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Potential role of dietary omega-3 essential fatty acids on some oxidant/antioxidant parameters in rats' corpus striatum

Sarsilmaz, M | Songur, A | Ozyurt, H | Kus, I | Ozen, OA | Ozyurt, B | Sogut, S


Omega-3 (omega-3) is an essential fatty acid (EFA) found in large amounts in fish oil. It contains eicosapentaenoic acid and docosahexaenoic acid (DHA). DHA is one of the building structures of membrane phospholipids of brain and necessary for continuity of neuronal functions. Evidences support the hypothesis that schizophrenia may be the result of increased reactive oxygen species mediated neuronal injury. Recent reports also suggest the protective effect of omega-3 EFA against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in antioxidant enzyme and oxidant parameters in the corpus str . . .iatum (CS) of rats fed with omega-3 EFA diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with omega-3 were decapitated under ether anesthesia, and CS was removed immediately. Thiobarbituric acid-reactive substances (TBARS) and nitric oxide (NO) levels as well as total superoxide dismutase (t-SOD) and xanthine oxidase (XO) enzyme activities in the CS were measured. Rats treated with omega-3 EFA had significantly lower values of TBARS (P < 0.001), NO (P < 0.002) and XO (P < 0.005) whereas higher values of t-SOD enzyme activity (P < 0.002) than the control rats. These results indicate that omega-3 EFA rich fish oil diet reduces some oxidant parameters in CS. This may be revealed by means of reduced CS TBARS levels as an end product of lipid peroxidation of membranes in treated rats. Additionally, reduced XO activity and NO levels may support this notion. On the other hand, although the mechanism is not clear, omega-3 EFA may indirectly enhance the activity of antioxidant enzyme t-SOD. Taken together, this preliminary animal study provides strong support for a therapeutic effect of omega-3 EFA supplemented to classical neuroleptic regimen in the treatment of schizophrenic symptoms and tardive dyskinesia. (C) 2003 Elsevier Ltd. All rights reserved Daha fazlası Daha az

Low-Density Lipoproteins Oxidized After Intestinal Ischemia/Reperfusion in Rats

Tekin I.O. | Sipahi E.Y. | Comert M. | Acikgoz S. | Yurdakan G.

Article | 2009 | Journal of Surgical Research157 ( 1 ) , pp.253 - 259

Background: Intestinal ischemia/reperfusion (I/R) is a complex phenomenon causing destruction of both local and remote tissues, as well as multiple-organ failure. We investigated the role of lipid peroxidation in damage to intestinal, liver, and lung tissues in this pathology. Materials and Methods: The superior mesenteric artery was blocked for 30 min followed by 24 h of reperfusion. Tissues were removed and the presence of oxidized LDL, the activities of the superoxide dismutase enzyme, malondialdehyde levels, and inducible nitric oxide synthase expression were each evaluated in the intestinal, liver, and lung tissues. Results: Wh . . .ile there was no staining in the control group tissues, ischemia/reperfusion resulted in positive oxidized LDL staining in all of the I/R test group tissue samples. Inducible nitric oxide synthase expression was significantly increased in the ischemia/reperfusion group tissues. Compared with those of the control group rats, the ischemia/reperfusion group tissues showed significantly higher malondialdehyde levels and lower superoxide dismutase activities. Conclusions: This study demonstrated for the first time that oxidized LDL accumulated in the terminal ileum, liver, and lung tissues after intestinal ischemia/reperfusion. This occurrence (or the presence of oxidized LDL) may be an indicator of ongoing oxidative stress and enhanced lipid peroxidation. Augmentation of inducible nitric oxide synthase expression may play a role in progression of inflammation and LDL oxidation. These data support the hypothesis that cellular oxidative stress is a critical step in reperfusion-mediated injury in both the intestine and end organs, and that antioxidant strategies may provide organ protection in patients with reperfusion injury, at least through affecting interaction with free radicals, nitric oxide, and oxidized LDL. © 2009 Elsevier Inc. All rights reserved Daha fazlası Daha az

