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Öğe Amikacin-induced acute renal injury in rats: protective role of melatonin(Wiley, 2003) Parlakpinar, H; Ozer, MK; Sahna, E; Vardi, N; Cigremis, Y; Acet, AIt is well established that some agents such as aminoglycosides generate free oxygen radicals, leading to an increased oxireductase production, which in turn increases tissue toxicity. The aim of this study is to test whether melatonin, the chief secretory product of the pineal gland and a highly effective antioxidant and free radical scavenger, reduces the nephrotoxicity caused by amikacin (AK). Herein, we investigated the physiologic and pharmacological role of melatonin in influencing AK-induced nephrotoxicity. For this, pinealectomized (Px) and sham operated (non-Px) rats were used. Both AK and melatonin were administered to all groups. We investigated the effects of melatonin on AK-induced changes in levels of malondialdehyde (MDA), a lipid peroxidation product, glutathione (GSH), an antioxidant whose levels are influenced by oxidative stress, and blood urea nitrogen (BUN) and serum creatine (Cr) levels. Morphologic changes in the kidney were also examined by using light microscopy. MDA levels were found to be higher in Px than in non-Px AK-treated animals. Melatonin administration to Px rats reduced MDA levels. In relative to non-Px rats, Px animals treated with AK had significantly lower GSH concentrations while melatonin administration elevated GSH levels in the kidney; however, this stimulatory effect of melatonin was not observed in non-Px AK-treated rats. Treatment with AK alone resulted in significantly higher plasma Cr and BUN levels. Repeated administration of melatonin prevented the AK-induced elevation of plasma Cr and BUN levels. Morphologic damage to renal tubules as a result of AK was more severe in the renal cortex than in the medulla. The damage to the kidney induced by AK was reversed by melatonin in the Px rats. In conclusion, these results show that physiologic melatonin concentrations are important in reducing AK-induced renal damage, while pharmacologic concentrations of melatonin did not add to the beneficial effect.Öğe The attenuation of vasospasm by using a SOD mimetic after experimental subarachnoidal haemorrhage in rats(Springer Wien, 2003) Aladag, MA; Turkoz, Y; Sahna, E; Parlakpinar, H; Gul, MBackground. Delayed cerebral vasoconstriction and brain ischemia, are critical problems in the management of a patient affected by rupture of an intracranial aneurysm. Overexpression of Cu-Zn superoxide dismutase (Cu-Zn SOD) can reduce the extent of cerebral vasospasm. We, therefore investigated if vasospasm, can be prevented by a novel, stable, and cell permeable SOD mimetic, MnTBAP [Mn(III) tetrakis (4-benzoic acid) porphyrin] which permeates the biological membranes and scavenges superoxide anions and peroxynitrite. Methods. 28 rats (225-250 g) were divided equally into four groups: group 1: control; group 2: SAH only; group 3: SAH plus placebo; and group 4: SAH plus MnTBAP We used a double haemorrhage method to produce SAH. Starting six hours after SAH, 5 mg/kg MnTBAP (Calbiochem, Darmstadt-Germany; Cat. No 475870)) or an equal volume of 0.9% saline (37degreesC) was administered by intraperitoneal injection twice daily for 5 days to groups 4 and 3 respectively. MnTBAP or 0.9% saline injections were continued up to fifth day after SAH and rats were sacrificied on the fifth day. Brain sections at the level of the pons were examined by light microscopy. Planimetric measurements were made for the cross-sectional areas of the lumen and the vessel wall (intima plus media) of the basilar artery by a micrometer. Finding. Administration of MnTBAP significantly attenuated the vasoconstriction of the basilar artery in group 4 compared with the groups 2 and 3 (p<0.001). Interpretation. These results suggest that this SOD mimetic (MnTBAP) attenuates delayed cerebral vasoconstriction following experimental SAH and that superoxide anions have a role in the pathogenesis of vasospasm after SAH.Öğe The beneficial effect of melatonin on chronic cyclosporin A nephrotoxicity in rats(Cambridge Med Publ, 2003) Esrefoglu, M; Kurus, M; Sahna, ECyclosporin A (CsA)-induced nephrotoxicity may be the consequence of oxidative stress. Anti-oxidant agents could be useful in reducing CsA toxicity. In this light microscopy study, tubular dilatation, atrophy, vacuolization and tubulointerstitial fibrosis were observed in rats given CsA, whereas in rats given CsA plus melatonin, no histological changes occurred. It is concluded that melatonin could be useful for reducing the nephrotoxic effects of CsA.