Gurel A. | Armutcu F. | Sahin S. | Sogut S. | Ozyurt H. | Gulec M. | Kutlu N.O.

Article | 2004 | Clinica Chimica Acta339 ( 01.Feb ) , pp.33 - 41

Background: The aim of this study was to determine the acute effects of antioxidant caffeic acid phenethyl ester (CAPE) and ?-tocopherol (vitamin E) on nitric oxide (NO) production, neutrophil infiltration, and antioxidant enzyme activities on an in vivo model of renal ischemia-reperfusion injury. Methods: Rats were divided into five equal groups each consisting six rats: sham operation, ischemia, ischemia-reperfusion (I/R), I/R plus CAPE, and I/R plus vitamin E groups. CAPE or vitamin E was administered intraperitoneally before reperfusion. After experimental procedure, rats were sacrificed and both ipsilateral and contralateral ki . . .dneys were removed and prepared for NO concentrations, myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Acute administration of vitamin E decreased NO concentrations in both ipsilateral and contralateral renal tissues compared to I/R group. SOD activity was increased in I/R and I/R+CAPE groups compared to sham operation group. The most prominent results were encountered in MPO activities, which did not change in contralateral kidneys in both ischemia and I/R groups. There was a significant decrease in ipsilateral MPO activity in ischemia group and a significant increase in I/R group compared to sham operation group. Pretreatment with intraperitoneal CAPE significantly diminished the tissue MPO activity indicating the prevention of the neutrophil sequestration into the kidney. Conclusion: There is a role for CAPE in attenuation in renal damage after I/R injury of the kidney, in part at least by inhibition of neutrophil sequestration. © 2003 Elsevier B.V. All rights reserved Daha fazlası Daha az

Yildirim Z. | Turkoz Y. | Kotuk M. | Armutcu F. | Gurel A. | Iraz M. | Ozen S.

Article | 2004 | Nitric Oxide - Biology and Chemistry11 ( 2 ) , pp.156 - 165

Reactive oxygen and nitrogen species have been implicated in the pathogenesis of bleomycin-induced lung fibrosis. The effects of aminoguanidine and erdosteine on the bleomycin-induced lung fibrosis were evaluated in rats. The animals were placed into five groups: Vehicle + vehicle, vehicle + bleomycin (2.5 U/kg), bleomycin + aminoguanidine (200 mg/kg), bleomycin + erdosteine (10 mg/kg), and bleomycin + erdosteine + aminoguanidine. Bleomycin administration resulted in prominent lung fibrosis as measured by lung hydroxyproline content and lung histology, which is completely prevented by erdosteine and aminoguanidine. A strong staining . . . for nitro tyrosine antibody in lung tissue and increased levels of lung NO were found in bleomycin group, that were significantly reduced by aminoguanidine and erdosteine. Aminoguanidine and erdosteine significantly prevented depletion of superoxide dismutase and glutathione peroxidase and elevated myeloperoxidase activities, malondialdehyde level in lung tissue produced by bleomycin. Data presented here indicate that aminoguanidine and erdosteine prevented bleomycin-induced lung fibrosis and that nitric oxide mediated tyrosine nitration of proteins plays a significant role in the pathogenesis of bleomycin-induced lung fibrosis. Also our data suggest that antifibrotic affect of antioxidants may be due to their inhibitory effect on nitric oxide generation in this model. © 2004 Elsevier Inc. All rights reserved Daha fazlası Daha az

Topal T. | Oztas Y. | Korkmaz A. | Sadir S. | Oter S. | Coskun O. | Bilgic H.

Article | 2005 | Journal of Pineal Research38 ( 4 ) , pp.272 - 277

Cyclophosphamide (CP), an alkylating antineoplastic agent, has potential urotoxicity including causing hemorrhagic cystitis (HC). HC is now accepted as a non-infectious inflammation and the pathogenesis of HC includes cytokine production which leads to inducible nitric oxide synthase (iNOS) induction. Moreover, overproduction of reactive oxygen species (ROS) during inflammation leads to extensive oxidative stress, cellular injury and apoptosis/necrosis via several mechanisms. Based on these facts, the aim of this study was to evaluate the protective effects of melatonin as an antioxidant, iNOS inhibitor and peroxynitrite scavenger a . . .gainst CP-induced urinary bladder damage. A total of 30 male Sprague-Dawley rats were divided into four groups. Three groups received a single dose of CP (100 mg/kg) intraperitoneally with the same times. Group 2 received CP only, group 3 received 5 mg/kg/day and group 4 received 10 mg/kg/day melatonin before and the day after CP administration. Group 1 served as the control. Increased iNOS induction, bladder malonyldialdehyde (MDA) levels and urinary nitrite-nitrate excretion were encountered in the CP-only group leading to severe cystitis. Melatonin exhibited significant protection against CP-induced cystitis by diminishing bladder oxidative stress and blocking iNOS and peroxynitrite production. Oxidants may have a major role in the pathogenesis of CP-induced cystitis and iNOS is an important mediator leading to peroxynitrite production. Melatonin ameliorates bladder damage induced by CP. Copyright © Blackwell Munksgaard, 2005 Daha fazlası Daha az

Akyol O. | Zoroglu S. | Armutcu F. | Sahin S. | Gurel A.

