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Publications (21)47.6 Total impact

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    ABSTRACT: Erythropoietin exerts hematopoietic effects by stimulating proliferation of early erythroid precursors. Nonhematopoietic effects of erythropoietin have also been shown. It may act as a new angiogenic factor in wound healing. This study aimed to investigate the effect of systemic administration of recombinant human erythropoietin on wound healing in mice. Dorsal incisional wounds were performed in mice, which were then divided into two groups; a group treated for 7 days with recombinant human erythropoietin, and a control group. Sacrificing animals on day 7, the wound tissues were collected for analysis of wound breaking strength, malondialdehyde, a marker of lipid peroxidation, hydroxyproline, an index of reparative collagen deposition, reduced glutathione levels, and for histological evaluation. The immunohistochemical determination of vascular endothelial growth factor (VEGF) which is believed to be the most prevalent angiogenic factor throughout the skin repair process, was also studied. The treatment significantly increased wound breaking strength by decreasing malondialdehyde and increasing hydroxyproline levels on day 7 after wounding. No statistically meaningful change was observed in reduced glutathione content. VEGF was immunostained significantly more on wound tissue of treated animals compared to the control group. Recombinant human erythropoietin treatment may be effective in wound healing due to inhibition of lipid peroxidation, deposition of collagen, and VEGF expression in wound area.
    Journal of Investigative Surgery 07/2009; 19(3):163-73. · 1.32 Impact Factor
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    ABSTRACT: Considering the implications that arose from several recent experimental studies using recombinant human erythropoietin in rodents, erythropoietin has been regarded as a pharmacological preconditioning agent. The purpose of the present study was to evaluate whether erythropoietin has a preconditioning effect against ischemia and reperfusion injury in the small intestine of the rat. Intestinal ischemia was induced in male Wistar rats by clamping the superior mesenteric artery for 30 min, followed by reperfusion for 180 min. Recombinant human erythropoietin (1000 or 3000 U/kg) or vehicle was administered intraperitoneally 24 h prior to ischemia. After collection of ileal tissue, evaluation of damage was based on measurements of the accumulation of polymorphonuclear neutrophils by technetium-99m-labeled leukocyte uptake, content of malondialdehyde, reduced glutathione, contractile responses to agonists, and an evaluation of histopathological features in intestinal tissue. Treatment with erythropoietin 24 h before ischemia significantly reduced the tissue content of malondialdehyde and increased that of reduced glutathione. Pretreatment also significantly suppressed leukocyte infiltration into the postischemic tissue, as evidenced by the lower content of myeloperoxidase and technetium-99m-labeled leukocytes. Physiological and histopathological improvements were also significant with the rHuEpo treatment. Results of the present study indicate that rHuEpo is an effective preconditioning agent in ischemic injury of the small intestine. Protection provided by recombinant human erythropoietin is closely related to the inhibition of oxidative stress and leukocyte infiltration, which might be among the possible protective mechanisms of erythropoietin in intestinal ischemia and reperfusion.
    Life sciences 02/2009; 84(11-12):364-71. · 2.56 Impact Factor
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    V H Ozacmak, H Sayan
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    ABSTRACT: Neuroprotective effects of estrogens and progesterone have been widely studied in various experimental models. The present study was designed to compare possible neuroprotective effects of 17alpha-estradiol, 17beta-estradiol, and progesterone on oxidative stress in rats subjected to global cerebral ischemia. Global cerebral ischemia was induced in ovariectomized female rats by four vessel occlusion for 10 min. Following 72 h of reperfusion, levels of malondialdehyde (MDA, oxidative stress marker), and reduced glutathione (GSH, major endogenous antioxidant) were assessed in hippocampus, striatum and cortex of rats treated with either 17alpha-estradiol, 17beta-estradiol, progesterone or estradiol + progesterone beforehand. Steroid administration ameliorated ischemia-induced decrease in GSH and increase in MDA levels. Our data offers additional evidence that estrogens and progesterone or combination of two exert a remarkable neuroprotective effect reducing oxidative stress.
