Person: YÜKSEL, MERAL
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YÜKSEL
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Publication Metadata only Oxygen radicals and nitric oxide in rat mesenteric ischaemia-reperfusion: Modulation by L-arginine and N-G-nitro-L-arginine methyl ester(WILEY, 1998) YALÇIN, AHMET SUHA; Haklar, G; Ulukaya-Durakbasa, C; Yuksel, M; Dagli, T; Yalcin, AS1. The aims of the present study were to detect changes in superoxide anion (O-2(.-)), nitric oxide (NO) and other reactive oxygen species (ROS) directly by measurement of chemiluminescence (CL) and to investigate the role of L-arginine, a nitric oxide synthase (NOS) substrate, and N-G-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, together with their molecular enantiomers D-arginine and D-NAME, in a rat mesenteric ischaemia-reperfusion (I/R) model. 2, Seventy-nine female Wistar albino rats were divided into eight groups, The first three groups underwent sham operation; group 1 was the control group, group 2 received L-arginine and group 3 received L-NAME. Ischaemia was produced in the remaining five groups by ligation of the superior mesenteric artery for 30 min followed by 60 min reperfusion, Group 4 rats were control I/R rats and groups 5-8 received either L-arginine, L-NAME, D-arginine or D-NAME, respectively. 3, Both luminol and lucigenin CL was significantly increased in I/R groups compared with sham-operated groups. L-Arginine significantly reduced CL measurements. D-Arginine was also protective, but not as much as L-arginine. Both L- and D-arginine had in vitro O-2(.-)-scavenging potential, as tested by the xanthine-xanthine oxidase system. N-G-Nitro-L-arginine methyl ester decreased lipid peroxidation values in addition to reducing CL measurements. Nitric oxide concentrations were significantly increased in VR groups in comparison with sham-operated groups. Peroxynitrite formation was increased by I/R. Treatment with L-NAME was beneficial by reducing NO concentrations in the reperfused ileum, 4, In our I/R model, O-2(.-), NO and other ROS were increased. Although NOS inhibitors were effective in reducing oxidative damage, increasing NO concentrations with L-arginine was also beneficial, presumably due to the ability of L-arginine to inhibit phagocyte adherence and its radical scavenging potential. In fact, NO may have different effects in terms of tissue injury or protection depending on the concentration of oxygen and the haemodynamic state of the tissue.Publication Metadata only Nitric oxide and endothelin relationship in intestinal ischemia/reperfusion injury(1998) DAĞLI, EMRULLAH TOLGA; Durakbasa, C. U.; Dagli, T. E.; Mouni, H.; Haklar, G.; Bilsel, A. S.; Yuksel, M.; Aktan, A. O.Gastrointestinal mucosal blood flow is dependent on a balanced release of vasoactive substances from endothelium. Nitric oxide (NO) may increase the flow by vasodilatation and/or antiaggregation whereas endothelin (ET) may decrease it by vasoconstriction and aggregation. NO and ET may have counterbalancing effects on each other in tissue damage. In order to test this hypothesis, in this study on rats, L-arginine to increase NO levels and N(G)-nitro-L-arginine methyl esther (L-NAME) to decrease NO levels have been used in an intestinal ischemia/ reperfusion (I/R) injury model and portal vein ET response was evaluated. Lipid peroxidation product measurements and chemiluminescence (CL) studies were also carried out in ileal tissue samples. Intestinal I/R injury caused an increase in portal venous ET levels with levels of 9.4+/-0.5 fmol/ml in sham operation and 14.8+/-1.6 fmol/ml in I/R group. ET level of L-NAME-sh group was lower than that of sham-operated group and also ET level of L-NAME-I/R group was lower than that of I/R group. This yielded the conclusion that inhibition of NO synthesis decreases portal venous ET levels in this model. Increased NO production by L-arginine caused increased ET levels in sham operated groups but this effect was not observed in I/R injury state. This study also showed that inhibition of NO synthesis has a protective role by reducing the reperfusion damage in this model. It is likely that NO and ET have a feedback effect on each other both under physiologic conditions and I/R injury.Publication Metadata only Adenosine protects against indomethacin-induced gastric damage in rats(1998) YEGEN, BERRAK; Bozkurt, A.; Yüksel, M.; Haklar, G.; Kurtel, H.; Yeğen, B. C.; Alican, I.This study examines the putative gastroprotective effect of adenosine on indomethacin-induced gastric lesions and the