Review | 2004 | In Vivo18 ( 3 ) , pp.377 - 390

The dominant research subject on schizophrenia, mood disorders, autism and other central nervous system diseases has been related to neurotransmitter system abnormalities. For example, the dopamine hypothesis states that schizophrenia is the result of dopaminergic hyperactivity. The therapeutic approach has also been directed towards finding agents which will modulate or regulate these neurotransmitter systems at any step. There is substantial and mounting evidence that subtle abnormalities of reactive oxygen species (ROS) and nitric oxide (NO) may underlie a wide range of neuropsychiatric disorders. NO has chemical properties that . . .make it uniquely suitable as an intracellular and intercellular messenger. It is produced by the activity of nitric oxide synthases which are present in peripheral tissues and in neurons. On the other hand, NO is known to be an oxygen radical in the central and peripheral nervous systems. NO has been implicated in a number of physiological functions such as noradrenaline and dopamine releases, memory and learning and certain pathologies such as schizophrenia, bipolar disorder and major depression. Evidence has been considered here for the proposal that an abnormality of NO metabolism may be a contributory factor in some neuropsychiatric disorders. The direct evidence for NO abnormalities in schizophrenia and other psychiatric disorders remains relatively limited to date, although there are some clinical and experimental studies. The suggestion that NO and other ROS may play a role in some neuropsychiatric disorders clearly has important implications for new treatment possibilities. The primary objective of the present review was to summarize and critically evaluate the current knowledge regarding a potential contribution of NO to the neuropathophysiology of schizophrenia as well as other neuropsychiatric disorders Daha fazlası Daha az

Ankarali S. | Ankarali H.C. | Marangoz C.

Article | 2009 | Physiological Research58 ( 4 ) , pp.591 - 598

It has been shown that nitric oxide (NO) increases aggression in male mice, whereas it decreases aggression in lactating female mice and prairie voles. It is also known that aggression can be exhibited at different levels in rodent species, strain or subtypes. The aims of this study were to investigate the proportion of aggressiveness in Wistar rats, the effect of intraperitoneally administered nonspecific nitric oxide synthase (NOS) inhibitor L-NAME (NG-nitro L-arginine methyl ester) on maternal aggression towards female intruders, and whether these effects are due to NO production or not. Rats were given saline intraperitoneally o . . .n the postpartum Day 2 and aggression levels were recorded. The same rats were given 60 mg/kg L-NAME or D-NAME (NG-nitro D-arginine methyl ester) on the postpartum Day 3 and their effects on aggression levels were compared to saline. While L-NAME administration did not cause any differences in the total number of aggressive behavior, aggression duration and aggression intensity, it reduced the proportion of animals showing aggressive behavior. In addition, the latency of the first aggression was significantly increased by L-NAME. In the D-NAME group, however, no significant change was found. Our results have shown that L-NAME reduces maternal aggression towards female intruders in Wistar rats through inhibition of NO production. These results suggest that the role of NO in offensive and defensive maternal aggression shares neural mechanisms. © 2009 Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic Daha fazlası Daha az

Sarsilmaz M. | Songur A. | Özyurt H. | Kuş I. | Özen O.A. | Özyurt B. | Sögüt S.

Conference Object | 2003 | Prostaglandins Leukotrienes and Essential Fatty Acids69 ( 4 ) , pp.253 - 259

Omega-3 (?-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 ?-3 EFA against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in antioxidant enzyme and oxidant parameters in the corpus striatum (C . . .S) of rats fed with ?-3 EFA diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with ?-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 ?-3 EFA had significantly lower values of TBARS ( Daha fazlası Daha az

Öztürk H. | Yagmur Y. | Buyukbayram H. | Dokucu A.I. | Gurel A.