Öğe Caffeic acid phenethyl ester (CAPE) attenuates cerebral vasospasm after experimental subarachnoidal haemorrhage by increasing brain nitric oxide levels(Pergamon-Elsevier Science Ltd, 2006) Aladag, MA; Turkoz, Y; Ozcan, C; Sahna, E; Parlakpinar, H; Akpolat, N; Cigremis, YBackground: Cerebral vasospasm, a medical complication of aneurysmal subarachnoid hemorrhage (SAH), is associated with high morbidity and mortality rates, even after the aneurysm has been secured surgically or endovascularly. Evidence accumulated during the last decade suggest that scavenging a vasodilator, nitric oxide (NO), by superoxide anions (O-2(-)), and activating a strong vasoconstructor, protein kinase C (PKC), are the two most important mechanisms in the pathogenesis of vasospasm. Our aim in this study was to determine whether caffeic acid phenethyl ester (CAPE), a non-toxic oxygen free radical scavenger, prevents vasospasm in an experimental rat model of SAH. Methods: Twenty eight rats (225-250 g) were divided into four groups equally: group 1, control group group 2, SAH group; group 3, SAH plus placebo group; and group 4, SAH plus CAPE group. We used double haemorrhage method for SAH groups. Starting 6 h after SAH, 10 mu mol/kg CAPE or an equal volume of 0.9% saline were administered by intraperitoneal injection twice daily for 5 days to SAH plus CAPE and SAH plus placebo groups, respectively. CAPE or 0.9% saline injections were continued up to 5th day after SAH. Rats were sacrificed on the 5th day. Brain sections at the level of the pons were examined by light microscopy. Measurements were made for the cross-sectional areas of the lumen and the vessel wall (intimae plus media) of basilar artery by a micrometer. The levels of malondialdehyde (MDA), reduced glutathione (GSH), and nitric oxide (NO) were measured in rat brain tissue. Results: Administration of CAPE significantly attenuated the vasoconstriction of the basilar artery. There were marked narrowing in the lumens of and thickening in the walls of basilar arteries in the SAH, and the SAH plus placebo compared with CAPE group (p < 0.001). We also observed that CAPE administration significantly decreased the tissue level of MDA, while significantly increased the tissue levels of GSH, NO in the SAH plus CAPE group compared to only SAH group, p < 0.05. Conclusions: Our results indicate that CAPE is effective in attenuating delayed cerebral vasoconstriction following experimental SAH. Our findings also suggest that the elevation of lipid peroxidation and reduction of NO bioavailability, resulting from the generation and the interaction of free radicals, have a significant role in the pathogenesis of vasospasm after SAH. (c) 2005 ISDN. Published by Elsevier Ltd. All rights reserved.Öğe Effects of aminoguanidine against renal ischaemia-reperfusion injury in rats(Wiley, 2006) Sahna, E; Parlakpinar, H; Cihan, OF; Turkoz, Y; Acet, AAminoguanidine is an inhibitor of nitric oxide synthase (NOS), with high selectivity for the inducible isoforrn (iNOS). In addition to being all inhibitor of NOS, aminoguanidine also exhibits antioxidant activity. Recent studies suggest that aminoguanidine reduces ischaemia-reperfusion (I/R)-induced damage. However, the role of aminoguanidine, in renal injury associated with I/R remains unknown. This Study was designed to investigate the effects of aminoguanidine on renal I/R injury. There were three groups of eight rats each. I/R was induced by occlusion of the left renal vessels for 60 min, followed by 24 h reperfusion in rats. Malondialdehyde (MDA) levels, a stable metabolite of the free radical-mediated lipid peroxidation cascade, were found to be significantly higher in the I/R group (30.3 +/- 0.1 nmol g(-1) tissue) than in the control group (10 +/- 0.05 nmol g(-1)). Aminoguanidine (100 mg kg(-1)) administration to rats significantly reduced the MDA values. We also demonstrated that I/R leads to structural change but aminoguanidine did not reverse this change. Aminoguanidine, according to the biochemical finding is protective but histopathological findings did not reveal protection against I/R injury in kidney. The effects of aminoguanidine on I/R-induced damage remain a subject for future investigations. Copyright (c) 2004 John Wiley & Soils, Ltd.Öğe Effects of captopril and losartan on myocardial ischemia-reperfusion induced arrhythmias and necrosis in rats(Academic Press Ltd Elsevier Science Ltd, 2002) Ozer, MK; Sahna, E; Birincioglu, M; Acet, AAngiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type I (AT(1)) receptor blockers improve ischemia-reperfusion induced arrhythmias and infarct size in several animal models. However, the effects of pretreatment with ACEIs or AT, receptor blockers on acute myocardial infarct size and arrhythmias are controversial. Thus, we sought to assess the comparative effects of pretreatment with ACEI captopril and AT(1)-receptor blocker losartan on myocardial infarct size and arrhythmias in a rat model of ischemia-reperfusion. We randomly assigned 92 male Wistar rats for arrhythmias (n = 60) and necrosis (n = 32) experiments. To produce arrhythmia, the left main coronary artery was occluded for 7 min, followed