    Physiological research / Academia Scientiarum Bohemoslovaca 01/2009; 58(6):909-12. · 1.53 Impact Factor
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    ABSTRACT: Studies have shown that nitric oxide (NO) may play a major role in sustaining mucosal integrity; however, NO has been also implicated in the pathogenesis of ischemia/reperfusion (I/R)-related tissue injury. We investigated the effects of L-arginine and NG-nitro L-arginine methyl ester (L-NAME) on the acetylcholine-induced contractile response of ileum and the levels of malondialdehyde (MDA) and reduced glutathione (GSH). Histopathological changes were also evaluated in ileal preparations. Male Wistar Albino rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (3 hours). Four groups were designed: sham-operated control; I/R; I/R and L-arginine pretreatment; and I/R and L-NAME pretreatment. After reperfusion, ileum specimens were collected to determine the parameters mentioned above. Following reperfusion, a significant decrease in acetylcholine-induced contractile response, an increase in lipid peroxidation, a decrease in GSH content, and mucosal damage of the ileal preparations were observed. We showed that decreased contractility, increased lipid peroxidation, and reduced GSH content have been reversed by L-arginine but not by L-NAME. Mucosal injury was significantly lowered in the L-arginine group. Treatment with L-arginine exerted a protective effect in intestinal I/R injury, which was mediated in part by regulating MDA and GSH levels, consequently ameliorating impaired contractile response and mucosal injury.
    Journal of pediatric gastroenterology and nutrition 02/2008; 46(1):29-35. · 2.18 Impact Factor
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    ABSTRACT: One of common pathophysiological states associated with central nervous system is chronic cerebral hypoperfusion (CH) that frequently occurs in conditions such as vascular dementia and Alzheimer's disease. Long term blockage of angiotensin II type 1 (AT(1)) receptor provides protection from ischemia induced injury of brain as well as reduction of cerebrovascular inflammation. Examining effect of the blockage on reduced glutathione (GSH), ascorbic acid (AA), and lipid peroxidation were of purpose in the present study. Modeling CH, rats were subjected to permanent occlusion of common carotid arteries bilaterally. AT(1 )receptor antagonist, candesartan, was given daily for 14 days after surgery. CH caused a significant increase in lipid peroxidation and decrease in GSH content of cerebral hippocampal tissue with no change in AA level. Candesartan (0.5 mg/kg, oral) not only reduced lipid peroxidation but also restored GSH significantly besides elevating AA and improving histopathological alterations. In conclusion, long term AT(1 )receptor blockage may be considered as novel therapeutic approach for protection from damage associated with CH. Underlying mechanism(s) may in part be related to suppressing oxidative stress and preserving brain antioxidant capacity.
    Neurochemical Research 08/2007; 32(8):1314-21. · 2.13 Impact Factor
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    ABSTRACT: Growing number of studies implicate that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, have beneficial effects on ischemia/reperfusion injury that are unrelated to their cholesterol-lowering action. In the present study, we aimed to evaluate possible effects of atorvastatin on oxidative stress, neutrophil accumulation, and contractile response of terminal ileum segments in rats subjected to intestinal ischemia/reperfusion. Intestinal ischemia/reperfusion model was generated by clamping the superior mesenteric artery for 30 min followed by reperfusion for 3 h. Oral administration of atorvastatin at a dose of 10 mg/kg/day lasted 3 days just before induction of intestinal ischemia. At the end of reperfusion period, terminal ileum samples were removed to determine the concentrations of malondialdehyde, reduced glutathione, and myeloperoxidase. Samples were collected also to assess histopathological alterations and contractile response to agonists. Ischemia/reperfusion significantly decreased contractile responses, and this decrease was attenuated by atorvastatin. Pretreatment with atorvastatin caused remarkable decrease in both oxidative stress and neutrophil accumulation. Atorvastatin appeared to be restoring amount of reduced glutathione back to about control level. Furthermore, the pretreatment lowered mucosal damage at histopathological level. Our results suggested that pretreatment with atorvastatin attenuated intestinal muscle dysfunction associated with ischemia/reperfusion. This remarkable effect of atorvastatin is accomplished at least by decreasing oxidative stress and neutrophil accumulation as well as preventing the depletion of reduced glutathione.