possible mechanisms involved. After 24 hr of starvation, the rats were treated either with indomethacin (Indo; 25 mg/kg, subcutaneously) alone or adenosine + Indo (Ado; 7.5 mg/kg, subcutaneously, three times a day), or the vehicle (5% NaHCO3, subcutaneously). The length of hemorrhagic lesions in the stomachs was expressed as the lesion index. The tissue-associated myeloperoxidase (MPO) activity and protein oxidation were measured in gastric tissue samples. Formation of reactive oxygen species in gastric tissues was measured by using luminol- and lucigenin-enhanced chemiluminescence. In other groups of rats, gastric mucosal permeability and gastric acid output were performed following the same treatment regimens. The gastric mucosal permeability was measured by determination of [51Cr]EDTA clearance in a perfused stomach preparation and gastric acid secretion studies were performed following pylorus ligation. The lesion index, the increase in lucigenin-enhanced chemiluminescence, and the increase in gastric mucosal permeability in Indo-treated rats were reversed by Ado pretreatment. Ado pretreatment also prevented the increase in gastric acid output and gastric volume in Indo-treated rats. Thus, these findings implicate that exogenous adenosine has a protective role on indomethacin-induced gastric lesions, possibly by inhibiting gastric hyperacidity and reactive oxygen formation and by preventing disruption of the mucosal integrity.Publication Metadata only The effect of antioxidant therapy on colonic inflammation in the rat(SPRINGER, 1999) YEGEN, BERRAK; Yavuz, Y; Yuksel, M; Yegen, BC; Alican, IUnder normal physiological conditions, chemical and antioxidant defenses protect tissues from the damaging effects of reactive oxygen metabolites (ROM). It has been proposed that ROMs are involved in the development of tissue injury in many inflammatory diseases and also in patients with colitis. In the present study we aimed to investigate the effects of antioxidant therapy on the extent of colonic inflammation and ROM levels in the injured tissues in a trinitrobenzene sulfonic acid-induced colitis model in the rat. Sprague-Dawley rats were pretreated with the antioxidants superoxide dismutase (30,000 U/kg s.c.) or catalase (400,000 U/kg s.c.) prior to induction of colitis and they were decapitated 24 h (acute group) or 6 days (chronic group) after the induction of colitis (each group consists of eight to ten rats). Pretreatment with the antioxidants reduced the macroscopic damage score significantly in both acute and chronic groups compared with untreated colitis groups, whereas they reduced the microscopic damage score and colonic wet weight only in the chronic group. The chemiluminescence assay - a technique to assess the presence of reactive oxygen species in the tissues - values of the groups pretreated with the antioxidants showed a tendency to decrease compared with the untreated colitis group, but they were not statistically significant. Based on these findings, pretreatment with the antioxidants superoxide dismutase or catalase has beneficial effects on the extent of colonic inflammation, particularly in the chronic period, and this may support the importance of antioxidant therapy to reduce the severity of inflammatory bowel disease in humans.Publication Metadata only The effects of free oxygen radical scavenger and platelet-activating factor antagonist agents in experimental acute pancreatitis(LIPPINCOTT WILLIAMS & WILKINS, 1999) HAKLAR, GONCAGÜL; Soybir, G; Koksoy, F; Ekiz, F; Yalcin, O; Fincan, K; Haklar, G; Yuksel, MThis study was done to evaluate the possible preventive effects of reactive oxygen species (ROS) scavenger agent desferrioxamine (DFX) and platelet-activating factor (PAF) antagonist agent: ginkgo biloba (GB) in an experimental acute pancreatitis model. Seventy-eight CD-1 mice were divided into six groups consisting of 10-13 mice. Induction of pancreatitis was achieved by cerulein injection in groups 2-5. The first group was control, whereas DFX and GB were used alone or in combinations as preventive agents in groups 3-5. DFX or GB were injected to the mice in groups 6 and 7 to evaluate any toxic effect. The assessment of the pancreatic edema and inflammation, the measurement of the amylase and the pancreatic weight and the measurement of the pancreatic tissue oxidative capacity by chemiluminescence method were the parameters to evaluate pancreatitis. Although the results indicate DFX and GB alone or in combinations have significant preventive roles, this was not a complete prevention.