A Yeşilkaya

Akdeniz University, Satalia, Antalya, Turkey

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Publications (22)29.07 Total impact

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    ABSTRACT: Purpose: The pathogenesis of pulmonary hypoplasia associated with congenital diaphragmatic hernia (CDH) remains unclear. Interactions between the epithelium and surrounding mesenchyme play an important role in normal lung morphogenesis. Epimorphin, a stromal protein, plays a role in epithelial morphogenesis and lung branching, both of which are involved in pulmonary hypoplasia. In this study, we aimed to examine the relationship between epimorphin and pulmonary hypoplasia associated with CDH in an animal model. Methods: Time-pregnant rats were exposed to nitrofen or vehicle on gestational day 9 (D9). Fetuses were harvested on D16 and D20, and were divided into control, hypoplastic lungs with CDH (CDH+), and hypoplastic lungs without CDH (CDH-). Both lungs of each fetus were removed and subjected to morphometric and molecular biologic analyses. Lung-to-body weight ratios were calculated. Pulmonary RNA was extracted, and relative mRNA level of epimorphin was determined by quantitative real-time PCR (qRT-PCR). Protein expression of epimorphin was investigated by Western blotting. Results: In groups D16 and D20, lung-to-body weight ratios in subgroups CDH+ were significantly lower than those of controls and CDH-. The relative mRNA expression levels of epimorphin were significantly increased in both lungs in subgroup CDH+ compared with controls and CDH- on D16. Pulmonary epimorphin gene expression levels were significantly decreased in CDH+ group on D20 compared to controls. Western blotting confirmed the qRT-PCR results showing decreased pulmonary epimorphin protein expression in CDH+ hypoplastic lungs compared to controls on D20. Conclusion: Our study shows that there is an association between the epimorphin expression and pulmonary hypoplasia associated with CDH. Although the cause-effect relationship is far from being established, epimorphin-related mechanisms have a more critical role in early (D16) developmental stage.
    No preview · Article · Aug 2014 · Pediatric Surgery International
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    ABSTRACT: Aim: Ang II stimulates vascular smooth muscle cells (VSMCs) and activates mitogen protein kinases (MAPKs) in culture media. p38 MAPK, a member of MAPK family, is stimulated by both Ang II and reactive oxygen species. This study was carried out to show Ang II stimulated p38 MAPK activation through Ras and subsequent NADPH oxidase activation in VSMCs. Material and Method: In our study, primary VSMCs isolated from rat aorta were stimulated by Ang II and with different inhibitors, and western blot was used to measure p38 MAPK phosphorylation. Results: The optimum p38 MAPK phosphorylation was observed at 100 nM Ang II concentration for 5 minutes and the next experiments were carried out under this conditions. To analyze the effect of Ras, which is an upstream mediator of p38 MAPK phosphorylation, VSMCs were incubated with a Ras spesific inhibitor FTS (Farnesyl thiosalicylic acid). After the stimulation of VSMCs by Ang II, p38 MAPK phosphorylation was inhibited. p38 MAPK phosphorylation was also completely inhibited in the presence of DPI (Diphenyl Iodinoum), a spesific NAD(P)H oxidase inhibitor, after Ang II stimulation. Conclusion: These findings demonstrate that Ang II stimulated p38 MAPK phosphorylation is through AT1 receptor and Ras-NAD(P)H oxidase dependent pathway in VSMCs. Understanding this pathway may contribute to the cellular mechanisms underlying in cardiovascular diseases.
