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1.
J Obstet Gynaecol ; 36(1): 34-8, 2016.
Article in English | MEDLINE | ID: mdl-26366935

ABSTRACT

It is controversial that uric acid (UA) levels are related to the severity of hypertension in preeclampsia (PE). Our aim in this study was to determine whether UA, xanthine oxidase activity (XOA), allantoin and nitrite levels are related to arterial blood pressure (BP) in PE. We formed a control group (n = 20) and a PE group (n = 20) for the study. Their BPs and plasma UA, XOA, allantoin and nitrite levels were measured. The values from the control and PE pregnant women were assessed via a Wilcoxon matched-pairs test. A Pearson correlation test was also performed. In addition, the diagnostic value of these tests was evaluated via receiver operating characteristic (ROC) analysis. The BP, UA, XOA and allantoin levels in the PE patients were found to be higher when compared with those of the pregnant controls. The UA, XOA and allantoin levels showed high correlations with BP in cases of PE. However, there was no superiority among the correlations. No differences were observed between the groups in terms of nitrite levels and the relationship between nitrite and BP. UA, XOA and allantoin levels may be high due to placental cell death because of abnormal trophoblastic activity observed in PE. Moreover, the reactive oxygen products that are created during the genetic material degradation may explain how UA, XOA and allantoin levels are related to BP. According to ROC analysis, UA, XOA and allantoin assays are reliable predictors for the determination of PE.


Subject(s)
Allantoin/blood , Hypertension/blood , Nitrites/blood , Pre-Eclampsia/blood , Uric Acid/blood , Xanthine Oxidase/blood , Adult , Arterial Pressure , Case-Control Studies , Female , Humans , Pre-Eclampsia/diagnosis , Pre-Eclampsia/physiopathology , Predictive Value of Tests , Pregnancy , ROC Curve , Severity of Illness Index , Young Adult
2.
Clin Exp Med ; 12(4): 265-72, 2012 Dec.
Article in English | MEDLINE | ID: mdl-22083509

ABSTRACT

Myricetin is a naturally occurring flavonoid that is known to decrease plasma glucose levels in diabetes; however, its influence on renal functions has not yet been determined. This study investigated the effect of myricetin on structural and functional changes occurring in diabetic nephropathy. Male Albino Wistar rats were divided into three groups: normoglycemic, diabetic and myricetin-treated diabetic. Diabetes was induced by intraperitoneal (ip) injection of streptozotocin (50 mg/kg), and rats having fasting blood glucose (FBG) levels greater than 200 mg/dl were included in the study. Treatment of myricetin (6 mg/day ip) was initiated 16 weeks after diabetes was confirmed. Light microscopy was performed on hematoxylin-eosin- and Masson's trichrome-stained sections to evaluate the effect of myricetin on structural changes in the kidney, while creatinine clearance, blood urea nitrogen (BUN), kidney weight, urine volume and protein were measured to assess kidney functions. Activities of glutathione peroxidase (GPx) and xanthine oxidase (XO) were also measured in renal tissues obtained from all experimental groups. Myricetin treatment significantly decreased glomerulosclerosis and reduced BUN, urinary volume and protein excretion, which was profoundly increased in diabetic rats. Decreased creatinine clearance measured in diabetic rats was significantly increased following myricetin treatment. Myricetin also restored altered renal activities of GPx and XO, which were decreased and increased in diabetic rats, respectively. In conclusion, myricetin improved altered renal functions and restored renal activities of GPx and XO in diabetic rats. Obtained data suggest that myricetin could be of therapeutic potential in diabetic nephropathy.


Subject(s)
Diabetes Mellitus, Experimental/complications , Diabetic Nephropathies/prevention & control , Flavonoids/administration & dosage , Hypoglycemic Agents/administration & dosage , Kidney/drug effects , Kidney/physiology , Animals , Blood Urea Nitrogen , Creatinine/metabolism , Diabetic Nephropathies/pathology , Histocytochemistry , Metabolic Clearance Rate , Microscopy , Proteinuria , Rats , Rats, Wistar , Treatment Outcome , Urine/chemistry
3.
Int J Neurosci ; 117(12): 1691-706, 2007 Dec.
Article in English | MEDLINE | ID: mdl-17987471