Protection of endotoxin-incluced oxidative renal tissue damage of rats by vitamin E or/and EGb 761 treatment

Coskun, O | Armutcu, F | Kanter, M | Kuzey, GM

Article | 2005 | JOURNAL OF APPLIED TOXICOLOGY25 ( 1 ) , pp.8 - 12

The aim of the present study was to evaluate the possible protective effects of vitamin E and EGb 761 treatments, alone or in combination, against oxidative renal tissue damage in experimentally induced endotoxaemic rats. Fifty healthy male Wistar albino rats, weighing 150-250 g and averaging 12 weeks old, were allotted randomly into one of five experimental groups: A (untreated), B (endotoxaemic), C (endotoxaemic + vitamin E treated), D (endotoaxemic + EGb 761 treated) and E (endotoxaemic + vitamin E and EGb 761 treated), each containing ten animals. Group A received only an intraperitoneal (i.p.) injection of 2 ml of normal saline . . . solution and served as the control. Groups B, C, D and E were administrated a single i.p. injection of 0.5 ml of endotoxin solution. In addition, groups C, D and E received i.p. injections of 600 mg kg(-1) body mt. of vitamin E and oral extract of 50 mg kg(-1) body wt. of EGb 761, alone or in combination, immediately after the endotoxin injection. The experiment lasted for 24 h. At the end of the experiment blood and tissue samples were obtained for biochemical and histopathological investigation. Endotoxin injection produced renal damage, increased lipid peroxidation and decreased antioxidant enzyme activity. Vitamin E or/and EGb 761 treatment decreased lipid peroxidation, increased antioxidant enzyme activity and also prevented renal tissue damage in experimentally induced endotoxaemic rats. In conclusion, vitamin E and EGb 761 treatment, alone or in combination, appears to be beneficial in preventing endotoxin-induced oxidative renal tissue damage and therefore shows potential for clinical use. Copyright (C) 2005 John Wiley Sons, Ltd Daha fazlası Daha az

The effect of CAPE on lipid peroxidation and nitric oxide levels in the plasma of rats following thermal injury

Hosnuter, M | Gurel, A | Babuccu, O | Armutcu, F | Kargi, E | Isikdemir, A

Article | 2004 | BURNS30 ( 2 ) , pp.121 - 125

Both experimental and clinical studies have shown that oxygen-derived free radicals rise in the plasma after thermal injury and participate in the pathogenesis of tissue damage. Hence, various antioxidant molecules have been used in treatment of burn injury both experimentally and clinically. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, is known to have potent antioxidant property. The purpose of the present study was to investigate the effects of CAPE on oxidative stress in plasma of burned rats. Experiment was designed in three groups of rats with 20% full-thickness burn: (a) sham burn . . .(n = 7); (b) burn only (n = 22); (c) burn + treatment with CAPE (n = 22). Plasma levels of malondialdehyde (MDA), nitric oxide (NO) and the activities of xanthine oxidase (XO), and superoxide dismutase (SOD) were used as both bio-indicators of oxidant status and determinant of antioxidant effect of CAPE. They were assessed by biochemical methods at 1st, 3rd, 7th, and 14th post-burn days. In conclusion, CAPE was shown to possess antioxidant activity by saving SOD activity, preventing XO activity and decreasing the levels of MDA, and NO. Our study showed that CAPE may be beneficial in burn injury. (C) 2003 Elsevier Ltd and ISBI. All rights reserved Daha fazlası Daha az

Dose-dependent neuroprotective effects of melatonin on experimental spinal cord injury in rats

