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Öğe Carbon tetrachloride-induced nephrotoxicity and protective effect of betaine in Sprague-Dawley rats(Elsevier Science Inc, 2003) Ozturk, F; Ucar, M; Ozturk, IC; Vardi, N; Batcioglu, KObjectives. To observe the changes in the antioxidative defense enzymes and to detect the alterations of renal microscopy after carbon tetrachloride (CCl4) administration in rats and to investigate the possible protective effects of betaine against CCl4-induced renal damage. Methods. Thirty-two adult Sprague-Dawley rats were divided into four groups as follows: control group, betaine group, CCl4 group, and CCl4 + betaine group. CCl4 was given subcutaneously at 1 mL/kg. In the CCl4 + betaine group, rats were pretreated with betaine, then exposed to CCl4 at the same dose. Betaine group rats received concentrated betaine solution. The rats were killed and the kidneys taken for enzyme analyses and histologic examination. Glutathione peroxidase, superoxide dismutase, and catalase activities were measured in right kidney homogenates. Left kidneys were processed for light microscopic evaluation. Results. In the CCl4-treated group, significant increases in kidney superoxide dismutase and catalase activities and significant decrease in glutathione peroxidase activity were observed (P < 0.01). These changes were found to be normalized in the CCl4 + betaine group. Betaine did not change the enzyme activities. Exposure to CCl4 resulted in glomerular and tubular alterations in the renal cortex. These alterations were found to be prevented by betaine pretreatment. Conclusions. These results indicate that exposure to CCl4 leads to renal damage in rats and betaine exerts an improvement on nephrotoxic effects of CCl4.Öğe Comparative study of the effect of ultrasound and electrostimulation on bone healing in rats(Lippincott Williams & Wilkins, 1998) Zorlu, U; Tercan, M; Ozyazgan, I; Taskan, I; Kardas, Y; Balkar, F; Ozturk, FThis study was performed to compare the effects of direct current with ultrasound on fracture healing. Thirty-two rats were subjected to the experiment. Each rat's right legs were used as the experimental sample, and their left legs were used as the control. Four groups were formed, each consisting of 16 ultrasound, 16 electrostimulation, 16 ultrasound control, and 16 electrostimulation control animals. Fibular osteotome was applied to the rats under anesthesia. In the electrostimulation and electrostimulation control groups, a stainless steel cathode electrode was installed in the fractured side. In the electrostimulation group, 10 mu A of direct current for 30 min, using a semi-invasive method, was given one day after fracture, for 15 days. On the control side, the aforementioned protocol was followed but sham treated. The ultrasound group was treated with 0.1 W/cm(2) ultrasound for 2 min every second day for 6 days after fracture (4 times). Rats were killed on the 7th and 14th days to investigate the macroscopic, radiologic, and histopathologic parameters of fracture healing. There was a difference (P < 0.05) between the electrostimulation and the electrostimulation control groups on the 7th day. There was a difference (P < 0.05) between the ultrasound and ultrasound control groups on the 14th day. After statistical evaluation of the experimental results, it was found that in both the ultrasound and the electrostimulation groups, the fracture healing had been accelerated more so than in the control groups. There was no observed statistical difference between ultrasound and electrostimulation effects.Öğe Comparison of chemopreventive effects of Vitamin E plus selenium versus melatonin in 7,12-dimethylbenz(a) anthracene-induced mouse brain damage(Elsevier Sci Ltd, 2004) Batcioglu, K; Karagözler, AA; Ozturk, IC; Genc, M; Bay, A; Ozturk, F; Aydogdu, NIn this work, the protective effect of Vitamin E plus selenium (Vit E + Se) and melatonin against 7,12-dimethylbenz(a)anthracene (7,12DMBA)-induced changes in superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT) and carbonic anhydrase (CA) activities and malonedialdehyde (MDA) levels of mouse brain were compared. 12-month old mice were divided into four groups each including 10 animals. The first group served as control group. The second group was treated with 7,12-DMBA (20 mg/(kg day)). The third group was treated with 7,12-DMBA and Vitamin E (90 mu g/(individual day)) and selenium (1.8 mu g/(individual day)) simultaneously. The fourth group was treated with 7, 12-DMBA and melatonin (4.2 mg/(kg day)) simultaneously. Treatment continued for 21 days after which the mice were sacrificed and brain homogenates were prepared. 7,12-DMBA treated group exhibited significantly decreased levels of brain SOD, GSHPx, CAT and CA activities and increased MDA levels as compared to control. Vitamin E + Se fully or partially restored enzyme inhibition except for SOD. Lipid peroxidation was also reduced in Vitamin E + Se treated group. Melatonin provided a better protection for SOD, GSHPx and CAT, and a plausible protection for CA activity. Protection against lipid peroxidation measured as MDA in melatonin treated group was appreciable although slightly lesser than the protection provided by Vitamin E + Se. The results imply that Vitamin E + Se and melatonin both provide chemoprevention against 7,12-DMBA-induced oxidative stress in mouse brain. (c) 2004 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved.Öğe Effects of chronic ethanol consumption on ?