ABSTRACT

The purpose of the present study was to investigate the effect of lipoic acid on lipid peroxidation, nitric oxide production, and visual evoked potentials (VEPs) in rats exposed to chronic restraint stress and to examine whether lipoic acid could prevent VEP alterations that occurred in stress together with lipid peroxidation. Forty male wistar rats, aged three months, were used in the present study. They were equally divided into four groups: control (C), the group treated with lipoic acid (L), the group exposed to restraint stress (S), and the group exposed to stress and treated with lipoic acid (LS). Chronic restraint stress was applied for 21 days (1 h/day) and lipoic acid (100 mg/kg/day) was injected intraperitonally to the L and LS groups for the same period. Brain and retina TBARS levels were significantly increased in the S group compared with the C group. Lipoic acid reduced retina and brain TBARS levels in the L and LS groups compared with their corresponding control groups. Restraint stress significantly increased nitrite and nitrate levels in both brain and retina in the stress group with respect to the control group. Lipoic acid produced a significant decrease in brain and retina nitrite and nitrate levels of the L and LS groups comparing with their corresponding control groups. All latencies of VEP components were prolonged in the S group with respect to the C group. The study found significant correlations between VEPs latencies and TBARS and nitrite and nitrate levels of retina and brain. Lipoic acid decreased the latencies of all VEP components in the LS group whereas it did not affect them in the L group with respect to their control groups. In summary, lipoic acid treatment was found effective in preventing VEP and TBARS alterations caused by stress.


Subject(s)
Antioxidants/pharmacology , Evoked Potentials, Visual/drug effects , Lipid Peroxidation/drug effects , Stress, Psychological/physiopathology , Thioctic Acid/pharmacology , Analysis of Variance , Animals , Disease Models, Animal , Male , Nitric Oxide/metabolism , Photic Stimulation/methods , Rats , Restraint, Physical/methods , Stress, Psychological/etiology , Thiobarbituric Acid Reactive Substances/metabolism
4.
Pharmacol Res ; 54(3): 247-52, 2006 Sep.
Article in English | MEDLINE | ID: mdl-16839772

ABSTRACT

OBJECTIVES: The aim of this study was to evaluate the effect of chronic restraint stress and alpha-lipoic acid (LA) administration on lipid peroxidation and antioxidant enzyme activities in rat peripheral organs. METHODS: Forty male wistar rats, aged 3 months were randomized to one of the following groups: control, restraint stress, LA treated and restraint stress+LA treated. Chronic restraint stress was applied for 21 days (1h/day) and LA (100 mg/kg/day) was administered intraperitoneally for the same period. RESULTS: Restraint stress had no statistically significant effect on lipid peroxidation, copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (CAT) and glutathione peroxidase (GPx) activity in rat liver and heart, when compared to the control group. Lipid peroxidation, determined by measuring malondialdehyde (MDA) levels, was found to be increased in the kidney of restraint stress treated rats, compared to controls. Restraint stress-induced lipid peroxidation in the kidney was significantly decreased via LA treatment. Administration of LA also enhanced GPx and decreased Cu/Zn SOD activity in rat kidney, liver and heart, compared to the control group. CONCLUSIONS: The presented data shows that LA is a protective agent against restraint stress--the inducer of lipid peroxidation in the kidney. These findings also suggest that LA-induced changes in antioxidant enzyme activities in rat peripheral organs may contribute to their versatile effects observed in vivo.


Subject(s)
Antioxidants/metabolism , Stress, Physiological/metabolism , Thioctic Acid/pharmacology , Animals , Catalase/metabolism , Glutathione Peroxidase/metabolism , Heart/drug effects , Lipid Peroxidation/drug effects , Liver/drug effects , Liver/enzymology , Male , Myocardium/enzymology , Rats , Rats, Wistar , Restraint, Physical , Stress, Physiological/enzymology , Stress, Physiological/etiology , Superoxide Dismutase/metabolism
5.
Mol Cell Biochem ; 290(1-2): 125-30, 2006 Oct.
Article in English | MEDLINE | ID: mdl-16758302

ABSTRACT

The aim of this study was determination and comparison of the levels of myeloperoxidase (MPO), xanthine oxidase (XO), and superoxide dismutase (SOD) in gastric mucosa of children who were infected and noninfected with Helicobacter pylori (HP). The MPO, and XO enzyme activities were detected via kinetic measurement, and the MPO, XO and SOD enzyme protein levels were detected via Western blot, in antral mucosa specimens of 43 patients who underwent upper gastrointestinal endoscopy with various indications. The diagnosis of HP infection was made with a positive rapid urease test and histopathologic detection. MPO activity and enzyme protein levels were measured in 14 [8 HP (+) and 6 HP (-)], and in 9 [5 HP (+) and 4 HP (-)] while XO activity and enzyme protein levels were measured in 16 [10 HP (+) and 6 HP (-)] and in 9 [5 HP (+) and 4 HP (-)] patients, respectively. SOD protein level was detected in 13 [7 HP (+) and 6 HP (-)] patients. Of 43 patients 25 were HP (+) and 18 were HP (-). MPO activities were 75.6 +/- 40.5 and 98.8 +/- 44.1 U/g. protein (p = 0.302) while XO activities were 0.5 +/- 0.3 and 0.4 +/- 0.2 U/g. protein in HP (+) and HP (-) patients, respectively (p = 0.625). Measured enzyme protein levels of MPO, XO and SOD were found statistically indifferent in HP (+) and HP (-) patients (p = 0.327, p = 0.086, and p = 0.775, respectively). The results of this study revealed that, MPO, XO and SOD conditions in gastric mucosa alone were not affected from HP presence. That's why MPO, XO, and SOD may not have important roles in the pathogenesis of HP related gastric disease in children.