Gul, S | Celik, SE | Kalayci, M | Tasyurekli, M | Cokar, N | Bilge, T

Article | 2005 | SURGICAL NEUROLOGY64 ( 4 ) , pp.355 - 361

Background: This report examines the dose-dependent effects of melatonin on early lipid peroxidation levels, ultrastructural changes, and neurological function in experimental spinal cord injury (SCI) by comparing them with therapeutic levels of methylprednisolone in rats. Methods: SCI was performed by an aneurysm clip placed extradurally at the level of T10. Rats were randomly divided into 6 groups of 10 rats each. Group 1 (sham) received only laminectomy; group 2 (control) received SCI; group 3 (placebo) received SCI and physiological saline; group 4 received methylprednisolone (30 mg/kg); groups 5 and 6 received melatonin at dose . . .s of 50 or 100 mg/kg, respectively, after SCI. Rats were neurologically tested 24 hours after trauma. Spinal cord samples were harvested for both lipid peroxidation levels and ultrastructural histopathological evaluation. Results: Neurological scores of rats were not different in SCI groups. Lipid peroxidation levels are significantly restricted only in methylprednisolone group at 24 hours. Melatonin-treated groups showed more ultrastructural improvement on electron microscopic studies when compared with methylprednisolone group. However, the therapeutic effects of melatonin were mainly observed on white matter of spinal cord in ultrastructural investigation. There was significant difference between metatonin dose groups increasing with dose. Conclusions: Results showed that melatonin has no significant dose-dependent effects on early lipid peroxidation but rather some neuroprotective effects on both axons and myelin sheaths of white matter in ultrastructural observations when compared with methylprednisolone. These effects significantly augmented with dose increase. (c) 2005 Elsevier Inc. All rights reserved Daha fazlası Daha az

Lipid peroxidation and homocysteine levels in Behcet's disease

Mungan, A. Gorkem | Can, Murat | Acikgoz, Serefden | Esturk, Emel | Altinyazar, Cevdet

Article | 2006 | CLINICAL CHEMISTRY AND LABORATORY MEDICINE44 ( 9 ) , pp.1115 - 1118

Background: The aim of this study was to investigate serum paraoxonase (PON1) activity in relation to homocysteine, malondialdehyde (MDA) and lipid parameters in active and inactive Behcet's disease, (BD). Methods: A total of 46 consecutive BD patients and 25 healthy control subjects were included in the present study. Results: Serum PON1 activity in both active and inactive BD was significantly lower compared with healthy subjects (p < 0.05). When compared to the control group, serum MDA levels were significantly higher in both active and inactive BD (p < 0.05). Serum C-reactive protein (CRP) and homocysteine concentrations were si . . .gnificantly higher in active BD than those in inactive BD and control subjects (p < 0.05). In addition, there was significant negative correlation between serum PON1 and MDA levels (r= -0.697, p < 0.05) and serum PON1 activity was also negatively correlated with homocysteine levels (r= -0.428, p < 0.05) in BD patients. Conclusions: Decreased PON1 could explain the increased lipid peroxidation and oxidative stress observed in BD. Also, according to our results, we suggest that homocysteine may contribute to decreased serum PON1 activity Daha fazlası Daha az

Experimental Obstructive Jaundice Results in Oxidized Low-Density-Lipoprotein Accumulation in Surgical Wound of Rats

Cakamak, G. Karadeniz | Tascilar, O. | Tekin, I. O. | Ucan, B. H. | Emre, A. U. | Gun, B. D. | Acikgoz, S.

Article | 2008 | ACTA CHIRURGICA BELGICA108 ( 6 ) , pp.725 - 731

Introduction : Mounting evidence suggests that impaired wound heating is a well-defined consequence in obstructive jaundice and, as redox-regulated processes are relevant to wound healing, it is not unreasonable to suppose that oxidative stress associated with lipid peroxidation in cholestasis might be a systemic phenomenon probably comprising all tissues and organs, including wounds. The aim of the present investigation was to analyse the lipid peroxidation status of surgical wounds, in terms of oxidized low-density-lipoprotein (oxLDL) accumulation in experimental obstructive jaundice. Methods : Sixteen Wistar-Albino rats weighing . . .200-230 gr were randomly divided into two groups. Group I (n = 8) was designed as the prolonged obstructive jaundice group and was subjected to bile duct ligation. Group II (Sham-control, n = 8) rats underwent laparotomy alone and bile duct was just dissected from the surrounding tissue. Histopathological evaluation. immunohistochemical screening and immunoflourescent staining of the surgical wound was conducted to the bile-duct ligated rats and control group on the 21(st) postoperative day. Results : Wound healing was found to be impaired in jaundiced rats histopathologically. When compared with the control group. significant positive oxLDL staining and intracellular accumulation of TNF-alpha, IL-2 and IL-6 was detected ill the wound sections of the prolonged obstructive jaundice group. Conclusion : Our present data is the first in the literature, indicating significant oxLDL accumulation in surgical wounds of cholestatic rats, which might be one of the results of systemic oxidative stress leading to deficient healing capacity as a consequence of persistent inflammation Daha fazlası Daha az