Article | 2002 | European Surgical Research34 ( 4 ) , pp.285 - 290

This study aimed to evaluate the effects of the nitric oxide donor molsidomine on the early stages of liver damage and biochemical changes in rats with bile duct ligation (BDL). Forty prepubertal male Sprague-Dawley rats weighing 125-140 g were studied. Group 1 rats (sham-control, n = 10) were not subjected to any surgical manipulation. Group 2 rats (BDL/untreated, n = 10) were subjected to BDL but no drug was administered. Group 3 rats (BDL/L-NAME, n = 10) received a daily dose of NG-nitro-L-arginine methyl ester (L-NAME) intraperitoneally for 7 days after BDL. Group 4 rats (BDL/molsidomine, n = 10) received a daily dose of molsido . . .mine by gastric tube for 7 days after BDL. After 1 week, biochemical and histological evaluations were performed and the liver hydroxyproline content was measured. Serum bilirubin and liver enzymes were significantly increased in the BDL/untreated, BDL/L-NAME and BDL/molsidomine groups in comparison with the sham-control group 1 week after BDL. However, the liver enzymes were significantly decreased in the BDL/molsidomine group in comparison with the BDL/untreated and BDL/L-NAME groups. In the BDL/L-NAME group, proliferation of portal and periportal biliary ductules with disorganization of the hepatocyte plates, dilated portal spaces and areas of polymorphonuclear leukocyte infiltration, fibrosis and hepatocyte necrosis were observed. In the BDL/molsidomine group, polymorphonuclear leukocyte infiltration, hepatocyte necrosis and fibrosis were rarely seen. The hydroxyproline content in the liver was increased 1 week after obstruction in the BDL/untreated and BDL/L-NAME groups when compared to BDL/molsidomine group. Collagen type-IV expression was not observed in the BDL/molsidomine group in contrast to the BDL/untreated and BDL/L-NAME groups. In conclusion, during 1 week of treatment, the nitric oxide donor molsidomine improved hepatic fibrosis in the hepatic parenchyma and did not affect serum bilirubin values, but positively affected the serum aspartate aminotransferase and alanine aminotransferase values. Copyright © 2002 S. Karger AG, Basel Daha fazlası Daha az

Gürel A. | Armutcu F. | Sögüt S. | Cihan A.

Article | 2003 | Ondokuz Mayis Universitesi Tip Dergisi20 ( 4 ) , pp.186 - 192

One of the most important reasons of liver destruction in obstructive jaundice is reactive oxygen derived compounds which are formed as a result of demolished liver circulation. In this experimental study, we investigated the effects of L-arginine and L-NAME on liver antioxidant system and lipid peroxidation in rats after ductus choledochus ligation (BDL). For this purpose, fifteen rats were divided randomly into three equal groups. BDL group (n=5): bile duct ligation was performed in rats. L-Arginine group (n=5): Anaesthetized rats were given L-arginine (1 mg/kg) for 7 days after BDL. L-NAME group (n=5): Anaesthetized rats were giv . . .en L-NAME (2 mg/kg) for 7 days after BDL. Liver tissue was removed in all rats under anesthesia seven days after surgical procedure. Tissue was homogenized and malondialdehyde (MDA) and nitric oxide levels, xanthine oxidase, superoxide dismutase (SOD) and catalase (CAT) levels were studied in the homogenate. Liver tissue MDA level of L-arginine group was significantly lower than control and L-NAME groups. Activity of SOD in L-arginine group was significantly lower than L-NAME and BDL groups. Activitiy of CAT and level of NO in L-arginine group were significantly lower than those of L-NAME group. Liver tissue MDA level of L-NAME group was significantly higher than BDL group. These findings show that L-arginine treatment is effective in prevention of oxidative liver destruction as a result of bile duct obstruction Daha fazlası Daha az

Demir E.O. | Demirtaş C.Y. | Paşaoğlu Ö.T.

Article | 2016 | Turkish Journal of Biochemistry41 ( 3 ) , pp.216 - 222

Objective: In our study, the short-term effects of caffeine on the renal antioxidant activity in rats were investigated. Methods: Caffeine was given orally at two different doses: 30 mg/kg and 100 mg/kg (a high non-toxic dose). The current study included 30 rats, which were divided into 3 groups: a control group and two caffeine-treated groups. Group 1 was given caffeine at 30 mg/kg and Group 2 was given caffeine at 100 mg/kg for 14 days. We measured advanced oxidation protein products (AOPP), malondialdehyde (MDA) and nitric oxide (NO) levels in the kidney tissue following caffeine administration. In addition, we also evaluated sup . . .eroxide dismutase (SOD), and glutathione S transferase (GST) activities in the kidney tissue. Results: Our results showed that caffeine administration decreased lipid peroxidation and advanced oxidation protein products in kidney. Especially, MDA levels in the kidney tissue of the caffeine-treated groups decreased significantly as a result of the dose. NO levels in the kidney tissue of the caffeine-treated groups were higher than those in the control group. GST activities in the kidney tissue of rats in the caffeine groups also increased significantly. In our study, we did not observe significant changes in renal SOD activities upon caffeine consuption. Conclusion: These results show that short-term consumption of two different doses of caffeine may protect against oxidative stress in the kidney tissue of rats. This effect is related to the caffeine dosage. Determining the mechanisms and antioxidant effects of caffeine at suitable dose requires advanced animal and human studies. © 2016, Turkish Biochemistry Society. All rights reserved Daha fazlası Daha az

Gurel A. | Altinyazar H.C. | Unalacak M. | Armutcu F. | Koca R.

