Person: ELÇİOĞLU, HATİCE KÜBRA
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ELÇİOĞLU
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HATİCE KÜBRA
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Publication Metadata only Octreotide ameliorates alendronate-induced gastric injury(ELSEVIER SCIENCE INC, 2004) ŞENER, GÖKSEL; Sener, G; Paskaloglu, K; Kapucu, C; Cetinel, S; Contuk, G; Ayanoglu-Dulger, GAlendronate causes serious gastrointestinal adverse effects. The aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue, improves the alendronate-induced gastric injury. Rats were administered 20 mg/kg alendronate by gavage for 4 days, either alone or following treatment with octreotide (0.1 ng/kg, i.p.). On, the last day, following drug administration, pilor ligation was performed and 2 h later,rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation (as assessed by malondialdehyde, MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined. Chronic oral administration of alendronate induced significant gastric damage, increasing lipid peroxidation (37.1 +/- 3.2 nmol/g) and myeloperoxidase activity (57.6 +/- 3.7 U/g), while tissue glutathione levels (0.9 +/- 0.1 mumol/g) decreased. Treatment with octreotide prevented this damage as well as the changes in biochemical parameters (MDA: 23.4 +/- 1.3 nmol/g; MPO: 31.68 U/g; GSH: 1.5 +/- 0.1 mumol/g). Findings of the present study suggest that alendronate induces oxidative gastric damage by a local irritant effect, and that octreotide ameliorates this damage by inhibiting neutrophil infiltration and reducing lipid peroxidation. Therefore, its therapeutic role as a ulcer healing agent must be further elucidated in alendronate-induced gastric mucosal injury. (C) 2004 Elsevier Inc. All rights reserved.Publication Metadata only Melatonin protects against gentamicin-induced nephrotoxicity in rats(2002) ŞENER, GÖKSEL; Sener, Göksel; Sehirli, A. Ozer; Altunbas, Hale Z.; Ersoy, Yasemin; Paskaloglu, Kübra; Arbak, Serap; Ayanoglu-Dulger, GülAcute renal failure is a major complication of gentamicin (GEN), which is widely used in the treatment of gram-negative infections. A large body of in vitro and in vivo evidence indicates that reactive oxygen metabolites (or free radicals) are important mediators of gentamicin nephrotoxicity. In this study we investigated the role of free radicals in gentamicin-induced nephrotoxicity and whether melatonin, a potent antioxidant could prevent it. For this purpose female Sprague-Dawley rats were given intraperitoneally either gentamicin sulphate (40 mg/kg), melatonin (10 mg/kg), gentamicin plus melatonin or vehicle (control) twice daily for 14 days. The rats were decapitated on the 15th day and kidneys were removed. Blood urea nitrogen (BUN) and creatinine levels were measured in the blood and malondialdehyde (MDA) and glutathione (GSH) levels, protein oxidation (PO) and myeloperoxidase (MPO) activity were determined in the renal tissue. Gentamicin was observed to cause a severe nephrotoxicity which was evidenced by an elevation of BUN and creatinine levels. The significant decrease in GSH and increases in MDA levels, PO and MPO activity indicated that GEN-induced tissue injury was mediated through oxidative reactions. On the other hand simultaneous melatonin administration protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by GEN treatment.Publication Metadata only L-Carnitine Ameliorates Oxidative Damage due to Chronic Renal Failure in Rats(2004) ŞENER, GÖKSEL; Şener G., Paskaloǧlu K., Şatiroglu H., Alican I., Kaçmaz A., Sakarcan A.Chronic renal failure (CRF) is associated with oxidative stress that promotes production of reactive oxygen species. L-Carnitine is a cofactor required for transport of long-chain fatty acids into the mitochondrial matrix. Recent research has shown that some clinical conditions (ie, anorexia, chronic fatigue, coronary heart disease, diphtheria, hypoglycemia, and male infertility) benefit from exogenous supplementation of L-carnitine. The aim of this study was to examine the role of L-carnitine in protecting the aorta, heart, corpus cavernosum, and kidney tissues against oxidative damage in a rat model of CRF. Male Wistar albino rats were randomly assigned to either the CRF group or the sham-operated control group, which had received saline or L-carnitine (500 mg/kg, i.p.) for 4 weeks. CRF was evaluated by BUN and serum creatinine measurements. Aorta and corporeal tissues were used for contractility studies or stored along with heart and kidney tissues for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels. Plasma MDA, GSH levels and erythrocyte superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were also studied. In the CRF group, the contraction and the relaxation of aorta and corpus cavernosum samples decreased significantly compared with controls and were partially reversed by L-carnitine treatment. In the CRF group, there were