by 7 min of reperfusion and to produce necrosis, the the left main coronary artery was occluded for 30 min, followed by 120 min of reperfusion. Captoptil (3 mg kg(-1)) and losartan (0.2 and 2 mg kg(-1)) were given intravenously 10 min before occlusion. Captopril reduced the incidences of ventricular fibrillation (VF) and mortality associated with irreversible VR whereas the studied doses of losartan did not. Captopril also decreased the number of ventricular beats on reperfusion. Losartan 2 mg kg(-1) reduced both the number of ventricular premature beats and the incidence of ventricular tachycardia (VT) on reperfusion, while losartan at dose of 0.2 mg kg(-1) had no effect on these arrhythmias. Compared to the control group, both captopril and losartan reduced myocardial infarct size in the rat model of ischemia-reperfusion, but this was statistically significant for captopril only. In this experimental model, although captopril did not reduce the incidence of reperfusion-induced VT, it was more effective than the AT(1)-receptor blocker losartan at preventing mortality associated with irreversible VF and to reduce myocardial infarct size in rat model of ischemia-reperfusion. (C) 2002 Elsevier Science 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 The effects of melatonin on focal cerebral ischemia-reperfusion model(Saudi Med J, 2004) Kavakli, A; Sahna, E; Parlakpinar, H; Yahsi, S; Ogeturk, M; Acet, A[Abstract Not Available]Öğe Effects of physiological and pharmacological concentrations of melatonin on ischemia-reperfusion arrhythmias in rats: can the incidence of sudden cardiac death be reduced?(Wiley, 2002) Sahna, E; Olmez, E; Acet, ACardiac arrhythmias during ischemia-reperfusion (I/R) are believed to be related to free radicals generated in the heart especially during the period of reperfusion. The pineal secretory product. melatonin, is known to be a potent free radical scavenger and its pharmacological concentrations have been shown to reduce the I/R-induced arrhythmias in isolated rat hearts. However, the physiological role of melatonin in the prevention of these arrhythmias is unknown. Rats were pinealectomized (Px) or sham-operated (non-Px) (control) 2 months before the I/R studies. To produce arrhythmias. left main coronary artery was occluded for 7 min, followed by 7 min reperfusion, in anesthetized rats. The incidence of mortality resulted from irreversible ventricular fibrillation (VF) was found significantly higher in the Px rats (63%) than in the control group (25%). Melatonin administration (0.4 mg,kg, either before ischemia or reperfusion) to Px rats significantly reduced the incidence of total (irreversible plus reversible) and irreversible VF and returned them to control values. On the other hand, melatonin administration (0.4 and 4 mg/kg) to non-Px rats failed to attenuate the I/R arrhythmias, significantly. These results suggest that physiological melatonin concentrations are important to reduce the I/R-induced VF and mortality. while pharmacological concentrations of melatonin did not increase its beneficial effect on these arrhythmias. As melatonin levels have been reported to decrease with age, melatonin replacement therapy may attenuate the incidence of sudden cardiac death especially in older patients,Öğe Efficacy of melatonin as protectant against oxidative stress and structural changes in liver tissue in pinealectomized rats(Urban & Fischer Verlag, 2004) Sahna, E; Parlakpinar, H; Vardi, N; Cigremis, Y; Acet, APrevious observations demonstrated that physiological levels of metatonin, the pineal secretory product, are important in protecting against oxidative stress-induced tissue damage. We investigated the effects of pinealectomy and administration of exogenous melatonin on liver tissue in rats. Pinealectomized (Px) and sham-operated (non-Px) rats were used. We evaluated structural changes, reduced glutathione (GSH) levels and matondialdehyde (MDA) levels. Rats were divided into three groups (10 rats in each group): control. (non-Px), Px+vehicle and Px+metatonin (4 mg/kg given daily intraperitoneally for 10 days). Liver GSH levels were significantly tower in Px rats than in the control group. Melatonin administration significantly increased GSH levels (p<0.05). Px caused a significant increase in MDA levels as compared with the control group and metatonin administration to Px rats significantly reduced MDA levels in the liver (p<0.05). Sinusoidal dilatation to a varying degree developed in all Px rats. Severity of mononuclear cell. infiltration and sinusoidal congestion were tower in Px+melatonin group than in the Px group. These findings suggest that a significant increase in oxidative and structural changes occur in rat livers after pinealectomy, which can be diminished by melatonin treatment. (C) 2004 Published by Elsevier GmbH.