-adrenergic-induced contractions and endothelium-dependent relaxations in rat thoracic aorta(Academic Press Ltd, 2000) Sahna, E; Kurcer, Z; Ozturk, F; Cengiz, N; Vardi, N; Birincioglu, M; Olmez, EThe effects of chronic oral administration of ethanol (7.2% daily during 24 weeks) on the contractions induced by phenylephrine (Phe) and the endothelium-dependent relaxation responses to acetylcholine (ACh) were studied in rat thoracic aorta. Ethanol pretreatment significantly attenuated the contractile responses to Phe, resulting in parallel shift of the concentration-response curve to the right. EC50 values of Phe were 64.6 +/- 11.2 and 95.5 +/- 8.5 nmol l(-1) in control and ethanol-fed rats, respectively. On the other hand, either calcium-induced contractions or relaxation responses to ACh and sodium nitroprusside were similar in the vessels of the control and ethanol-treated rats. These results suggest that chronic ethanol ingestion significantly attenuates the alpha(1)-adrenergic-induced contractions but does not affect the relaxation responses mediated by nitric oxide in rat aortic rings. (C) 2000 Academic Press.Öğe Gentamicin-induced nephrotoxicity and protective effect of caffeic acid phenethyl ester in rats(Wiley, 2005) Vardi, N; Parlakpinar, H; Ozturk, F; Acet, AThe objective of this study was to investigate the beneficial effects of caffeic acid phenethyl ester (CAPE) on gentamicin (GM)-induced nephrotoxicity in Wistar rats. Twenty-one adult Wistar rats were divided into three groups as follows: control group, GM and GM + CAPE group. Control group rats were injected with 5% ethanol, GM group rats were treated with 100 mg/kg GM and GM + CAPE group were pretreated with 10 mu mol/kg CAPE for 2 days, then exposed to GM at the same dose. Drug injections were applied for 12 days. Twenty-four hours after the last injection, rats were killed and kidneys were quicky removed. Tissue malondialdehyde (MDA) measurements and microscopic examination of kidneys were performed. In the GM group, significant increases in MDA levels were observed (P < 0.05). These changes were found to be normalized in the GM + CAPE group. Exposure to GM caused necrosis of tubular epithelial cells. Necrosis of tubules were found to be prevented by CAPE pretreatment. In conclusion, CAPE exerted an improvement on GM-induced nephrotoxicity, possibly, at least in part through inhibition of the production of oxygen free radicals that cause lipid peroxidation.Öğe Melatonin protects against myocardial doxorubicin toxicity in rats: role of physiological concentrations(Wiley, 2003) Sahna, E; Parlakpinar, H; Ozer, MK; Ozturk, F; Ozugurlu, F; Acet, ADoxorubicin (Dox) is a widely used antineoplastic drug. Oxygen radical-induced injury of membrane lipids is considered to be the most important factor responsible for the development of Dox-induced cardiotoxicity. The pineal secretory product, melatonin, is known to be a potent free radical scavenger and its pharmacological concentrations have been shown to reduce Dox-induced cardiac damage. However, the physiological role of melatonin in the prevention of this damage is unknown. We investigated physiological and pharmacological effects of melatonin on Dox-induced changes in the levels of malondialdehyde (MDA), a lipid peroxidation product, and morphological changes in heart. Rats were pinealectomized (Px) or sham-operated ( control) 2 months before the studies. Melatonin was administered [ 4 mg/kg, intraperitoneally (i.p.)] 1 hr before or 24 hr after the administration of a single dose of Dox ( 20 mg/kg, i.p.) and continued for 2 days. The levels of MDA Dox was found to be significantly higher in the Px rats (55.9 +/- 0.6 nmol/g tissue) than intact control animals (42.6 +/- 0.4). Dox administration to Px and non-Px rats significantly increased the MDA levels. Pre- and post-treatment with melatonin in both Px and intact rats significantly reduced MDA levels. Morphological changes parallelled the MDA alterations. These findings strongly suggest that both physiological and pharmacological concentrations of melatonin are important in protecting the heart from Dox-induced damage in rats. It would seem valuable to test melatonin in clinical trials for prevention of possible heart damage associated with Dox.Öğe The protective effects of physiological and pharmacological concentrations of melatonin on renal ischemia-reperfusion injury in rats(Springer, 2003) Sahna, E; Parlakpinar, H; Ozturk, F; Cigremis, Y; Acet, AReactive oxygen species have been implicated in the pathophysiology of renal ischemia reperfusion (I/R) injury. The pineal secretory product melatonin is known to be a potent free radical scavenger and antioxidant. This study was designed to investigate the effects of physiological and pharmacological concentrations of melatonin on I/R injury. Rats were pinealectomized (Px) or sham-operated (control) 2 months before the I/R studies. There were eight groups of eight rats each. After a right nephrectomy to produce damage, left renal vessels were occluded for 60 min, followed by 24 h reperfusion, in rats. Malondialdehyde (MDA) levels resulting from I/R were significantly higher in the pinealectomized rats than in the control group. Melatonin administration (4 mg kg(-1) i.p. either before ischemia or reperfusion) to Px and sham-operated rats significantly reduced the MDA values and returned them to the control values. Morphological changes in the groups were similar to the MDA levels. Serum levels of blood urea nitrogen and creatine were unchanged. These results suggest that physiological and pharmacological melatonin concentrations are important for the reduction of I/R-induced damage. We also demonstrated that melatonin, even when administrated just before reperfusion, had a protective effect on I/R injury. It would seem valuable to test melatonin in clinical trials for the prevention of possible I/R injury.