significant increases in tissue MDA with marked reductions in GSH levels in all tissues and plasma compared with controls. In the plasma SOD, CAT and GSH-Px activities were also reduced. All these effects were reversed by L-carnitine as well. The increase in MDA level and the concomitant decrease in GSH level of tissues and plasma and also suppression of the antioxidant enzyme activities in plasma demonstrate that oxidative mechanisms are involved in CRF-induced tissue damage. L-carnitine, possibly via its free radical scavenging and antioxidant properties, ameliorates oxidative organ injury and CRF-induced dysfunction of the aorta and corpus cavernosum. These results suggest that L-carnitine supplementation may have some benefit in CRF patients.Publication Metadata only Melatonin treatment protects against diabetes-induced functional and biochemical changes in rat aorta and corpus cavernosum(ELSEVIER SCIENCE BV, 2004) ŞENER, GÖKSEL; Paskaloglu, K; Sener, G; Ayanoglu-Dulger, GEnhanced oxidative stress due to diabetes is accepted to lead to endothelial dysfunction, and this is known to play a key role in the pathogenesis of diabetic vascular diseases and complications. This study was designed to determine the possible protective effect of melatonin and/or insulin treatment on the functional and biochemical changes caused by hyperglycemia in aorta and corpus cavernosum of diabetic rats. Wistar albino male rats were rendered diabetic by injecting streptozotocin (60 mg/kg, intraperitoneally (i.p.)). Melatonin (10 mg/kg, i.p.) and/or insulin (6 U/kg, subcutaneously (s.c.)) were administered for 8 weeks. In the diabetic group, the contractile responses of aortic strips to phenylephrine were significantly impaired (EC50 5.5 x 10(-7) M in diabetic and EC50 1.47 x 10(-7) M in the control group, P<0.001). Treatment with melatonin (EC50 4.6 x 10(-7) M) or insulin+melatonin (EC50 1.68 x 10(-7) M, p<0.001) improved the contractile responses. Acetylcholine caused a dose-dependent relaxation response (EC50 1.58 x 10(-7) M) which was impaired in the diabetic group (EC50 26 x 10(-7) M, P<0.001). There was less impairment in melatonin-, insulin- and insulin+melatonin-treated groups (EC50 11.61 X 10(-7), 7.3 x 10(-7) and 1.41 X 10(-7) M, respectively, P<0.01). Contractile responses to phenylephrine were also impaired in the corpus cavemosurn strips (EC50 2.06 x 10-5 M in diabetic and 0.94x 1 0-5 M in the control group, P<0.001). In the melatonin- (EC50 1.59x 10(-5) M) and insulin+melatonin-treated (EC50 1.53 X 10(-5) M, P<0.5) groups contractile responses were improved. In the diabetic group, the relaxation responses of corpus cavemosum strips to acetylcholine were impaired (EC50 24.12 x 10(-5) M, P<0.001), and treatment with melatonin (EC50 0.68 x 10(-5) M), insulin (EC50 0.53 x 10(-5) M) or insulin+melatonin (0.98 x 10(-5) M, P<0.001) restored the responses to acetylcholine. In diabetic tissues, malondialdehyde levels were increased while glutathione levels were decreased, demonstrating oxidative damage. This was also prevented by treatment with melatonin or the melatonin and insulin combination. The diabetic state enhances the generation of free radicals, and both melatonin and insulin treatments reduced this oxidative stress; however, treatment with the combination was the most efficient in preventing diabetes-induced damage. Thus, our results suggested that giving diabetic patients adjuvant therapy with melatonin may have some benefit in controlling diabetic complications. (C) 2004 Elsevier B.V. All rights reserved.Publication Metadata only Melatonin reverses urinary system and aorta damage in the rat due to chronic nicotine administration(ROYAL PHARMACEUTICAL SOC GREAT BRITAIN, 2004) ŞENER, GÖKSEL; Sener, G; Kapucu, C; Paskaloglu, K; Ayanoglu-Dulger, G; Arbak, S; Ersoy, Y; Alican, IWe have evaluated the changes in contractile activity and oxidant damage of corpus cavernosum, urinary bladder, kidney and aorta after chronic nicotine administration in rats. The effects of melatonin on these parameters were investigated also. Male Wistar albino rats were injected intraperitoneally with nicotine hydrogen bitartrate (0.6 mg kg(-1) daily for 21 days) or saline. Melatonin (10 mg kg(-1), i.p.) was administered either alone or with nicotine injections. Corpus cavernosum, bladder and aorta were used for contractility studies, or stored with kidneys for the measurement of malondialdehyde and glutathione levels. Corpus cavernosum, bladder, and aorta samples were examined histologically and the extent of microscopic tissue damage was scored. In the nicotine-treated group, the contraction of corpus cavernosum, bladder and aorta samples and the relaxation of corporeal and aorta tissues decreased significantly compared with controls. However, melatonin treatment restored these responses. In the nicotine-treated group, there was a significant increase in the malondialdehyde levels of the