Person: ŞENER, GÖKSEL
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ŞENER
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GÖKSEL
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Publication Open Access Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats(BIOSCIENTIFICA LTD, 2006-05) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, G.; Kabasakal, L.; Atasoy, B. M.; Erzik, C.; Velioglu-Ogunc, A.; Cetinel, S.; Contuk, G.; Gedik, N.; Yegen, B. C.The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pre-treated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and turnout necrosis factor-alpha (TNF alpha) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P < 0.05-0.001). Similarly, serum TNFa and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.Publication Metadata only Allopurinol improves endothelial function and reduces oxidant-inflammatory enzyme of myeloperoxidase in metabolic syndrome(SPRINGER HEIDELBERG, 2008) ŞENER, GÖKSEL; Yiginer, Omer; Ozcelik, Fatih; Inanc, Tugrul; Aparci, Mustafa; Ozmen, Namik; Cingozbay, Bekir Yilmaz; Kardesoglu, Ejder; Suleymanoglu, Selami; Sener, Goksel; Cebeci, Bekir SitkiObjective In this study, we tested in patients with metabolic syndrome whether allopurinol through decreasing oxidative stress improves endothelial function, and ameliorates inflammatory state represented by markers of myeloperoxidase, C-reactive protein (CRP) and fibrinogen. Methods In a randomized, double-blind fashion; subjects with metabolic syndrome were treated with allopurinol (n = 28) or placebo (n = 22) for one month. Before and after treatment, blood samples were collected and the flow-mediated dilation (FMD) and isosorbide dinitrate (ISDN)-mediated dilation of the brachial artery were performed. Results Baseline clinical characteristics of the allopurinol and placebo groups demonstrated no differences in terms of clinical characteristics, endothelial function and inflammatory markers. After the treatment with allopurinol, FMD was increased from 8.0 +/- 0.5 % to 11.8 +/- 0.6% (P < 0.01), but there were no change in the placebo group. In both groups, ISDN-mediated dilation is unaffected by the treatment. As a marker of oxidative stress, allopurinol significantly reduced malondialdehyde. Moreover, myeloperoxidase levels were reduced by the treatment with allopurinol (56.1 +/- 3.4 ng/ml vs. 44.4 +/- 2.4 ng/ml, P < 0.05) but there were no change in the placebo group. Surprisingly, neither CRP nor fibrinogen levels were affected by the treatment in both groups. Conclusion Xanthine oxidoreductase inhibition by allopurinol in patients with metabolic syndrome reduces oxidative stress, improves endothelial function, ameliorates myeloperoxidase levels and does not have any effect on CRP and fibrinogen levels.Publication Metadata only The effect of pentoxifylline on intestinal ischemia/reperfusion injury(2001) ŞENER, GÖKSEL; Şener, Akgün, Şatiroǧlu, Topaloǧlu, Keyer-UysalThe small intestine is highly sensitive to oxygen free radical-induced injury. Post-ischemic intestinal tissue damage appears to be due to the formation of oxygen radicals. Free radical initiated lipid peroxidation (LP) following intestinal ischemia/reperfusion (I/R) may disrupt mucosal integrity. Indirectly, the radicals trigger the accumulation of neutrophils within the affected tissue, initiating inflammatory processes that lead to severe mucosal lesions. In the present study we investigated the effect of pentoxifylline (PTX), a potent inhibitor of tumour necrosis factor production, on I/R induced intestinal injury. Wistar albino rats were divided into four groups: (1) Sham operation (S); (2) Sham operation + PTX (50 mg/kg i.v.) (S + PTX); (3) 1 h ischemia + 2 h reperfusion (I/R); and (4) I/R + PTX. Animals were sacrificed at the end of the reperfusion period and ileum samples were obtained. Malondialdehyde (MDA) levels, an end product of LP, glutathione (GSH) levels, a key antioxidant, and myeloperoxidase (MPO) activity (an index of polymorphonuclear neutrophils) stimulation, were determined in ileum homogenates. The results of the present study indicate that ischemia/reperfusion results in a significant increase in MDA content and MPO activity with a significant decrease in GSH content. Treatment with PTX returns these biomarkers to control values. A mechanism of this protective effect may involve inhibition of neutrophil oxidative burst.Publication Metadata only Ginkgo biloba extract protects against mercury(II)-induced oxidative tissue damage in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2007) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goksel; Sehirli, Ozer; Tozan, Ayfer; Velioglu-Ovunc, Ayliz; Gedik, Nursal; Omurtag, Gulden Z.Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5 mg/kg mercuric chloride (HgCl2; Hg group) either saline or EGb (150 mg/kg) was administered for 5 days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl2 induced oxidative damage Caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects. (c) 2006 Published by Elsevier Ltd.Publication Metadata only Mesna (2-mercaptoethane sulfonate) prevents ischemia/reperfusion induced renal oxidative damage in rats(PERGAMON-ELSEVIER SCIENCE LTD, 2004) ŞENER, GÖKSEL; Kabasakal, L; Sehirli, AO; Cetinel, S; Cikler, E; Gedik, N; Sener, GReoxygenation of the ischemic tissue promotes the generation of various reactive oxygen metabolites (ROM) which are known to have deleterious effects on various cellular functions. This study was designed to determine the possible protective effect of mesna (2-Mercaptoethane Sulfonate) on renal ischemia/reperfusion (I/R) injury. Wistar albino rats were unilaterally nephrectomized, and 15 days later they were subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Mesna (MESNA, 150 mg/kg, i.p.; an effective dose against I/R injury) or vehicle was administered twice, 15 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion period, rats were killed by decapitation. Kidney samples were taken for histological examination or determination of the free radicals, renal malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Renal tissue collagen content, as a fibrosis marker was also determined. Creatinine and urea concentrations in blood were measured for the evaluation of renal function. The results demonstrated that renal I/R caused nephrotoxicity, as evidenced by increases in blood urea and creatinine levels, which was reversed by MESNA treatment. Increased free radical levels, as assessed by nitroblue-tetrazolium test were reduced with MESNA. Moreover, the decrease in GSH and increases in MDA levels, and MPO activity induced by I/R indicated that renal injury involves free radical formation. Treatment of rats with MESNA restored the reduced GSH levels while it decreased MDA levels as well as MPO activity. Increased collagen contents of the kidney tissues by I/R were reversed back to the control levels by MESNA treatment. Since MESNA administration reversed these oxidant responses, improved renal function and microscopic damage, it seems likely that MESNA protects kidney tissue against I/R induced oxidative damage. (C) 2004 Elsevier Inc. All rights reserved.Publication Metadata only Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice(ELSEVIER SCIENCE BV, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sener, GokselThe protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pretreated with beta-D-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemilummescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, P-D-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-D-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity. (c) 2006 Elsevier B.V. All rights reserved.Publication Metadata only Protective effects of resveratrol against acetaminophen-induced toxicity in mice(WILEY, 2006) VELİOĞLU ÖĞÜNÇ, AYLİZ; Sener, Goksel; Toklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Gedik, NursalThis investigation elucidates the role of free radicals in acetaminophen (AA)-induced toxicity and the possible protection by resveratrol (RVT). BALB-c mice were injected with a single dose of 900 mg/kg AA to induce toxicity, while RVT administred in a dose of 30 mg/kg i.p. following AA. Mice were sacrificed 4 h after AA injection to determine serum ALT, AST and tumor necrosis factor-alpha (TNF-alpha) levels in blood, and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity and collagen contents in liver tissues. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probe. ALT, AST levels and TNF-alpha were increased significantly after AA treatment, and reduced with RVT. AA caused a significant decrease in GSH levels while MDA levels and MPO activity were increased in liver tissues. On the other hand when RVT administered following AA, depletion of GSH and accumulation of MDA and neutrophil infiltration were reversed back to control. Furthermore increased luminol and lucigenin CL levels in the AA group reduced by RVT treatment. Our results implicate that AA causes oxidative damage in hepatic tissues and RVT, by its potent antioxidant effects protects the liver tissue. These data suggest that RVT may be of therapeutic use in preventing hepatic oxidative injury due to AA toxicity. (c) 2006 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only Melatonin reduces cholesterol accumulation and prooxidant state induced by high cholesterol diet in the plasma, the liver and probably in the aorta of C57BL/6J mice(2004) ŞENER, GÖKSEL; Sener, Göksel; Balkan, Jale; Cevikbaş, Ugur; Keyer-Uysal, Meral; Uysal, MüjdatWe examined the hypolipidemic and antioxidative effects of melatonin in plasma, liver and aorta of C57BL/6J mice fed on a high cholesterol (HC) diet. Mice were fed normal mice chow containing 1.5% cholesterol and 0.5% cholic acid for 4 months with or without melatonin (10 mg/L in drinking water) treatment. HC diet was observed to increase cholesterol, triglyceride and diene conjugate (DC) levels in plasma and liver. There was a tendency towards an increase in cholesterol level in the aorta following HC diet. In addition, aortic DC levels were higher than those of control group. No fatty streaks or plaques developed in the aorta of mice following HC diet, but in some sections, derangement of the endothelial layer was detected. Melatonin treatment was found to reduce plasma, liver cholesterol and DC levels as well as liver triglyceride levels in hypercholesterolemic mice. Aortic cholesterol and DC levels were also reduced in hypercholesterolemic mice when given melatonin, although not statistically significant. There were no differences in aortic histopathological findings of mice fed on a HC diet with and without melatonin treatment. In conclusion, our results indicate that melatonin reduces HC diet-induced cholesterol accumulation and prooxidant state in the plasma, liver and probably in the aorta.Publication Metadata only 2-mercaptoethane sulfonate (MESNA) protects against biliary obstruction-induced oxidative damage in rats(ELSEVIER IRELAND LTD, 2006) ERCAN, FERİHA; Sener, G; Kabasakal, L; Sehirli, O; Ercan, F; Gedik, NThe aim of this study was to assess the antioxidant and antifibrotic effects of chronic administration of 2-mercaptoethane sulfonate (MESNA) on oxidative liver damage and fibrosis induced by biliary obstruction in rats. Liver fibrosis was induced in male Wistar albino rats by bile duct ligation and scission (BDL). MESNA (150 mg/kg, i.p.) or saline was administered for 28 days. At the end of the experiment, rats were killed by decapitation. Serum aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels were determined to assess liver function. Tumor necrosis factor-alpha (TNF-alpha) and lactate dehidrogenase (LDH) were also assayed in serum samples. Liver tissues were taken for determination of the free radicals, hepatic malondialdehyde (MDA) levels, an end product of lipid peroxidation; glutathione (GSH) levels, a key antioxidant; myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. Hepatic collagen content, as a fibrosis marker was also determined. Serum AST, ALT, LDH and TNF-alpha levels were elevated in the BDL group as compared to control group, while this increase was significantly decreased by MESNA treatment. BDL caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased in the liver tissue. These changes were reversed by MESNA treatment. Collagen contents of the liver tissue was increased by BDL (P < 0.001), and reversed back to the control levels with MESNA. Since MESNA administration alleviated the BDL-induced oxidative injury of the liver and improved the hepatic functions, it seems likely that MESNA with its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis and oxidative injury due to biliary obstruction. (c) 2006 Published by Elsevier Ireland Ltd.Publication Metadata only The protective effects of melatonin against water avoidance stress-induced mast cell degranulation in dermis(ELSEVIER GMBH, 2005) ERCAN, FERİHA; Cikler, E; Ercan, F; Cetinel, S; Contuk, G; Sener, GNontraumatic psychological water avoidance stress has been shown to induce mucosal. degeneration, inflammatory cell infiltration and mast cell degranulation in stomach, ileum, colon and urinary bladder. Many skin disorders, such as atopic dermatitis and psoriasis, worsen during stress and seem to be related with infiltration and activation of mast cells releasing vasoactive and proinflammatory mediators. Melatonin is a free radical scavenger and has cytoprotective effects in inflammatory conditions. The aim of the present study was to investigate the effects of melatonin on water avoidance stress (WAS)-induced degranulation of mast cells in the dermis. Wistar rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing to acute WAS, one group of animals was treated with 10mg/kg metatonin (aWAS+mel. group). In the cWAS+mel group, treatment with melatonin lasted for 5 days. Dermal mast cells were stained with toluidine blue and investigated using light microscopy. Numbers of mast cells were increased in both aWAS and cWAS groups, but numbers of degranulated mast cells were increased significantly only in the cWAS group when compared to the control group. Numbers of mature granulated and degranulated mast cells were decreased in the cWAS+mel. group when compared to the cWAS group. In conclusion, chronic metatonin treatment reduced WAS-induced infiltration and activation of mast cells in dermis and may provide a useful therapeutic option in stress-induced skin disorders. (c) 2004 Elsevier GmbH. All rights reserved.