    European Journal of Pharmacology 06/2007; 562(1-2):138-47. · 2.59 Impact Factor
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    V Haktan Ozacmak, Hale Sayan
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    ABSTRACT: To examine the effects of adenosine and A1 receptor activation on reperfusion-induced small intestinal injury. Rats were randomized into groups with sham operation, ischemia and reperfusion, and systemic treatments with either adenosine or 2-chloro-N(6)-cyclopentyladenosine, A1 receptor agonist or 8-cyclopentyl-1,3-dipropylxanthine, A1 receptor antagonist, plus adenosine before ischemia. Following reperfusion, contractions of ileum segments in response to KCl, carbachol and substance P were recorded. Tissue myeloperoxidase, malondialdehyde, and reduced glutathione levels were measured. Ischemia significantly decreased both contraction and reduced glutathione level which were ameliorated by adenosine and agonist administration. Treatment also decreased neutrophil infiltration and membrane lipid peroxidation. Beneficial effects of adenosine were abolished by pretreatment with A1 receptor antagonist. The data suggest that adenosine and A1 receptor stimulation attenuate ischemic intestinal injury via decreasing oxidative stress, lowering neutrophil infiltration, and increasing reduced glutathione content.
    World Journal of Gastroenterology 02/2007; 13(4):538-47. · 2.55 Impact Factor
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    ABSTRACT: In this study, we investigated thyroid hormones, thyroid stimulating hormone (TSH), prostaglandin D(2) (PGD(2)) and prostaglandin E(2) (PGE(2)) levels in rapid-eye-movement (REM) sleep-deprived rats compared with controls. The aim of the present study was to detect the effect of REM sleep deprivation (RSD) especially on hypothalamic prostaglandin levels. Twenty-seven male rats were randomly assigned in three groups as dry cage control, yoked control, and RSD. RSD rats were sleep deprived for 10 consecutive days. At the end of 10th day all rats were sacrificed for measurement. Our results indicated that total triiodothyronine (T(3)) and thyroxine (T(4)) decreased in the RSD group while there was no change in TSH. We also measured hypothalamic PGD(2) and PGE(2) levels, but we could not find any significant change between groups.
    Prostaglandins Leukotrienes and Essential Fatty Acids 12/2005; 73(5):391-6. · 2.73 Impact Factor
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    ABSTRACT: We investigated the combinative effects of L-arginine and melatonin on the contractile responses of terminal ileum after the intestinal ischemia-reperfusion (I/R), in vivo. Male rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (180 min). We have observed a dramatic decrease in spontaneous basal activity and Ach-induced contractile response. Our data clearly showed that the contractility decrease was ameliorated by L-arginine but not by L-NAME. Melatonin has reversed the inhibition of contractility caused by I/R injury in part. We did not observe an augmentation in the contractility of ileum when we use melatonin and L-arginine in combination, in fact, melatonin decreased the protective effect of L-arginine in intestinal I/R injury.
    Fundamental and Clinical Pharmacology 11/2005; 19(5):533-5. · 1.99 Impact Factor
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    ABSTRACT: Free radicals derived from molecular oxygen have been reported to be responsible for changes in motility and mucosal damage observed in intestinal ischemia-reperfusion injury. Melatonin has been considered as an antioxidant that prevents injuries resulted from I/R in various tissues. The present study was designed to determine the effect of melatonin on the contractile responses of acetylcholine (Ach) and KCl, on malondialdehyde (MDA), a product of lipid peroxidation, and reduced glutathione (GSH) levels and to assess histopathological changes in the smooth muscle of terminal ileum subjected to ischemia-reperfusion. The intestinal ischemia-reperfusion was induced by occlusion of superior mesenteric artery of rat for 30 min, followed by a period of reperfusion for 3 h. Melatonin at doses of 10 or 50 mg/kg was administered via the tail vein in 5 min prior to reperfusion. Following reperfusion, segments of terminal ileum were rapidly taken and transferred into isolated organ bath and responses to Ach and KCl were recorded. Samples of terminal ileum were also taken for measuring the MDA and GSH levels. EC50 values of these contracting substances were seriously reduced in the ischemia-reperfusion group compared to that of the sham-operated control group. The decreased contraction response to Ach and KCl was significantly ameliorated by a dosage of 50 mg/kg of melatonin, while not by a dosage of 10 mg/kg. Similar pattern of the effect was observed in the tissue levels of MDA and GSH as well as in histological improvement. Melatonin appeared to be restoring the amounts of tissue MDA and GSH back to about control levels. These results suggest that the high dose of melatonin not only physiologically but also biochemically and morphologically could be useful to normalize contractility injured by oxidative stress in intestinal ischemia-reperfusion.