    Full-text · Article · Jan 2012 · Türk Biyokimya Dergisi / Turkish Journal of Biochemistry
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    Alper Tokay · Arzu çetin · Fatih Uzuner · Akin Yesilkaya
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    ABSTRACT: Aim: In this study, we have evaluated the procedure of transient transfection efficiency of vascular smooth muscle cells (VSMCs) with Lipofectamine (Life Technologies) and FuGENE (ROCHE, FuGENE HD Reagent) transfection reagents using the pCH110 eukaryotic assay vector containing the lacZ reporter gene. We also did try these attainments to transfect VSMCs with RasN17 DNA and affirmed our findings. Material Methods: Plasmid pcH110, which has been purified by cesium chloride gradient centrifugation, was used in all transfections as the assay vector. And c-H-Ras was observed via Western-blot technique. Results: Briefly, the transfection with FuGENE has been given the best results, comparing with Lipofectamin. Under our culture conditions for VSMCs, FuGENE transfection efficiency could be augmented by simply increasing the amount of plasmid DNA 1.5–3 times above the recommended concentration without any visible cytotoxicity. With the FuGENE reagent, optimal transfection efficiency was obtained for primary culture of VSMCs within the recommended concentrations, but at the top of the range. The results indicate that optimization of the transfection process should include plasmid DNA concentrations above the levels suggested by the manufacturers, in order to accomplish the highest transfection efficiency. And, these finding was also supported with our Western-blot results when VSMCs have been transiently transfected with RasN17 DNA. Conclusion: According to the difficulty of transfections of primary cell culture, we used FuGENE reagent with different DNA and plasmid ratio describes by the manufacturer and obtained better transfection efficiency in primary cultured vascular smooth muscle cells. Our findings, precisely implicates to use FuGENE reagent for to get a better transfection efficiency in primary cultured cells, especially in primary cultured VSMCs.
    Full-text · Article · Jan 2012 · Turkish Journal of Biochemistry
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    ABSTRACT: Regular exercise has blood pressure-lowering effects, as shown in different types of experimental hypertension models in rats, including the nitric oxide synthase (NOS) inhibition model. We aimed to investigate possible mechanisms implicated in the exercise effect by evaluating the vasoreactivity of resistance arteries. Exercise effects on agonist-induced vasodilatory responses and flow-mediated dilation were evaluated in vessel segments of the rat chronic NOS inhibition model. Normotensive and hypertensive rats were subjected to swimming exercise (1 h/day, 5 days/wk, 6 wk), while rats in other sedentary and hypertensive groups did not. Hypertension was induced by oral administration of the nonselective NOS inhibitor l-NAME (25 mg/kg day) for 6 wk. Systolic blood pressure, as measured by the tail-cuff method, was significantly decreased by the training protocol in exercising hypertensive rats. The vasoreactivity of resistance arteries was evaluated by both wire and pressure myography studies. An impaired nitric oxide-mediated relaxation pathway in untrained hypertensive rats led to decreased relaxation responses in vessels with intact endothelium. Exercise training significantly improved the responses to acetylcholine and flow-mediated dilation in exercise-trained hypertensive rats in parallel with a decrease in blood pressure. On the other hand contraction (norepinephrine and KCl) and relaxation (sodium nitroprusside) responses of vascular smooth muscle were not different between the groups. Vascular endothelial NOS protein expression was found to be increased in both exercising groups. In conclusion, these results revealed evidence of an increased role of the nitric oxide-dependent relaxation pathway in exercising hypertensive rats.
    No preview · Article · Jul 2009 · Journal of Applied Physiology
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    ABSTRACT: Angiotensin II (Ang II) induces a rapid increase in mitogen-activated protein kinase (MAPK) activity through the Ang II type 1 receptor in cultured rat vascular smooth muscle cells (VSMCs). In the present study, we examined the effects of the phospholipase C (PLC) inhibitor U73122, the protein kinase C (PKC) inhibitor GF109203X, and the Ras inhibitor farnesylthiosalicylic acid (FTS) on Ang II-induced activation of p42/p44 MAPKs in cultured VSMCs. Phosphorylation was shown using the Western blot technique with specific phospho-antibodies against MAPK proteins. The PLC inhibitor U73122 abolished the Ang II-induced MAPK activity, while the PKC inhibitor GF109203X only decreased it. There was also an inhibition observed with the Ras inhibitor, FTS on Ang II-induced MAPK activity. These data suggest that Ang II-induced MAPK phosphorylation through the Ang II type 1 receptor could be mediated by Ras and/or PLC-dependent phosphorylations but not by PKC phosphorylation.
