Person: ŞENER, GÖKSEL
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ŞENER
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GÖKSEL
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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 Protective effect of melatonin and omeprazole against alendronat-induced gastric damage(SPRINGER, 2005) ŞENER, GÖKSEL; Sener, G; Goren, FO; Ulusoy, NB; Ersoy, Y; Arbak, S; Dulger, GAAlendronate causes serious gastrointestinal adverse effects. We aimed to investigate if free radicals have any role in the damage induced by alendronate and if melatonin or omeprazole is protective against this damage. Rats were administered 20 mg/kg alendronate by gavage for 4 days, either alone or following treatment with melatonin or omeprazole. On the last day, following drug administration, pilor ligation was performed, and 2 hr later rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation, and myeloperoxidase and glutathione levels, as well as the histologic appearance of the stomach tissues, were determined. Chronic oral administration of alendronate induced significant gastric damage, increasing lipid peroxidation and myeloperoxidase activity, while tissue glutathione levels decreased. Treatment with omeprazole or melatonin prevented this damage as well as the changes in biochemical parameters, and melatonin appeared to be more efficient than omeprazole in protecting the mucosa. Intraperitoneal administration of alendronate did not cause much gastric irritation. Findings of the present study suggest that alendronate induces oxidative gastric damage by a local irritant effect and that melatonin and omeprazole are protective against this damage due to their antioxidant properties.Publication Metadata only Melatonin protects against oxidative organ injury in a rat model of sepsis(SPRINGER, 2005) YEGEN, BERRAK; Sener, G; Toklu, H; Kapucu, C; Ercan, F; Erkanli, G; Kacmaz, A; Tilki, M; Yegen, BCPurpose. Based on the potent antioxidant effects of melatonin, we investigated the putative protective role of melatonin against sepsis-induced oxidative organ damage in rats. Methods. Sepsis was induced by cecal ligation and puncture (CLP) in Wistar albino rats. Animals subjected to CLP and sham-operated control rats were given saline or melatonin 10 mg/kg intraperitoneally 30 min before and 6 h after the operation. The rats were killed 16 h after the operation and the biochemical changes were investigated in the liver, kidney, heart, lung, diaphragm, and brain tissues by examining malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. We also examined the tissues microscopically. Results. Sepsis resulted in a significant decrease in GSH levels and a significant increase in MDA levels and MPO activity (P < 0.05-P < 0.001) showing oxidative damage, which was confirmed by histological examination. Melatonin clearly reversed these oxidant responses and the microscopic damage, demonstrating its protective effects against sepsis-induced oxidative organ injury. Conclusion. The increase in MDA levels and MPO activity and the concomitant decrease in GSH levels demonstrate the role of oxidative mechanisms in sepsis-induced tissue damage. Melatonin, by its free radical scavenging and antioxidant properties, ameliorated oxidative organ injury. Thus, supplementing antiseptic shock treatment with melatonin may be beneficial in the clinical setting.Publication Metadata only Protective effect of aqueous garlic extract against renal ischemia/reperfusion injury in rats(MARY ANN LIEBERT, INC, 2005) ŞENER, GÖKSEL; Kabasakal, L; Sehirli, O; Cetinel, S; Cikler, E; Gedik, N; Sener, GOxygen free radicals are important components involved in pathophysiological tissue alteration observed during ischemia/reperfusion (I/R). This study was designed to determine the possible protective effect of aqueous garlic extract (AGE) on renal I/R injury. Wistar albino rats were unilaterally nephrectomized and subjected to 45 minutes of renal pedicle occlusion followed by 6 hours of reperfusion. AGE (I mL/kg, i.p., corresponding to 500 mg/kg) or vehicle was administered twice: 15 minutes 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 levels of free radicals; renal malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration. Renal tissue collagen content, as a fibrosis marker, was also determined. Creatinme and urea concentrations in blood were measured for the evaluation of renal function. The results revealed that I/R-induced nephrotoxicity, as evidenced by increases in blood urea and creatinine levels, was reversed by AGE treatment. The levels of free radicals, as assessed by the nitro blue tetrazolium test, were increased. Moreover, the decrease in GSH levels and the increases in MDA levels and MPO activity induced by I/R indicated that renal injury involves free radical formation. Treatment of rats with AGE (1 mL/kg) restored the reduced GSH levels, while it decreased free levels of radicals and MDA as well as MPO activity. Collagen contents of the kidney tissues increased by I/R were reversed back to the control levels with AGE. Since AGE administration reversed these oxidant responses and improved renal function and damage at the microscopic level, it seems likely that AGE protects kidney tissue against I/R-induced oxidative damage.Publication Metadata only Protective effect of beta-glucan against oxidative organ injury in a rat model of sepsis(ELSEVIER, 