Öğe Melatonin administration prevents the nephrotoxicity induced by gentamicin(Wiley, 2000) Özbek, E; Turkoz, Y; Sahna, E; Ozugurlu, F; Mizrak, B; Ozbek, MObjective To investigate the effect of melatonin on the antioxidant enzyme activity and renal tubular necrosis induced by gentamicin. Materials and methods Twenty-four adult male Sprague-Dawley rats were divided into three equal groups. In group 1, the rats were injected with vehicle (controls), in group 2 they were injected with gentamicin for 5 days and in group 3 injected with gentamicin plus melatonin for 5 days. At 24 h after the last injection, rats were killed and the renal cortex separated from the medulla. Most of the cortex was homogenized but a small sample was fixed in formaldehyde solution for histological examination by light microscopy. Blood samples were also taken to assess the serum levels of urea, creatinine, Na+, K+ and gamma-glutamyl transpeptidase (gamma-GT); before death, urine samples were analysed for protein content. Crude extracts of the cortex were used to deter-mine lipoperoxides, reduced glutathione (GSH-Px), catalase and superoxide dismutase (SOD). The results were compared using the Mann-Whitney U-test. Results Compared with the controls rats, gentamicin caused hyperproteinuria, an increase in the level gamma-GT In serum, a marked increase in lipoperoxides and a signifcant decrease of GSH-Px, catalase and SOD activity in the kidney. In the rats in group 3 there was a marked restoration in lipid peroxidation, GSH-Px, catalase, SOD activity and proteinuria, and in gamma-GT in serum. In rats in group 2 there was widespread tubular necrosis (grade 2-4) but in rats in group 3 there was a merited reduction in the extent of tubular damage. There was no significant difference in serum levels of Na+, K+, blood urea nitrogen and creatinine. Conclusion These results indicate that melatonin prevents the tubular necrosis induced by gentamicin in rats, presumably because it is a potent antioxidant and restores antioxidant enzyme activity in the rat kidney.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 Myocardial ischemia-reperfusion in rats: reduction of infarct size by either supplemental physiological or pharmacological doses of melatonin(Wiley, 2002) Sahna, E; Acet, A; Ozer, MK; Olmez, EMyocardial ischemia reperfusion (I/R) represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. I/R injury is believed to be a consequence of free radical generation in the heart especially during the period of reperfusion. The pineal secretory product, melatonin, is known to be a potent free radical scavenger and pharmacological concentrations have been shown to reduce the I/R-induced cardiac damage in isolated rat hearts. However, the physiological role of melatonin in the prevention of this damage is unknown. Rats were pinealectomized or sham-operated (control) 2 months before the I/R studies. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 in reperfusion, in anesthetized rats. Infarct size, expressed as the percentage of the risk zone, was found significantly higher in pinealectomized rats (49 +/- 4%) than in the control group (34 +/- 6%). Melatonin administration (4 mg/kg, either before ischemia or reperfusion) to pinealectomized rats significantly reduced the infarct size values and returned the to the control values. On the other hand, melatonin administration (4 mg/kg) to sham-operated rats failed to attenuate significantly the I/R-induced infarct size. These results suggest that physiological melatonin concentrations are important in reducing the I/R-induced myocyte damage, while pharmacological concentrations of melatonin did not add to the beneficial effect. As melatonin levels have been reported to decrease with age, melatonin replacement therapy may attenuate I/R-induced myocardial injury, especially in older patients.Öğe Physiological and pharmacological concentrations of melatonin protect against cisplatin-induced acute renal injury(Blackwell Munksgaard, 2002) Parlakpinar, H; Sahna, E; Ozer, MK; Ozugurlu, F; Vardi, N; Acet, ACisplatin [cis -diaminedichloroplatinum(II), CDDP] is a widely used antineoplastic drug. However, it has major side-effects such as acute tubular necrosis (ATN). There are a number of studies concerning the role of reactive oxygen radical species in the pathophysiology of CDDP-dependent ATN. Several antioxidant agents have been reported to prevent this side-effect but there is no study regarding the protective action of either physiological or pharmacological concentrations of melatonin. Melatonin, the chief secretory product of the pineal gland, is a direct free radical scavenger and indirect antioxidant. We investigated the effects of melatonin on CDDP-induced changes of renal malondialdehyde (MDA), a lipid peroxidation product, and blood urea nitrogen (BUN) and serum creatine (Cr). The morphological changes in kidney were also examined using light microscopy. The rats were divided into two groups: pinealectomized (Px) and sham-operated (non-Px). Both CDDP and melatonin were administered to all groups. MDA levels were found to be higher in Px than non-Px animals. CDDP administration to Px or non-Px rats increased renal MDA levels and melatonin administration either before or after CDDP injection caused significant decreases in MDA in kidney compared with those in rats treated with CDDP alone. Serum levels of BUN and Cr did not change as a result of any treatment. Morphological tubule damage because of CDDP was more severe in the renal cortex than in the medulla. The damage to the kidney induced by CDDP was reversed by melatonin. The results show that pharmacological and physiological concentrations of melatonin reduce CDDP-induced renal injury.