    Full-text · Article · Feb 2007 · Pharmacology
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    ABSTRACT: We investigated the effects of lipopolysaccharide (LPS) administration on plasma nitrite, nitrotyrosine and 6-keto prostaglandin F1alpha, (PGF1alpha) levels and the related resultant changes in function and histochemistry of aorta in rats. Plasma nitrite and PGF1alpha nitrotyrosine levels were analysed after 5 mg/kg intravenous LPS was administered to rats compared with those in non-treated rats. The distribution of nitrotyrosine in the aorta was studied immunohistochemically. The contractile responses of aortic rings to phenylephrine (PE) from both the LPS-treated and control rats were studied in the organ baths. There were increases in plasma nitrite, PGF1alpha, and nitrotyrosine concentrations of LPS-treated rats compared to non-treated rats. Immunoreactivity of nitrotyrosine residues were detected in the endothelial and smooth muscle cells in LPS-treated but not in control rat aorta. The contractile responses to PE of the LPS-treated rat aortic rings were significantly reduced as compared with those of control rat's. Incubation of the aortic rings from LPS-treated rats with cyclooxygenase inhibitor indomethacine or with a combination of indomethacine and nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) increased the contractile responses to the levels observed in control rats suggesting that both prostanoids and particularly nitric oxide (NO) are involved in the reduced contractile responses in LPS-treated rats. These results supported the view that LPS might cause an increment in both NO and PGI2 levels. This increase in the NO and PGI2 levels may be responsible from the reduction in responses of aorta to contractile agents in LPS-treated rats. Increased peroxynitrite formation in LPS-treated rats may lead to nitration of the tyrosil residues of the proteins in the aorta.
    No preview · Article · Apr 2006 · Journal of physiology and biochemistry
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    ABSTRACT: Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.
    Full-text · Article · Nov 2005 · Journal of Applied Physiology
  • M U Senturk · U K Senturk · P Y Basak · O Kuru · A Yesilkaya

    No preview · Article · Oct 2003 · Journal of the European Academy of Dermatology and Venereology
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    ABSTRACT: Regular training lowers blood pressure in hypertensive humans and other animals. We investigated the response to 4 weeks of treadmill exercise training in hypertensive male Wistar rats receiving the nitric oxide synthase inhibitor N ω-nitro-L-arginine methyl ester (L-NAME). The rats were on either a short- (4 weeks) or long-term (10 weeks) L-NAME treatment protocol and were subjected to running exercise that started concomitantly in the short-term group and in the 6th week in the long-term group. Four weeks of exercise training induced a fall in mean arterial pressure in both the short- [mean (SEM) 137.6 (4.0) mmHg] and long-term hypertensive groups [161.4 (2.3) mmHg] compared to their sedentary hypertensive controls [160.4 (3.3) mmHg and 176.8 (8.9) mmHg, respectively]. Exercise also increased muscle nitric oxide synthase activity in both of the trained hypertensive groups. Muscle nitrite levels were higher in the exercising short-term hypertensive group compared to both the sedentary control and the sedentary hypertensive groups, and were not different between the sedentary and exercising long-term hypertensive groups. Increased wall thickness of the aortic and mesenteric vessels was observed in the hypertensive groups, but was prevented in the exercising long-term hypertensive group. In rat, exercise reduces the elevated blood pressure in L-NAME-induced hypertension via increasing nitric oxide synthase activity. Changes in vessel structure with exercise training may also be involved in the blood-pressure-lowering effects.
    No preview · Article · Jul 2002 · Arbeitsphysiologie
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    ABSTRACT: Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.
