Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary artery endothelial cells (PAEC) were isolated from broilers by the method of tissue explantation. The cells were identified using morphological features and immunocytochemical staining using a specific antiserum against factor VIII related antigen. Xanthine/Xanthine oxidase (X/XO) served as the oxygen free radical (OFR) generating system. In vitro model of oxidative injury of PAEC was established based on the X/XO system. The effect of OFR on the growth and viability of PAEC was determined with methylthiazol tetrazolium (MTT) colorimetric assay. Malondialdehyde (MDA, a product of lipid peroxidation) in culture medium of PAEC was detected by a thiobarbituric acid colorimetric assay. The results showed that PAEC survive in vitro and can be subcultured for 5-6 passages. Morphological and immunocytochemical observations of cultured cells demonstrated specific characteristics of endothelial cells. PAECs were severely damaged by OFR. The viability of cells was reduced by the X/XO system, and a dose-dependent decrease in cell viability was found with increasing XO dosages. OFR promoted lipid peroxidation of PAEC and increased the MDA concentration in culture media. These results suggest that OFR can injure the endothelial cells from broiler pulmonary arteries in vitro, which confirms previous results obtained in vivo. Oxidative injury may play an important role in the pathogenesis of pulmonary hypertension syndrome in broiler.
 ...
PMID:The injury effect of oxygen free radicals in vitro on cultured pulmonary artery endothelial cells from broilers. 1705 46

Evaluation of prophylactic effects of omeprazole and/or vitamin E on the formation of free oxygen radicals (FOR) and bowel histopathology in the newborn rat model of hypoxia/reoxygenation (H/R) that resembles human necrotizing enterocolitis (NEC). Eighty newborn rats were randomly divided into eight groups. H/R was done using airtight chamber. Rats were exposed to 100% CO2 for 15 min followed by a reoxygenation for the next 15 min with 100% O2. Group 1 (n = 10) was the control group. Group 2 (n = 10) rats received vitamin E. In Group 3 (n = 10) omeprazole was administrated. Group 4 (n = 10) rats received omeprazole and vitamin E. Group 5 (n = 10) rats were subjected to H/R two times for 2 days and one time for 3 days. Group 6 (n = 10) received vitamin E in addition to H/R for 5 days and in Group 7 (n = 10) omeprazole in addition to H/R for 5 days. In Group 8 (n = 10), vitamin E and omeprazole and H/R were applied for 5 days. Rats were killed at the end of the each process and bowel specimens were harvested for histopathological and biochemical investigations. We administrated vitamin E intramuscularly 300 unit/kg per day and omeprazole orally 20 mg/kg per day. Malondialdehyde (MDA), xanthine oxidase (XO), xanthine dehydogenase (XDH) and XO/(XO + XDH) were measured. Vitamin E and/or omeprazole treated rats had significantly less XO% levels than H/R only group (0.36, 0.38 and 0.57, respectively). Similarly, the MDA levels were significantly lower in vitamin E and/or omeprazole received rats than H/R only rats (88.8, 97.9 and 122.6, respectively). All rats treated with omeprazole and/or vitamin E had better biochemical and histopathological levels compared to H/R rats (p < 0.05). Histopathological results show that Group 5 (H/R only) had significantly more intestinal damage when compared with Group 6 (vitamin E + H/R), Group 7 (omeprazole + R/H) and Group 8 (vitamin E + omeprazole + H/R) (p < 0.001). Grade 2 and 3 intestinal damages were only in Group 5 and there were no statistical difference between in Groups 6, 7 and 8 (p > 0.001). Omeprazole and/or vitamin E may protect the biochemical and histopathological intestinal damage of H/R injury in rats. These drugs may be beneficial in the prophylaxis of NEC in humans as well.
 ...
PMID:Protective effects of vitamin E and omeprazole on the hypoxia/reoxygenation induced intestinal injury in newborn rats. 1842 13