Article | 2007 | Oral Diseases13 ( 6 ) , pp.570 - 574

Objectives: Recurrent aphthous ulceration (RAU) is one of the most common oral mucosal disorders found in humans. Although the exact etiology of RAU is unkown, local and systemic conditions, and genetic, immunologic, and infectious factors all have been identified as potential etiopathogenic agents. The aim of our study was to compare serum xanthine oxidase (XO) and adenosine deaminase (AD) activities, and malondialdehyde (MDA), nitric oxide (NO) and uric acid (UA) levels in a group of patients affected by RAU and in a group of healthy controls. Subjects and methods: A total of 26 patients with minor RAU were included in the study. . . .Twenty-six healthy volunteers were selected to form the control group. AD and XO activities, and UA, NO, and MDA levels were studied in the serum samples of all patients and controls. Results: Serum XO and AD activities, and MDA, NO, and UA levels were significantly higher in RAU patients than in controls. Conclusion: Increased XO and AD activities, NO and UA levels and lipid peroxidation were thought to take part in the pathogenesis of RAU. Hence the effects of XO inhibitors in the treatment of RAU should be evaluated in future studies. © 2007 The Authors Daha fazlası Daha az

Hekimoglu A. | Bilgin H.M. | Kurcer Z. | Ocak A.R.

Article | 2010 | Archives of Gynecology and Obstetrics281 ( 1 ) , pp.23 - 28

Purpose: The relationship between increasing ratio of progesterone in estrogen/progesterone combination and oxidative stress (OS) was investigated. Methods: Thirty non-pregnant Wistar Albino female rats were divided into five groups and bilaterally ovariectomized (Ovx) except sham group. Groups: Sham + 0.3 cc seaseme oil, Ovx + 0.3 cc seaseme oil, Ovx + estradiol propionate (E2) (1 µg/kg), Ovx + E2 + medroxyprogesterone acetate (MPA) 1 mg/kg, Ovx + E2 + MPA 20 mg/kg. Hormones were applied for three consecutive days after 28 days of ovariectomy. Their uteri and blood samples were collected and nitric oxide (NO), malondialdehyde (MDA) . . ., total oxidative status (TOS) and total antioxidant capacity (TAC) levels were determined. Results: E2 + MPA1 treatment decreased NO, MDA and TOS levels and increased TAC levels in uterus. Plasma NO levels elevated in all groups and MDA production increased due to E2 treatment when compared to ovariectomy. E2 + MPA20 treatment increased TOS levels, while TAC levels decreased when compared to ovariectomy in plasma. Conclusions: Using E2 plus low dose progesterone may prevent pathologies resourced of OS. © 2009 Springer-Verlag Daha fazlası Daha az

Korkmaz A. | Oter S. | Sadir S. | Coskun O. | Topal T. | Ozler M. | Bilgic H.

Article | 2005 | Journal of Urology173 ( 5 ) , pp.1793 - 1796

Purpose: It was previously shown that nitric oxide (NO) produced by inducible NO synthase (iNOS) is responsible for cyclophosphamide (CP) induced cystitis. In this study we evaluated whether peroxynitrite is also responsible for CP induced bladder damage in rats. Materials and Methods: A total of 38 male albino Wistar rats were divided into 4 groups. Group 1 served as controls and was given 2 ml saline, while 3 groups received a single dose of CP (200 mg/kg) at the same intervals. Group 2 received CP only, group 3 received the selective iNOS inhibitor aminoguanidine (AG) (100 mg/kg) and group 4 received the peroxynitrite scavenger e . . .bselen (2-phenyl-1,2-benzisoselenazol-3[2H]-one) (20 mg/kg). Results: CP injection resulted in severe cystitis with continuous macroscopic hemorrhage, strong edema, inflammation and ulceration. Moreover, bladder tissue malondialdehyde levels, iNOS activation and urine nitrite-nitrate levels were dramatically increased. AG histologically protected bladder against CP damage and decreased urine nitrite-nitrate levels, bladder malondialdehyde and iNOS induction. Ebselen showed results similar to those of AG without changing the urinary nitrite-nitrate level and iNOS activity. Conclusions: These results suggest that not only nitric oxide, but also peroxynitrite may be important in the pathogenesis of CP induced cystitis. Copyright © 2005 by American Urological Association Daha fazlası Daha az