    Full-text · Article · Dec 2001 · Journal of Applied Physiology
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    O Erdoğan · S Yildiz · A Başaran · A Demirbaş · A Yeşilkaya
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    ABSTRACT: Removal of free oxygen radicals, generated during reperfusion of an ischemic organ by scavengers protects the tissue from reperfusion injury. The calcium channel blocker verapamil is an effective cytoprotective agent, preventing against reperfusion injury. The effects of verapamil were investigated previously using hepatic, renal or cardiac ischemia-reperfusion injury models. We investigated the effects of intravenous and intraportal administration of verapamil in prevention from the injury caused by free oxygen radicals generated during hepatic ischemia-reperfusion in rats. Thirty six male Sprague-Dawley rats after laparotomy were subjected to hepatic ischemia for 30 and 45 min followed by 60 min of reperfusion. Two minutes before ischemia the rats were pretreated by intravenous or intraportal administration of verapamil. The levels of glutathione and thiobarbituric acid reacting substances (TBARs) referred to as malonyldialdehyde (MDA) and the serum levels of transaminases were measured in liver tissue 1 and 24 h after the onset of reperfusion. Statistical analysis of the data by Student's t-test showed statistically significant differences between the group pretreated intraportally with verapamil and the other groups. Verapamil given intraportally exerted more beneficial effect. Therefore, we conclude that intraportal verapamil administration reduces the ischemia-reperfusion injury caused by free oxygen radicals.
    Full-text · Article · Mar 2001 · Polish journal of pharmacology
  • D K Korgun · S Bilmen · A Yesilkaya
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    ABSTRACT: In the present study, we measured the concentrations of reduced glutathione (GSH) and malonyldialdehyde (MDA) and the activities of glutathione peroxidase (GSH-Px), glutathione S-transferase (GSH-S-T), superoxide dismutase (SOD), catalase (CAT) and glucose-6-phosphate dehydrogenase (G-6-PD) in erythrocytes obtained freshly from adult male donors which was preserved with CPDA-1 anticoagulant (citrate,phosphate, dextrose, adenine) on different days of storage. At the end of the study, storage-associated alterations in antioxidant activities were noted and discussed. GSH, GSH-Px, GSH-S-T, SOD, CAT and G-6-PD activities decreased, but erythrocyte MDA levels, as anindex of lipid peroxidation, increased during the storage period. According to our results, glutathione-dependent antioxidant systems in erythrocytes might be depleted during long storage in blood bags.
    No preview · Article · Feb 2001 · Research communications in molecular pathology and pharmacology
  • Akin Yesilkaya · Resul Altinayak · Dijle Kipmen Korgun
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    ABSTRACT: To examine the antioxidant effect of bilirubin (BR) on leukocyte, we treated leukocytes obtained from healthy subjects with an oxidant and various concentrations of BR. High concentrations of BR decreased thiobarbituric acid reactive substances (TBARS) and catalase activities, increased superoxide dismutase (SOD) activity, but had no effect on glutathione (GSH) concentration. Our results showed that under physiological conditions, BR has an antioxidant effect only in high concentrations.
    No preview · Article · Aug 2000 · General Pharmacology
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    ABSTRACT: Nitric oxide (NO) plays a major role in vascular regulation. Modulation of NO synthesis is known to influence blood pressure. Inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME; 72 mg/kg/day, p.o., 21 days) resulted in 60% increase in blood pressure in rats. Red blood cell (RBC) transit time measured by the cell transit analyzer increased significantly in the L-NAME treated group, in comparison to normotensive rats. RBC aggregation measured in autologous plasma, by a photometric rheoscope also increased significantly in the hypertensive rats. RBC cytosolic free calcium concentration was also significantly higher in the hypertensive animals. Incubation of RBC from hypertensive and control animals with NO donor, sodium nitroprusside (SNP; 10-1000 microM) for 60 minutes resulted in a dose-dependent decrease in RBC aggregation, however aggregation index was significantly higher in hypertensive group at each SNP concentration. Incubation with SNP had no effect on RBC deformability in the control group, while a slight decrease in RBC transit time was observed only at 10 microM SNP in the hypertensive group. These results imply that NO may play a role in the regulation of rheological properties of RBC and the alterations in these properties may at least in part be involved in the development of L-NAME induced hypertension.