Subject(s)
Gastric Mucosa/enzymology , Helicobacter Infections/enzymology , Helicobacter pylori/pathogenicity , Peroxidase/metabolism , Superoxide Dismutase/metabolism , Xanthine Oxidase/metabolism , Adolescent , Child , Child, Preschool , Female , Helicobacter pylori/enzymology , Humans , Male
6.
J Enzyme Inhib Med Chem ; 20(3): 293-6, 2005 Jun.
Article in English | MEDLINE | ID: mdl-16119201

ABSTRACT

Intravenous nitroglycerin (GTN) has been used as an anti-ischemic agent for the therapy of unstable and post-infarction angina. Nitric oxide (NO) and S-nitrosothiols constitute the biologically active species formed via nitroglycerin bioactivation. Increased levels of reactive oxygen species can diminish the therapeutic action of organic nitrates by scavenging donated NO and oxidizing tissue thiols important in nitrate biotransformation. Studies reported here show that the red cell activity of antioxidant enzymes, catalase and glutathione peroxidase, are significantly decreased after intravenous nitroglycerin treatment. Catalase activity (739.6 +/- 92.3 k/gHb) decreased to 440.1 +/- 111.9 and 459.8 +/- 130.7 k/gHb after 1 and 24 hr GTN infusion, respectively. Similarly, glutathione peroxidase activity (5.8 +/- 1.8 U/gHb) decreased to 3.2 +/- 1.7 and 3.8 +/- 1.1 U/g Hb after 1 and 24 hr GTN infusion, respectively. The reported decrease in antioxidant enzyme activities can lead to an oxidant milieu and contribute to the generation of nitrate tolerance.


Subject(s)
Antioxidants/pharmacology , Erythrocytes/enzymology , Nitroglycerin/pharmacology , Antioxidants/metabolism , Catalase/blood , Female , Glutathione Peroxidase/blood , Glutathione Peroxidase/metabolism , Humans , Infusions, Intravenous , Male , Middle Aged , Nitrates/metabolism , Nitroglycerin/administration & dosage , Sulfhydryl Compounds/metabolism
7.
Regul Toxicol Pharmacol ; 42(1): 77-82, 2005 Jun.
Article in English | MEDLINE | ID: mdl-15896446

ABSTRACT

Sodium metabisulfite (Na2S2O5) is used as an antioxidant and antimicrobial agent in a variety of drugs and functions as a preservative in many food preparations. In addition to their antioxidant activity, sulfites oxidize to sulfite radicals (SO3-) initiating lipid peroxidation. This study was performed to elucidate the effect of subchronic Na2S2O5 (520 mg/kg/day) ingestion on hepatic and renal antioxidant enzyme activities and lipid peroxidation in albino rats. The antioxidant effect of l-carnitine was also tested in rats treated with Na2S2O5. Plasma uric acid levels were monitored in all rats included in the study. Malondialdehyde (MDA) levels significantly increased in Na2S2O5 treated rats vs. controls, with kidney values of 2.21+/-0.21 vs. 1.22+/-0.35 and liver values of 79.85+/-19.5 vs. 31.36+/-5.0 nmol/mg protein, respectively. Selenium-glutathione peroxidase (GPx) activity was significantly increased in Na2S2O5 treated rats vs. controls, with kidney values of 38.22+/-2.21 vs. 8.09+/-0.76 and liver values of 31.11+/-6.37 vs. 11.70+/-1.02 U/g protein, respectively. Sodium metabisulfite treatment increased plasma uric acid levels in rats that were included in the study. No protective effect of l-carnitine was observed against lipid peroxidation in both liver and kidneys of rats treated with Na2S2O5. The presented data confirm the prooxidant activity of sulfites and suggest that increased GPx activity and plasma uric acid levels may partially reduce the observed renal and hepatocellular oxidative damage caused via the ingestion of sulfites.


