. G6PD activities were found to be decreased in erdosteine + cisplatin group compared to cisplatin group. There were minimal changes in LDH and MDH activities of the two study groups compared with the control group. The results obtained suggested that the glucose metabolizing metabolic pathways of renal tissue were partially affected from cisplatin toxicity and erdosteine have some protective effects on these enzyme activities. (C) 2004 Elsevier Ltd. All rights reserved.Öğe Erdosteine prevents bleomycin-induced pulmonary fibrosis in rats(Elsevier, 2004) Sogut, S; Ozyurt, H; Armutcu, F; Kart, L; Iraz, M; Akyol, O; Ozen, SOxidative stress plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. Therefore, erdosteine, an antioxidant, is expected to have an inhibitor potential against the disease. Rats were given one dose of bleomycin in pulmonary fibrosis groups and saline in controls. The first dose of oral erdosteine (10 mg/kg/day) was given 2 days before the bleomycin injection to achieve the plateau level in blood and continued until killing. At day 14, fibrotic changes were evaluated, using Aschoft's criteria and lung hydroxyproline content. Bleomycin produced a fivefold increase in fibrosis score that was decreased by 87% by erdosteine (P>0.001) and almost twofold increases in hydroxyproline content which were completely prevented by erdosteine. Myeloperoxidase activities and MDA levels, which were significantly higher in the bleomycin group, were then significantly attenuated by erdosteine. These results revealed that oral erdosteine may prevent the development of acute pulmonary inflammation caused by bleomycin injection via the repression of neutrophil accumulation and lipid peroxidation, resulting in the inhibition of subsequent lung fibrosis. (C) 2004 Elsevier B.V. All rights reserved.Öğe Inhibitory effect of caffeic acid phenethyl ester on bleomycine-induced lung fibrosis in rats(Elsevier, 2004) Özyurt, H; Sögüt, S; Yildirim, Z; Kart, L; Iraz, M; Armutçu, F; Temel, IBackground: Pulmonary fibrosis (PF) induced by anticancerogenic bleomycin (BLM) is one of the more common side effects encountered during cancer treatment. It has been suggested in the last decades that the main responsible agent in PF is reactive oxygen species which were generated also in normal physiological conditions in the human body. In this experimental study, we investigated the preventive or attenuating effects of caffeic acid phenethyl ester (CAPE) that has been demonstrated to have anti-inflammatory, cytocytatic, anti cancerogenic, antiprolipherative and antioxidant effects on BLM-induced PF. Methods: Thirty-six Sprague-Dawley rats were divided randomly into four groups as sham operation, BLM, BLM + vitamin E (vit E), and BLM + CAPE groups. BLM (7.5 mg/kg, single dose) was applied intratracheally, and CAPE and vit E intraperitoneally in the appropriate groups. At the end of the fibrosis processes, lung tissues were removed and the levels of tissues hydroxyproline (OH-proline), malondialdehyde (MDA) and NO as well as the activities of superoxide dismutase (SOD), catalase (CAT) and myeloperoxidase (MPO) were determined. Also, the weights of the rats were recorded at 7th and 14th days of the experiments. Results: BLM application to the rats resulted in a significant increase in the OH-proline level as compared to the controls. Administration of CAPE and vit E led to the remarkable reduction of total lung OH-proline levels compared to the rats treated with BLM alone (p < 0.0001). There were a decreases in antioxidant enzyme (SOD and CAT) activities while an increase in MPO activity in BLM group was found vs. the control group (p < 0.0001). CAPE had a regulator effect on these parameters: the increase in CAT and SOD activities and the decrease in MPO activity were seen after CAPE application. NO, MDA and OH-proline levels were increased in BLM group vs. the control group. CAPE was more effective in decreasing the tissue levels of NO, MDA and OH-proline than vit E. MPO activity, as a good marker of neutrophil sequestration to the tissues, in the BLM group was decreased by CAPE approximately to the control group. Conclusion: We suggest that CAPE is more effective on the prevention of BLM-induced fibrosis via antioxidant and free radical scavenger properties than vit E at the doses used in the present study. CAPE has some attenuating effects on BLM-induced PF affecting both oxidant and antioxidant systems as well as neutrophils sequestration. (C) 2003 Elsevier B.V. All rights reserved.Öğe Role of caffeic acid phenethyl ester, an active component of propolis, against cisplatin-induced nephrotoxicity in rats(Wiley, 2004) Özen, S; Akyol, Ö; Iraz, M; Sögüt, S; Özugurlu, F; Özyurt, H; Odaci, EWe have investigated the effect of caffeic acid phenethyl ester (CAPE) on cisplatin-induced nephrotoxicity in rats. Administration of a single dose of cisplatin resulted in the elevation of blood area nitrogen and creatinine in serum, as well as nitric oxide in kidney tissue of rats. Cisplatin also caused reduction of catalase (P < 0.0001), superoxide dismutase (P = 0.149) and glutathrone peroxidase (P < 0.0001) activities in kidney tissue. Although cisplatin caused elevation in malondialdehyde levels and myeloperoxidase activities in kidney tissue, they were not statistically significant. Caffeic acid phenethyl ester was found to be protective against cisplatin-induced antioxidant enzyme reductions. Treatment with free-radical scavenger CAPE attenuated the increase in plasma blood area nitrogen and kidney nitric oxide levels, and showed histopathological protection against cisplatin-induced acute renal failure. Extensive epithelial cell vacuolization, swelling, desquamation and necrosis were observed in the kidney of the cisplatin-treated rat. There were also larger tubular lumens in cisplatin-treated rats than those of the control and the CAPE groups. Caffeic acid phenethyl ester caused a marked reduction in the extent of tubular damage. It is concluded that administration of cisplatin imposes an oxidative stress to renal tissue and CAPE confers protection against the oxidative damage associated with cisplatin. This mechanism may be attributed to its free-oxygen-radical scavenging activity. Copyright (C) 2004 John Wiley Sons, Ltd.