    Full-text · Article · Feb 2000 · Clinical hemorheology and microcirculation
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    ABSTRACT: Fetal distress (FD) adversely affects fetal gastric physiology and histology, increasing gastric acid secretion and disturbing gastric protective mechanism. Considering these findings, an experimental study was planned to test whether ranitidine prevents FD-related gastric physiological and histological changes during late gestational period. In this study, a rabbit model of FD was created by way of intermittent maternal aortic occlusion. In group 1 (SC), saline treated animals underwent control operation. In group 2 (SD), FD was created in saline treated animals. In group 3 (RC), ranitidine treated animals underwent control operation. In group 4 (RD), FD was created in ranitidine treated animals. Blood lactic acid levels of the fetuses were 2.3 +/- 1.0 mg/L in SC group and 4.7 +/- 1.8 mg/L in group SD (p < 0.01); 2.5 +/- 0.9 mg/L in group RC and 6.7 +/- 2.5 mg/L in group RD (p < 0.01). Fetal gastric acid secretion was 5.94 +/- 2.13 microEq/h in group SC and 8.26 +/- 2.24 microEq/h in group SD (p < 0.05); 6.63 +/- 2.3 microEq/h in group RC and 6.04 +/- 2.43 microEq/h in group RD (p < 0.05). Fetal gastric PGE2 level was 16.4 +/- 2.65 microg/g-wet weight in group SC and 7.62 +/- 1.86 microg/g-wet weight in group SD (p < 0.01); 15.6 +/- 2.61 microg/g-wet weight in group RC and 8.44 +/- 1.44 microg/g-wet weight in group RD (p < 0.01). In addition, histopathological examination showed normal gastric structure in groups SC and RC, but there were mild erosive and hemorrhagic changes in groups SD and RD. Because prophylactic ranitidine significantly decreased gastric acid secretion, but did not prevent harmful histopathologic effects in FD, it is suggested that gastric damage cannot be avoided by decreasing gastric acid secretion alone. However PGE2 analogs with or without H2 receptor blockers may have a potential role to prevent FD-related gastric damage.
    No preview · Article · Feb 1999 · American Journal of Perinatology
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    ABSTRACT: 1. The effects of halothane and isoflurane anesthesia on red blood cell (RBC) deformability, lipid peroxidation and antioxidant enzymes were tested in rabbits. 2. RBC transit time was significantly increased to 2.12 +/- 0.07 msec after 1-hr halothane anesthesia preceded by 6 mg/kg pentobarbital injections from 1.98 +/- 0.07 msec preanesthesia value (p < 0.05). Thiobarbituric acid-reactive substances also were increased significantly, being 23.35 +/- 2.75 nmol/gHb and 33.11 +/- 5.34 nmol/gHb before and after anesthesia, respectively (p < 0.05). 3. Under halothane anesthesia without prior pentobarbital injection or under isoflurane anesthesia with or without pentobarbital injection, no significant alterations were observed in these parameters. 4. RBC superoxide dismutase activity was decreased in the group anesthetized with the pentobarbital-halothane combination. The impaired RBC deformability and increased oxidant damage might be related to the free radical formation during the metabolism of halothane. Pentobarbital can potentiate this effect either by inducing cytochrome P-450 or by altering antioxidant defense. 5. Alterations in RBC mechanical properties may contribute to the tissue perfusion problems that develop after surgery under general anesthesia.
    No preview · Article · Jul 1998 · General Pharmacology
  • A Yeşilkaya · A Yeğin · S Ozdem · TA Aksu
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    ABSTRACT: Recently, it has been suggested that bilirubin may act as a potent biological chain-breaking antioxidant. To observe the effects of free bilirubin on antioxidant reactions in cumene hydroperoxide-treated erythrocytes (15 g hemoglobin/dl), we added bilirubin at four different concentrations (0.5, 1, 5, and 10 mg/dl). We measured the thiobarbituric acid-reactive substance and reduced glutathione levels, and some antioxidant enzyme activities, namely superoxide dismutase, catalase, and glucose-6-phosphate dehydrogenase. Thiobarbituric acid-reactive substance and chemiluminescent signals decreased during the incubation. Superoxide dismutase activities also decreased but not as much as in the control group. Glucose-6-phosphate dehydrogenase activities and reduced glutathione levels increased, but catalase activities remained the same as the control group. Our results suggest that bilirubin--in the concentrations we have used--partially prevented the oxidant effects of cumene hydroperoxide.