2005) ERCAN, FERİHA; Sener, G; Toklu, H; Ercan, F; Erkanli, GSepsis leads to various organ damage and dysfunction. One of the underlying mechanisms is thought to be the oxidative damage due to the generation of free radicals. In this study, we investigated the putative protective role of beta-gluican against sepsis-induced oxidative organ damage. Sepsis was induced by caecal ligation and puncture (CLP) in Wistar albino rats. Sham operated (control) and sepsis groups received saline or beta-glucan (50 mg/kg, po) once daily for 10 days and 30 min prior to and 6 h after the CLP. Sixteen hours after the surgery, rats were decapitated and the biochemical changes were determined in the brain, diaphragm, kidney, heart, liver and lung tissues using malondialdehyde (N4DA) content - an index of lipid peroxidation - glutathione (GSH) levels - a key antioxidant - and myeloperoxidase (MPO) activity - an index of neutrophil infiltration. Serum TNF-alpha levels were assessed by RIA method. Tissues were also examined under light microscope to evaluate the degree of sepsis-induced damage. The results demonstrate that sepsis significantly decreased GSH levels and increased the MDA levels and MPO activity (p < 0.05-p < 0.001) causing oxidative damage. Elevated plasma TNF-alpha levels in septic rats significantly reduced to control levels in beta-glucan treated rats. Since -glucan administration reversed these oxidant responses, it seems likely that beta-glucan protects against sepsis-induced oxidative organ injury. (c) 2005 Elsevier B.V. All rights reserved.Publication Metadata only Protective effects of Ginkgo biloba against acetaminophen-induced toxicity in mice(SPRINGER, 2006) ERCAN, FERİHA; Sener, G; Omurtag, GZ; Sehirli, O; Tozan, A; Yuksel, M; Ercan, F; Gedik, NBackground: The analgesic acetaminophen (AAP) causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. It was reported that these toxic effects of AAP are due to oxidative reactions that take place during its metabolism. Objective: In this study, we aimed to investigate the possible beneficial effect of Ginkgo biloba (EGb), an antioxidant agent, against AAP toxicity in mice. Methods: Balb/c mice were injected i.p. with: (1) vehicle, control (C) group; (2) a single dose of 50 mg/kg Ginkgo biloba extract, EGb group; (3) a single dose of 900 mg/kg i.p. acetaminophen, AAP group, and (4) EGb, in a dose of 50 mg/kg after AAP injection, AAP + EGb group. 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 were measured. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lusigenin probe. Tissues were also examined microscopically. Results: ALT, AST levels, and TNF-alpha were increased significantly (p < 0.001) after AAP treatment, and reduced with EGb. Acetaminophen caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased (p < 0.001) in liver tissues. These changes were reversed by EGb treatment. Furthermore, luminol and lusigenin CL levels in the AAP group increased dramatically compared to control and reduced by EGb treatment (p < 0.01). Conclusion: Our results implicate that AAP causes oxidative damage in hepatic tissues and Ginkgo biloba extract, by its antioxidant effects protects the tissues. Therefore, its therapeutic role as a tissue injury-limiting agent must be further elucidated in drug-induced oxidative damage.Publication Open Access Melatonin protects against mercury(II)-induced oxidative tissue damage in rats(BLACKWELL MUNKSGAARD, 2003-12) ŞENER, GÖKSEL; Sener, G; Sehirli, AO; Ayanoglu-Dulger, GMercury exerts a variety of toxic effects in the body. Lipid peroxidation, DNA damage and depletion of reduced glutathione by Hg(II) suggest an oxidative stress-like mechanism for Hg(II) toxicity. Melatonin, the main secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. N-Acetylcysteine, a precursor of reduced glutathione and an antioxidant, is used in the therapy of acute heavy metal poisoning. In this study the protective effects of melatonin in comparison to that of N-acetylcysteine against Hg-induced oxidative damage in the kidney, liver, lung and brain tissues were investigated. Wistar albino rats of either sex (200-250 g) were divided into six groups, each consisting of 8 animals. Rats were intraperitoneally injected with 1) 0.9% NaCl, control (C) group; 2) a single dose of 5 mg/kg mercuric chloride (HgCl2), Hg group; 3) melatonin in a dose of 10 mg/kg, I hr after HgCl2 injection, Hg-melatonin group; 4) melatonin in a dose of 10 mg/kg one day before and 1 hr after HgCl2 injection, melatonin-Hg-melatonin group; 5) N-acetylcysteine in a dose of 150 mg/kg, I hr after HgCl2 injection, Hg-N-acetylcysteine group, and 6) N-acetylcysteine in a dose of 150 mg/kg one day before and I hr after HgCl2 injection, N-acetylcysteine-Hg-N-acetylcysteine group. Animals were killed by decapitation 24 hr after the injection of HgCl2. Tissue samples were taken for determination of malondialdehyde, an end-product of lipid peroxidation; glutathione (GSH), a key antioxidant, and myeloperoxidase activity, an index of neutrophil infiltration. The results revealed that HgCl2 induced oxidative tissue damage, as evidenced by increases in malondialdehyde levels. Myeloperoxidase activity was also increased, and GSH levels were decreased in the liver, kidney and the lungs. All of these effects were reversed by melatonin or N-acetylcysteine treatment. Since melatonin or N-acetylcysteine administration reversed these responses, it