Publications by authors named "Dengiz G"

The aim of this study was to evaluate and compare the effects of 5-lipoxygenase enzyme (5-LO) inhibitor zileuton and cysteinyl leukotriene receptor (CysLT1R) antagonist montelukast in testicular torsion/detorsion (T/D) injury model in rats. Rats were anaesthetised with 75 mg kg(-1) ketamine hydrochloride and 8 mg kg(-1) xylazine intraperitoneal before the operation. Torsion was created by rotating the right testis 720° clockwise and maintained by fixing the testis.

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Objectives: To determine whether angiotensin and endothelin have any role in testicular ischemia reperfusion injury by investigating the effects of the angiotensin converting enzyme inhibitor enalapril, selective non-peptide angiotensin-II type I blocker losartan and dual endothelin receptor blocker bosentan.

Methods: Rats were anesthetized with thiopental sodium (50 mg/kg i.p.

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Reactive oxygen species (ROS) have been implicated in the etiology of indomethacin-induced gastric mucosal damage. This study investigated amiodarone's protective effects against oxidative gastric mucosal damage induced by indomethacin. Amiodarone is a widely used antiarrhythmic agent.

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Montelukast, a selective reversible cysteinyl leukotriene D(4)-receptor (LTD(4) receptor) antagonist, is used in the treatment of asthma. We have investigated alterations in the glutathione (GSH) and activity levels of antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione reductase (GR)] and myeloperoxidase (MPO), as markers of the ulceration process following oral administration of montelukast, lansoprazole, famotidine, and ranitidine, respectively, in rats with indomethacin-induced ulcers. In the present study, we found that 1) montelukast, lansoprazole, famotidine, and ranitidine all reduced the development of indomethacin-induced gastric damage, with this reduction occurring at a greater magnitude for montelukast, famotidine, and lansoprazole than for ranitidine; 2) montelukast and ranitidine both alleviated increases in the activity levels of CAT and GST enzymes resulting from gastric injury; 3) montelukast and ranitidine both ameliorated depressions in the GSH and activity levels of SOD and GR enzymes caused by indomethacin administration; and 4) all doses of montelukast, lansoprazole, and ranitidine decreased amplification of MPO activity resulting from induced gastric injuries.

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Amiodarone is a widely used anti-arrhythmic agent. We have investigated alterations in the glutathione (GSH) level and the activities of anti-oxidative enzymes (superoxide dismutase, catalase, glutathione s-transferase and glutathione reductase) and myeloperoxidase, as marker of acute inflammation, following oral administration of amiodarone and diclofenac in rats with carrageenan-induced paw edema. In the present study, we found that 1) Amiodarone reduced the development of carrageenan-induced paw edema, to a greater degree than diclofenac; 2) Amiodarone and diclofenac alleviated increases in the activities of catalase and glutathione s-transferase enzymes resulting from edema; 3) Amiodarone and diclofenac ameliorated depressions in the GSH level and the activities of superoxide dismutase and glutathione reductase enzymes caused by carrageenan injection; and 4) All doses of amiodarone and diclofenac caused an amplification in myeloperoxidase activity resulting from induced paw edema.

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The aim of this paper was to investigate the protective effect of the T-type calcium channel blocker in a model of acute local inflammation (histamine-induced). The intraplantar injection of histamine elicited an inflammatory response that was characterized by a time-dependent increase in paw oedema and neutrophil infiltration in paw tissue. The maximal increase in paw volume was observed at 90 min after histamine administration (maximal paw volume: 0.

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