Öğe Protective effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia-reperfusion-induced apoptotic cell death(Elsevier Ireland Ltd, 2005) Parlakpinar, H; Sahna, E; Acet, A; Mizrak, B; Polat, AOcclusion of coronary artery causes cardiomyocyte dysfunction. Reperfusion relieves ischemia by providing cells with metabolites and oxygen, thereby preventing extensive tissue damage. Although reperfusion salvages the myocardium, it also initiates a series of events including myocardial apoptosis and necrosis. The common inducers of apoptosis include reactive oxygen species (ROS). Caffeic acid phenethyl ester (CAPE) is known as an antioxidative, anti-inflammatory effects, may protect myocardial ischemia-reperfusion (MI/R)-induced apoptosis. We have previously reported that CAPE reduced MI/R-induced necrosis. Therefore, this study was focused to investigate protective effect of CAPE on the distinct form of cell death; apoptosis in an in vivo rat model. To produce MI/R, a branch of the descending left coronary artery was occluded for 30 min followed by 2 h reperfusion. ECG changes, blood pressure (BP), and heart rate (HR) were measured before occlusion and continued both occlusion and reperfusion. CAPE (50 mu mol/kg) was given 10 min before ischemia via juguler vein. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the terminal deoxynucleotidyl transferase (TdT)-mediated d UTP-biotin nick and labeling (TUNEL) method. Also, cysteine aspartate specific proteinase (caspase)-3 and caspase-9 activities a universal effector of apoptosis, were determined. Trunk blood was extracted to determine the serum contents related to oxidant-antioxidant status. In hemodynamic parameters, there was no significant difference in HR or BP values among any group. CAPE administration had no a significant effect on hemodynamic parameters during ischemia or reperfusion. Control group revealed extensive TUNEL-positive cardiomyocytes especially in free wall of left ventricule, interventiculare septum and nearly apex zone. Intensity of TUNEL-positive cardiomyocytes reduced as a result of CAPE treatment compared to control group in the same sections. Result of the caspase activities was found to correlate with TUNEL evaluation. CAPE also, ameliorated antioxidant status. We propose that CAPE acts in the heart as a potent scavenger of free radicals to prevent the apoptotic effect of I/R. Further studies are needed to elucidate the mechanisms of apoptotic death machinery. (C) 2004 Elsevier Ireland Ltd. All rights reserved.Öğe Protective effects of melatonin on myocardial ischemia-reperfusion induced infarct size and oxidative changes(Acad Sciences Czech Republic, Inst Physiology, 2005) Sahna, E; Parlakpinar, H; Turkoz, Y; Acet, AFree radicals, calcium overloading and loss of membrane phospholipids play an important role in the development of ischemia/reperfusion (I/R) injury. Melatonin is a well-known antioxidant and free radical scavenger. Melatonin may also reduce the intracellular calcium overloading and inhibit lipid peroxidation. This study was designed to investigate the effects of melatonin on the I/R-induced cardiac infarct size in an in vivo rat model. We also investigated glutathione (GSH) levels, an antioxidant the levels of which are influenced by oxidative stress, and malondialdehyde (MDA) levels, which is an index of lipid peroxidation. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Melatonin (10 mg/kg) or vehicle was given 10 min before ischemia via the jugular vein. Infarct size, expressed as the percentage of the risk zone, was found significantly greater in I/R group than in the melatonin-treated I/R group. MDA levels were significantly higher, but GSH levels were lower in the I/R group than in the control group. Melatonin significantly reduced the MDA values and increased the GSH levels. These results suggest that oxidative stress contributes to myocardial I/R injury and melatonin administration exerts a mitigating effect on infarct size. Furthermore, the results indicated that melatonin improves the antioxidant capacity of the heart and attenuates the degree of lipid peroxidation after I/R.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.