    Life Sciences 03/2005; 76(14):1575-88. · 2.56 Impact Factor
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    ABSTRACT: Previous studies have indicated a pivotal role of reactive oxygen species in the pathomechanism of gastric ulcer. Recent studies demonstrated that thymoquinone (TQ) had an antioxidant effect on injuries caused by various toxic agents in different experimental models. The present study was planned to test whether TQ, the main constituent of the volatile oil of Nigella sativa seeds, was capable to exert beneficial effects on acute gastric ulcer model in rats. We examined antiulcerative and antioxidant effects of TQ on ethanol (EtOH)-induced gastric lesions in rats. The data we collected showed that gastric ulcer caused by absolute EtOH induction resulted in an increase in lipid peroxidation, represented by malondialdehyde level as well as by superoxide dismutase level, an antioxidant enzyme, whereas it resulted in a decrease in glutathione content in rat stomach tissue. Thymoquinone (20 mg/kg) administration reduced the ulcer index and the malondialdehyde level, and reversed the glutathione depletion. However, it did not statistically change the high superoxide dismutase activity induced by EtOH. These results suggest that TQ could inhibit the development of EtOH-induced gastric ulcer, and gastroprotective action of TQ might be in part dependent on its antioxidant property.
    Nutrition Research. 01/2005;
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    ABSTRACT: Taurine has several biological processes such as hypoglycemic action, antioxidation, detoxification, etc. To assess the effect of taurine administration on the guinea pigs with hyperglycemia, blood glucose, C-peptide levels together with morphologic alterations in the pancreatic ultrastructure were investigated in terms of hypoglycemic action and malondialdehyde and total sulfhydryl group levels with regard to oxidation-antioxidation relation. Animals were divided into four groups of six. Glucose supplementation group was administrated a single dose of glucose (400 mg/kg, i.p.) injection. Glucose and taurine supplementation group was administrated glucose treatment (a single dose, 400 mg/kg, i.p.) following taurine (a single dose, 200 mg/kg, i.p.). Taurine and glucose supplementation group was administered taurine treatment (a single dose, 200 mg/kg, i.p.) following glucose treatment (a single dose, 400 mg/kg, i.p.). Control animals received no treatment. Blood samples were collected at the end of the experiments for the determination of glucose, C-peptide (indicator of insulin secretion), lipid peroxidation (thiobarbituric acid reactive substances), and total sulfhydryl groups levels. Pancreatic tissue samples were then collected and processed for transmission electron microscopy. The findings showed that glucose supplementation following taurine administration significantly decreased blood glucose level by increasing C-peptide level and the pancreatic secretion stimulated morphologically and insignificantly changed thiobarbituric acid reactive substances and total sulfhydryl group levels. These observations suggest that taurine administration may be useful in hyperglycemia because of its hypoglycemic and protective effects.
    Amino Acids 01/2005; 27(3-4):327-33. · 3.91 Impact Factor
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    ABSTRACT: Studies have shown that ischemia-reperfusion (I/R) produces free radicals leading to lipid peroxidation and to damage of the nervous tissue. Melatonin, a main secretory product of the pineal gland, has free radical scavenging and antioxidant properties and has been shown to diminish I/R injury in many tissues. There are a limited number of studies related to the effects of melatonin on I/R injury in the peripheral nervous system. Therefore, in the present study, the protective effect of melatonin was investigated in rats subjected to 2 hr of sciatic nerve ischemia followed by 3 hr of reperfusion. Following reperfusion, nerve tissue samples were collected for quantitative assessment of malondialdehyde (MDA), an oxidative stress marker, and superoxide dismutase (SOD), a principal antioxidant enzyme. Samples were further evaluated at electron microscopic level to examine the neuropathological changes. I/R elevated the concentration of MDA significantly while there was a reduction at SOD levels. Melatonin treatment reversed the I/R-induced increase and decrease in MDA and SOD levels, respectively. Furthermore, melatonin salvaged the nerve fibers from ischemic degeneration. Histopathologic findings in the samples of melatonin-treated animals indicated less edema and less damage to the myelin sheaths and axons than those observed in the control samples. Our results suggest that administration of melatonin protects the sciatic nerve from I/R injury, which may be attributed to its antioxidant property.