corporeal tissue, bladder, kidney and aorta, with marked reductions in glutathione levels compared with controls. Melatonin treatment reversed these effects also. Melatonin administration to nicotine-treated animals caused a marked reduction in the microscopic damage of the tissues compared with those of the untreated group. In this study, nicotine-induced dysfunction of the corpus cavernosum, bladder and aorta of rats was reversed by melatonin treatment. Moreover, melatonin, as an antioxidant, abolished elevation in lipid peroxidation products, and reduction in the endogenous antioxidant glutathione, and protected the tissues from severe damage due to nicotine exposure.Publication Metadata only Melatonin treatment protects against ischemia/reperfusion-induced functional and biochemical changes in rat urinary bladder(2003) ŞENER, GÖKSEL; Sener, Göksel; Sehirli, Ahmet Ozer; Paskaloğlu, Kübra; Dülger, Gül Ayanoğlu; Alican, InciReactive oxygen metabolites play important roles in ischemia/reperfusion (I/R) injury in several systems. The aim of this study was to investigate the role of melatonin against I/R injury of the rat urinary bladder. The abdominal aorta was clamped to induce ischemia for 30 min, then the animals were subjected to 60 min of reperfusion. Melatonin (10 mg/kg, i.p.) or the vehicle (control 1% alcohol i.p.) was administered before I/R. After decapitation, the bladder was removed and the tissue was either used for functional studies or stored for measurement of products of lipid peroxidation (LP), glutathione (GSH) levels and myeloperoxidase activity (MPO). Bladder strips were suspended in oxygenated Tyrode's buffer at 37 degrees C and isometric contractions to carbachol (CCh; 10(-8)-10(-4) m) were recorded. In the I/R group, the contractile responses of the bladder strips were lower than those of the control group (P < 0.01-0.001) and were reversed by treatment with melatonin (P < 0.05-0.001). LP which was higher in I/R group compared with control (27.68 +/- 1.69 and 10.59 +/- 1.27 nmol/g, respectively; P < 0.001) was partially reversed by melatonin (19.01 +/- 1.85 nmol/g; P < 0.01). Similarly, GSH showed a decrease in the I/R group compared with controls (0.27 +/- 0.03 and 0.43 +/- 0.04 micromol/g, respectively; P < 0.05) and melatonin prevented this effect completely (0.45 +/- 0.04 micromol/g; P < 0.05). MPO activity in the I/R group (4.19 +/- 0.08 U/g) was significantly higher than that of the control group (1.41 +/- 0.08 U/g; P < 0.001) and melatonin treatment reduced MPO levels compared with I/R alone (3.16 +/- 0.07; P < 0.001). Melatonin almost completely reversed the low contractile responses of rat urinary bladder strips to CCh and prevented oxidative tissue damage following I/R.Publication Metadata only Melatonin treatment protects against sepsis-induced functional and biochemical changes in rat ileum and urinary bladder(PERGAMON-ELSEVIER SCIENCE LTD, 2004) ŞENER, GÖKSEL; Paskaloglu, K; Sener, G; Kapucu, C; Ayanoglu-Dulger, GSepsis is commonly associated with enhanced generation of reactive oxygen metabolites, which lead to multiple organ dysfunction. The aim of this study was to examine the role of melatonin, a potent antioxidant, in protecting the intestinal and bladder tissues against damage in a rat model of sepsis. Sepsis was induced by cecal ligation and perforation (CLP) in Wistar Albino rats. Sham operated (control) and CLP group received saline or melatonin (10 mg/kg, ip) 30 minutes prior to and 6 hours after the operation. Sixteen hours after the surgery, rats were decapitated and the intestinal and urinary bladder tissues were used for contractility studies, or stored for the measurement of malondialdehyde (MDA) content -an index of lipid peroxidation-, glutathione (GSH) levels -a key antioxidant- and myeloperoxidase (MPO) activity- an index of neutrophil infiltration-. Heal and bladder MDA levels in the CLP group were significantly increased (p < 0.001) with concomitant decreases in GSH levels (p < 0.01 -p < 0.001) when compared to the control group. Similarly, MPO activity was significantly increased (p < 0.001) in both ileum and bladder tissues. On the other hand, melatonin treatment significantly reversed (p < 0.001) the elevations in MDA and MPO levels, while reduced GSH levels were increased back to the control levels (p < 0.01-p < 0.001). In the CLP group, the contractility of the ileal and bladder tissues decreased significantly compared with controls. Melatonin treatment of the CLP group restored these responses. In this study, CLP induced dysfunction of the ileal and bladder tissue of rats was reversed by melatonin treatment. Moreover, melatonin, as an antioxidant, abolished the elevation in lipid peroxidation products and myeloperoxidase activity, and reduction in the endogenous antioxidant glutathione and thus protected the tissues against sepsis-induced oxidative damage. (C) 2003 Elsevier Inc. All rights reserved.