    No preview · Article · Feb 1998 · International Journal of Clinical & Laboratory Research
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    ABSTRACT: Although effects of stress on the stomach have been extensively investigated in children and adults, our knowledge about effects of fetal distress (FD) on the fetal stomach is quite limited. Therefore, an experimental study was planned to evaluate the effects of FD on fetal gastric physiology and histology. In this study, a model of FD was created by way of intermittent maternal aortic occlusion in pregnant rabbits. In total, 21 fetuses of 6 pregnant rabbits were available for surgical and laboratory procedures. Laboratory examinations showed that (1) fetal gastric acid secretion was 4.24 +/- 2.68 muEq/h in the control group and 18.08 +/- 6.34 muEq/h in the distress group (p < 0.01) and (2) fetal gastric PGE2 level was 16.59 +/- 6.15 mg/g wet weight in the control group and 9.86 +/- 3.46 mg/g wet weight in the distress group (p < 0.05). Histopathologically, there were mild hemorrhagic and errosive changes in the distressed fetuses, but not in control fetuses. These findings support that FD adversely affects fetal gastric physiology through two mechanisms consisting of increased gastric acid secretion and decreased fetal gastric protection in rabbits. Consequently, gastric injury should be noted as a potential problem among hypoxia-associated abnormalities encountered in the distressed fetus.
    No preview · Article · Sep 1997 · American Journal of Perinatology
  • G Yücel · A Yeşilkaya · T A Aksu · A Yeğin · Y Alicigüzel
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    ABSTRACT: Erythrocytes and hemolysates from 10 normal and 10 glucose-6-phosphate dehydrogenase-deficient individuals were incubated with cumene hydroperoxide, and free radical-induced lipid peroxidation was monitored by chemiluminescence. Chemiluminescence intensities in erythrocytes of normal and deficient subjects were similar in the presence or absence of glucose-6-phosphate dehydrogenase substrates. Hemolysates of normal and deficient subjects also showed similar chemiluminescence in the absence of substrates. However, with the addition of substrates to the incubation medium, deficient hemolysates reached maximum chemiluminescence intensity within a shorter period, and maximum values were higher than in normal hemolysates. We believe this offers a new means of detection of glucose-6-phosphate dehydrogenase-deficient patients.
    No preview · Article · Feb 1997 · International Journal of Clinical & Laboratory Research
  • A Yeşilkaya · A Yeğin · G Yücel · Y Alicigüzel · T A Aksu
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    ABSTRACT: We studied the effect of cumene hydroperoxide, t-butyl hydroperoxide, and hydrogen peroxide on intact healthy human erythrocytes (15 g hemoglobin/dl) using chemiluminescence to monitor peroxidation. We measured the chemiluminescence spectrum, the process of hemolysis, the pH shift, and absorbance spectrum during the incubation with chemicals producing oxidative stress. Maximum chemiluminescence was reached with cumene hydroperoxide at about 50 min, but with t-butyl hydroperoxide at 100 min. The effect of organic hydroperoxide was concentration dependent, whereas the effect of hydrogen peroxide was independent of concentration. Peroxides induced hemolysis after 30 min. The pH shift to alkaline was observed in the first 20-min period. Incubation with organic hydroperoxides induced a decrease in absorption at 580, 545, and 345 nm. Hydrogen peroxide induced a decrease in the same period of time but this returned to the normal range by 120 min. There was no change in absorption at 420 nm with any of the peroxidative agents. Our results suggest that low-level chemiluminescence is a useful model for studying hydroperoxide-induced peroxidation in human erythrocytes.
    No preview · Article · Feb 1996 · International Journal of Clinical & Laboratory Research