seems likely that melatonin or N-acetylcysteine can protect all these tissues against HgCl2-induced oxidative damage.Publication Metadata only L-Carnitine ameliorates methotrexate-induced oxidative organ injury and inhibits leukocyte death(SPRINGER, 2006) YEGEN, BERRAK; Sener, G; Eksioglu-Demiralp, E; Cetiner, M; Ercan, F; Sirvanci, S; Gedik, N; Yegen, BCMethotrexate (MTX), a folic acid antagonist widely used for the treatment of a variety of tumors and inflammatory diseases, affects normal tissues that have a high rate of proliferation, including the hematopoietic cells of the bone marrow and the gastrointestinal mucosal cells. To elucidate the role of free radicals and leukocytes in MTX-induced oxidative organ damage and the putative protective effect of L-carnitine (L-Car), Wistar albino rats were administered a single dose of MTX (20 mg/kg) followed by either saline or L-Car (500 mg/kg) for 5 days. After decapitation of the rats, trunk blood was obtained, and the ileum, liver, and kidney were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content. Our results showed that MTX administration increased the MDA and MPO activities and collagen content and decreased GSH levels in all tissues, while these alterations were reversed in L-Car-treated group. The elevated serum TNF-alpha level observed following MTX treatment was depressed with L-Car. The oxidative burst of neutrophils stimulated by Annexin V was reduced in the saline-treated MTX group, while L-Car abolished this inhibition. Similarly, flow cytometric measurements revealed that leukocyte apoptosis was increased in MTX-treated animals, while L-Car reversed these effects. Severe degeneration of the intestinal mucosa, liver parenchyma, and glomerular and tubular epithelium observed in the saline-treated MTX group was improved by L-Car treatment. These results suggest that L-Car, possibly via its free radical scavenging and antioxidant properties, ameliorates MTX-induced oxidative organ injury and inhibits leukocyte apoptosis. Thus, supplementation with L-Carnitine as an adjuvant therapy may be promising in alleviating the systemic side-effects of chemotherapeutics.Publication Metadata only Gastroprotective effect of leukotriene receptor blocker montelukast in alendronat-induced lesions of the rat gastric mucosa(ELSEVIER SCI LTD, 2005) ŞENER, GÖKSEL; Sener, G; Kapucu, C; Cetinel, S; Cikler, E; Ayanoglu-Dulger, GAlendronate causes serious gastrointestinal adverse effects. We aimed to investigate if montelukast, a leukotriene receptor antagonist, is protective against this damage. Rats were administered 20 mg/kg alendronate by gavage for 4 days, either alone or following treatment with montelukast (10 mg/kg). On the last day, following drug administration, pilor ligation was performed and 2 h later, rats were killed and stomach, liver and kidney tissues were removed. Gastric acidity, gastric tissue ulcer index values and malondialdehyde (MDA); an end product of lipid peroxidation, and glutathione (GSH) levels; a key antioxidant, as well as myeloperoxidase (MPO) activity; an indirect marker of tissue neutrophil infiltration were determined, and the histologic appearance of the stomach, liver and kidney tissues were studied. Chronic oral administration of alendronate induced significant gastric damage, increasing myeloperoxidase activity and lipid peroxidation, while tissue glutathione levels decreased. Similarly, in the alendronate group MDA levels and MPO activities of liver and kidney tissues were increased and GSH levels were decreased. Treatment with montelukast prevented the damage as well as the changes in biochemical parameters in all tissues studied. Findings of the present study suggest that alendronate is a local irritant that causes inflammation through neutrophil infiltration and oxidative damage in tissues, and that montelukast is protective against this damage by its anti-inflammatory effect. (C) 2004 Elsevier Ltd. All rights reserved.Publication Metadata only Protective effects of taurine on protamine sulfate induced bladder damage(SPRINGER, 2006) ERCAN, FERİHA; Zeybek, Ali; Saglam, Beyhan; Cikler, Esra; Cetinel, Sule; Ercan, Feriha; Sener, GokselThe present study was designed to investigate the putative protective effects of taurine on protamine sulfate (PS) induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate buffered solution (control group) or PS (PS group) dissolved in phosphate buffered solution. In the PS + taurine (PS+Tau) group, after the PS instillation, taurine (50 mg/kg) was injected intraperitoneally for 3 days. Histopathological changes were investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) (a biomarker of oxidative damage) and glutathione (GSH) (a biomarker of protective oxidative injury) levels. In the PS group ulcerated areas, an irregular mucus layer, inflammatory cell infiltration, and increased number of mast cells were observed. In the PS+Tau group, a relatively normal urothelial topography, glycosaminoglycan layer, and decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction lead us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in GSH levels in the PS+Tau group compared to PS group was in accordance with morphological findings. Based on the results, taurine treatment significantly prevented PS induced degenerative morphological and biochemical changes of urinary bladder mucosa.
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