    Journal of Pineal Research 11/2004; 37(3):143-8. · 7.30 Impact Factor
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    ABSTRACT: Nitric oxide (NO) has been reported to function in both cytoprotective and cytotoxic tissue ischemia-reperfusion (I/R). In this study, we evaluated the effects of L-arginine, the substrate for NO, and NG-nitro L-arginine methyl ester (L-NAME), NO synthase (NOS) inhibitor on super oxide dismutase (SOD) enzyme activity, malondialdehyde (MDA), a marker of lipid peroxidation, nitrate levels, and histopathological structure in rat sciatic nerve 2 h after ischemia, followed by 3 h of reperfusion. Reperfusion resulted in a significant increase in lipid peroxidation level and a decrease in nitrate level of the sciatic nerve. The increased level of lipid peroxidation was partly reduced by NOS inhibition. The decrease in sciatic nerve SOD level, observed in group subjected to I/R, was prevented by inhibition of NOS by L-NAME. These results were supported by histological findings that in the L-arginine-treated group, degenerations of both myelin sheath and axon were observed, while in the L- NAME-treated group, no pathological changes were detected. Our results suggested that excessive NO formation accelerates lipid peroxidation, as well as axonal degeneration on the early reperfusion period of the sciatic nerve.
    International Journal of Neuroscience 04/2004; 114(3):349-64. · 1.22 Impact Factor
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    ABSTRACT: The process of wound healing begins immediately following surface lesions or just after exposure to radiation, chemical agents or extreme temperatures. Taurine (2-aminoethane sulfonic acid), an amino acid containing sulfur, is found in almost all tissues in mammals, playing various important physio-logical roles in each organ. Taurine exhibits an antioxidant effect and is also known to have effects on cell proliferation, inflammation and collagenogenesis. Many antioxidants have been used to eliminate the negative effects of oxygen free radicals on wound healing. The objective of the present study was to examine the wound healing effect in mice of taurine-chitosan gel, which releases taurine slowly over a long time period. Fifty mM of taurine in 1.5% chitosan polymer (TAU-GEL) and 1.5% chitosan polymer (CHI-GEL) were applied to full thickness skin wounds of mice once a day for seven days. After seven days of treatment, lipid peroxide formation-malondialdehyde (MDA) and hydroxyproline (HPX) levels and the tensile strength of wound tissues were measured. All results were compared with those of the untreated control group (CONT). The structural alterations in the skin layers were also histologically investigated. It was found that locally administered TAU-GEL form significantly increased wound tensile strength by decreasing the MDA and increasing HPX levels. These results were supported by histological findings. All observations suggest that taurine gel may be effective in wound healing.
    Amino Acids 02/2002; 22(2):187-98. · 3.91 Impact Factor
  • H Sayan, A Babül, B Ugurlu
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    ABSTRACT: Oxygen free radicals are implicated in the pathophysiology of ischemia-reperfusion (I/R) injury in skeletal muscle. Nitric oxide (NO) and prostaglandin E2 (PGE2) are important regulators of the microcirculation in skeletal muscle. The effects of L-arginine, substrate for NO, and N(G)-nitro L-arginine methyl ester (L-NAME) on PGE2 synthesis, lipid peroxidation and reduced glutathione (GSH) levels was investigated in the rat gastrocnemius muscle after 3 h of reperfusion following 2 h of ischemia. Lipid peroxidation and GSH levels showed a non-significant changes in the I/R groups compared to the control group. According to these results, it can be assumed that skeletal muscle can resist 2 h of ischemia followed by 3 h of reperfusion-induced oxidative stress. PGE2-like activity in the gastrocnemius muscle increased in the L-NAME treated and I/R groups. L-arginine administration reversed the increase in PGE2-like activity of reperfused skeletal muscle. These findings support the conclusion that endothelium-derived PGE2 synthesis increases during reperfusion and suggest that PGE2 may have a protective role in the maintenance of endothelial function.