omega-3 fatty acid treatment in cardiac syndrome X: a double-blind, randomized, placebo-controlled clinical study

Bozcali, Evin | Babalik, Erhan | Himmetoglu, Solen | Mihmanli, Ismail | Toprak, Sadik

Article | 2013 | CORONARY ARTERY DISEASE24 ( 4 ) , pp.328 - 333

Objective We conducted a clinical trial to examine the effect of omega-3 fatty acids in patients with cardiac syndrome X (CSX). We aimed to evaluate the potential impact of omega-3 fatty acids on endothelial function, oxidative stress, and symptom relief in the CSX. Methods and results Eighteen patients with CSX were enrolled according to a double-blind, randomized, placebo-controlled design. Patients were randomized to omega-3 fatty acids (1440 mg/day, n = 8) or placebo (n = 10) for 4 months. We assessed plasma levels of malondialdehyde (MDA), endothelium-dependent vasodilatation [flow-mediated dilatation (FMD)], endothelium-indepe . . .ndent vasodilatation [nitroglycerin-mediated dilatation (NMD)], and status of symptom [score with Seattle Angina Questionnaire (SAQ)] before and after the treatment. After 4 months, patients who were treated with omega-3 fatty acids showed significant increases in the FMD (from 47 +/- 48 to 104 +/- 23%, Daha fazlası Daha az

Oxidized low-density-lipoprotein accumulation is associated with liver fibrosis in experimental cholestasis

Karadeniz, Gueldeniz | Acikgoz, Serefden | Tekin, Ishak Ozel | Tascylar, Oge | Gun, Banu Dogan | Comert, Mustafa

Article | 2008 | CLINICS63 ( 4 ) , pp.531 - 540

OBJECTIVE: The aim of the present study was to examine the probable relationship between the accumulation of oxLDL and hepatic fibrogenesis in cholestatic rats. INTRODUCTION: There is growing evidence to support the current theories on how oxidative stress that results in lipid peroxidation is involved in the pathogenesis of cholestatic liver injury and fibrogenesis. One of the major and early lipid peroxidation products, OxLDL, is thought to play complex roles in various immuno-inflammatory mechanisms. METHODS: A prolonged (21-day) experimental bile duct ligation was performed on Wistar-albino rats. Biochemical analysis of blood, h . . .istopathologic evaluation of liver, measurement of the concentration of malondialdehyde (MDA) and superoxide-dismutase (SOD) in liver tissue homogenates, and immunofluorescent staining for oxLDL in liver tissue was conducted in bile-duct ligated (n = 8) and sham-operated rats (n = 8). RESULTS: Significantly higher levels of MDA and lower concentrations of SOD were detected in jaundiced rats than in the sham-operated rats. Positive oxLDL staining was also observed in liver tissue sections of jaundiced rats. Histopathological examination demonstrated that neither fibrosis nor other indications of hepatocellular injury were found in the sham-operated group, while features of severe hepatocellular injury, particularly fibrosis, were found in jaundiced rats. CONCLUSION: Our results support the finding that either oxLDLs are produced as an intermediate agent during exacerbated oxidative stress or they otherwise contribute to the various pathomechanisms underlying the process of liver fibrosis. Whatever the mechanism, it is clear that an association exists between elevated oxLDL levels and hepatocellular injury, particularly with fibrosis. Further studies are needed to evaluate the potential effects of oxLDLs on the progression of secondary biliary cirrhosis Daha fazlası Daha az

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