Subject(s)
Kidney/drug effects , Liver/drug effects , Oxidants/pharmacology , Sulfites/pharmacology , Animals , Carnitine/pharmacology , Glutathione Peroxidase/pharmacology , Humans , Kidney/chemistry , Kidney/enzymology , Lipid Peroxidation/drug effects , Lipid Peroxidation/physiology , Liver/chemistry , Liver/metabolism , Male , Malondialdehyde/chemistry , Malondialdehyde/metabolism , Oxidants/chemistry , Oxidants/metabolism , Rats , Rats, Wistar , Sulfites/metabolism , Uric Acid/blood
8.
Food Chem Toxicol ; 43(7): 1093-101, 2005 Jul.
Article in English | MEDLINE | ID: mdl-15833385

ABSTRACT

Stress and sulfite can stimulate numerous pathways leading to an increased production of free radicals which generate a peroxidation cascade producing lipid peroxidation, protein oxidation, DNA damage and cell death, and contribute to the occurrence of pathologic conditions. The purpose of our study was to investigate the effects of stress and sulfite on visual evoked potentials (VEPs) and to examine the relationship between lipid peroxidation and VEP changes. Forty male wistar rats, aged three months were used. They were equally divided into four groups: control (C), the group exposed to restraint stress (R), the group treated with sulfite (S) and the group exposed to stress and treated with sulfite (RS). Chronic restraint stress was applied for 21 days (1h/day) and sodium metabisulfite (520 mg/kg/day) was given by gavage for the same period. All latencies of VEP components were prolonged in the R, S and RS groups with respect to the C group. Brain and retina TBARS levels were found to be increased in those groups compared to the C group. Our results strongly suggest that the latency prolongations of all VEP components may have resulted from the enhancement of lipid peroxidation. Correlation analysis between brain and retina TBARS levels and VEP latencies also support this conclusion. Our data in regard to latency prolongations of all VEP components in the stress group exposed to sulfite, reflected an additive effect of sulfite toxicity on VEP components. Therefore it could be suggested that chronic exposure to stress and sulfite together is associated with a considerable health risk.


Subject(s)
Evoked Potentials, Visual/drug effects , Lipid Peroxidation/drug effects , Stress, Psychological/metabolism , Stress, Psychological/physiopathology , Sulfites/toxicity , Animals , Body Weight/drug effects , Eating/drug effects , Male , Rats , Restraint, Physical , Thiobarbituric Acid Reactive Substances/metabolism
9.
J Lab Clin Med ; 142(3): 172-7, 2003 Sep.
Article in English | MEDLINE | ID: mdl-14532905

ABSTRACT

Oxidative stress is an important pathogenic constituent in diabetic endothelial dysfunction. The aim of this study was to investigate whether an increase in oxidative stress related to xanthine oxidoreductase occurs in diabetes. Liver, brain, heart, and kidney xanthine oxidase (XO), xanthine dehydrogenase (XDH), antioxidant enzymes (glutathione peroxidase, superoxide dismutase, catalase), and nitrite levels were measured in control and early and late diabetic rat models. Although diabetes had no impact on liver XO and XDH activity, XDH activity in heart, kidney, and brain was significantly greater in late diabetic rats than in controls. Selenium glutathione peroxidase (GPx) activity was found to be lower in the liver, brain, kidney, and heart of late diabetic rats than in controls. The measured decrease in selenium GPx activity was also observed in early diabetic heart, kidney, and brain. No significant change was observed in liver, brain, and kidney copper/zinc superoxide dismutase (Cu/Zn SOD) activity in early and late diabetic rat models compared with that in controls, whereas heart Cu/Zn SOD activity was significantly decreased in both early and late diabetic rats. Liver and brain catalase activity remained similar among the different experimental groups, whereas increased heart and kidney catalase activity was observed in both early and late diabetic rats. Liver, kidney, and brain nitrite levels were found to be increased in early diabetic rat models compared with those in controls. These data suggest that the increased XDH and decreased selenium GPx activity observed in the later stages of diabetes leads to enhanced oxidative stress in the heart, kidney, and brain, resulting in secondary organ damage associated with the disease.


Subject(s)
Antioxidants/metabolism , Diabetes Mellitus, Experimental/metabolism , Xanthine Oxidase/metabolism , Animals , Brain/enzymology , Catalase/metabolism , Glutathione Peroxidase/metabolism , Kidney/enzymology , Myocardium/enzymology , Nitrites/metabolism , Oxidative Stress/physiology , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Xanthine Dehydrogenase/metabolism
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