    Prostaglandins Leukotrienes and Essential Fatty Acids 11/2001; 65(4):179-83. · 2.73 Impact Factor
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    ABSTRACT: Irradiation decreases incisional healing and produces oxygen radicals that damage cells. Because of the lipid component in the membrane, lipid peroxidation is reported to be particularly susceptible to radiation damage. Glutathione acts as a cosubstrate in the enzymatic repair of radiation damage. The aim of this study is to examine the role of granulocyte macrophage-colony stimulating factor (GM-CSF) in incisional skin wounds by investigating lipid peroxidation and reduced glutathione levels in the irradiated rats. Rats were irradiated with cobalt 60 and a dorsal skin incision was made 2 days after irradiation. Rats were divided into four groups: group 1: control; group 2: GM-CSF administered; group 3: irradiated control group; group 4: irradiated and GM-CSF administered group. By irradiation, a marked lipid peroxidation increase was demonstrated. Two days after irradiation, in animals given total body irradiation (TBI), application of a single topical dose of GM-CSF decreased lipid peroxidation of the tissue decreased significantly. By drug administration, the GSH content of the skin increased both in the irradiated and non-irradiated groups. Our results suggest that GM-CSF modulate lipid peroxidation and GSH of the skin wound.
    European Journal of Surgical Oncology 12/2000; 26(7):701-4. · 2.61 Impact Factor
  • D Kiliç, H Sayan
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    ABSTRACT: Radiation-induced gastrointestinal toxicity is important for subjects receiving radiation to the pelvis. Eicosanoids and free radicals may be involved in the mechanism. rHuGM-CSF is a subcutaneously administered drug which may reduce some side effects of radiation. This experimental study was undertaken to determine the effectiveness of rHuGM-CSF on PGE(2)-like activity of the small intestine in rats. Thirty-two adult male Wistar-Albino rats entered the study to be randomized to one of the four groups: Group I. Control; II. Drug administered; III. Irradiated; IV. Irradiated and drug administered. Radiation was by total body irradiation, 800 rads with Cobalt 60. On the 9th day the animals were killed and biopsies were taken from the terminal ileum. PGE(2)-like activity was evaluated. Animals were weighed on the day of irradiation and end of the experiment. A statistically significant difference was found according to pre- and post-treatment weights in the irradiated and nonirradiated drug administered groups (Groups II and IV) (P=0.035 and 0.018, respectively). PGE(2)-like activity in the intestinal tissue was statistically significant higher in the drug-treated animals, both in non-irradiated and irradiated groups. Surprisingly, irradiation was found to decrease the PGE(2)-like activity in the intestinal tissue (P=0.008). rHuGM-CSF was found to increase PGE(2)-like activity in the intestinal tissue. The cellular mechanisms underlying this must be clearly determined and weighed carefully in considering the drug for clinical usage.
    Prostaglandins Leukotrienes and Essential Fatty Acids 07/2000; 62(6):349-53. · 2.73 Impact Factor
  • N A Güzel, H Sayan, D Erbas
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    ABSTRACT: The purpose of this study was to investigate the effects of staying at a moderate altitude (2,300 m, 7 d) on the levels of plasma nitrite, exhaled nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD). Measurements were obtained from 9 female (mean age 18.3 +/- 2) and 9 male (mean age 19.3 +/- 3.7) cross-country volunteer skiers: before, during (1st day, 7th day) and after staying at a moderate altitude. Exhaled nitric oxide levels were measured only before and after staying at the altitude. Nitrite levels increased throughout the stay at the altitude, while MDA levels decreased. In parallel with the nitrite levels, SOD activities were also found to have increased. Exhaled NO values were decreased after the stay at the moderate altitude. These results show that altitude hypoxia causes decreased in NO levels in the lung but increased systemic NO levels in the blood due to inhibition of erythrocyte lipid peroxidation.
    The Japanese Journal of Physiology 05/2000; 50(2):187-90. · 1.04 Impact Factor
  • Pathophysiology. 01/1998; 5:72-72.