It has been known that contrast medium may cause contrast-induced nephropathy in risk groups. This study sought to establish possible effects of ionic high-osmolar contrast medium administration with or without antecedent cisplatin treatment on oxidant/antioxidant status in rat kidney tissues, as well as to investigate a possible protective role of antioxidant ascorbic acid in this regard. Thirty-five female, 14-week-old Wistar-albino rats were used in this study. They were divided into five groups of seven rats (sham, contrast, contrast + ascorbic acid, contrast + cisplatin, and contrast + cisplatin + ascorbic acid). Ascorbic acid was given in a dose of 250 mg/kg/day orally throughout the study period, and cisplatin (10 mg/kg) as a single i.v. dose on the fourth day. Ionic high-osmolar contrast medium (3 gr/kg iodine as a single dose) was administered by i.v. route on the fifth day. After the animals were sacrificed on the sixth day, their kidney tissues were removed surgically to be used in the analyses. Malondialdehyde (MDA) level and activities of antioxidant (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px] and catalase [CAT]) and oxidant (xanthine oxidase [XO]) enzymes were measured in these samples. Serum urea and creatinine levels were measured to evaluate kidney functions. Histopathological investigation of the tissues was also performed. It was observed that contrast medium administration caused increases in MDA levels in the kidney tissues, either alone or together with antecedent cisplatin treatment. However, ascorbic acid prevented the increases in MDA levels in the kidney tissues. Histopathological findings revealed that ionic high-osmolar contrast medium administration alone led to mild acute structural damage, but contrast medium administration together with antecedent cisplatin usage caused severe tubular necrosis. Ascorbic acid supplementation prevented these changes, to a great extent. The results suggest that ionic high-osmolar contrast medium administration, either alone or together with antecedent cisplatin treatment, leads to accelerated oxidative reactions in rat kidney tissues, and ascorbic acid protects in part the kidney tissues against this oxidant stress.
 ...
PMID:Ionic high-osmolar contrast medium causes oxidant stress in kidney tissue: partial protective role of ascorbic acid. 1856 39

We recently reported that excessive superoxide anion radical (O(2)(-)) was generated in the jugular vein during reperfusion in rats with forebrain ischemia/reperfusion using a novel electrochemical sensor and excessive O(2)(-) generation was associated with oxidative stress, early inflammation, and endothelial injury. However, the source of O(2)(-) was still unclear. Therefore, we used allopurinol, a potent inhibitor of xanthine oxidase (XO), to clarify the source of O(2)(-) generated in rats with forebrain ischemia/reperfusion. The increased O(2)(-) current and the quantified partial value of electricity (Q), which was calculated by the integration of the current, were significantly attenuated after reperfusion by pretreatment with allopurinol. Malondialdehyde (MDA) in the brain and plasma, high-mobility group box 1 (HMGB1) in plasma, and intercellular adhesion molecule-1 (ICAM-1) in the brain and plasma were significantly attenuated in rats pretreated with allopurinol with dose-dependency in comparison to those in control rats. There were significant correlations between total Q and MDA, HMGB, or ICAM-1 in the brain and plasma. Allopurinol pretreatment suppressed O(2)(-) generation in the brain-perfused blood in the jugular vein, and oxidative stress, early inflammation, and endothelial injury in the acute phase of forebrain ischemia/reperfusion. Thus, XO is one of the major sources of O(2)(-)- in blood after reperfusion in rats with forebrain ischemia/reperfusion.
 ...
PMID:Xanthine oxidase is one of the major sources of superoxide anion radicals in blood after reperfusion in rats with forebrain ischemia/reperfusion. 1978 28

ABSTRACT In this study, the aim was to investigate possible effects of Electromagnetic Radiation (EMR) use on oxidant and antioxidant status in erythrocytes and kidney, heart, liver, and ovary tissues from rats, and possible protective role of vitamin C. For this aim, 40 Wistar albino female rats were used throughout the study. The treatment group was exposed to EMR in a frequency of 900 MHz, the EMR plus vitamin C group was exposed to the same EMR frequency and given vitamin C (250 mg/kg/day) orally for 4 weeks. There were 10 animals in each group including control and vitamin C groups. At the end of the study period, blood samples were obtained from the animals to get erythrocyte sediments. Then the animals were sacrificed and heart, kidney, liver, and ovary tissues were removed. Malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), xanthine oxidase (XO), and adenosine deaminase (ADA) enzyme activities were measured in the tissues and erythrocytes. It was observed that MDA level, XO, and GSH-Px activities significantly increased in the EMR group as compared with those of the control group in the erythrocytes. In the kidney tissues, it was found that MDA level and CAT activity significantly increased, whereas XO and ADA activities decreased in the cellular phone group as compared with those of the control group. However, in the heart tissues it was observed that MDA level, ADA, and XO activities significantly decreased in the cellular phone group as compared with those of the control group. The results suggest that EMR at the frequency generated by a cell phone causes oxidative stress and peroxidation in the erythrocytes and kidney tissues from rats. In the erythrocytes, vitamin C seems to make partial protection against the oxidant stress.
 ...
PMID:Effects of Electromagnetic Radiation Use on Oxidant/Antioxidant Status and DNA Turn-over Enzyme Activities in Erythrocytes and Heart, Kidney, Liver, and Ovary Tissues From Rats: Possible Protective Role of Vitamin C. 2002 Sep 24

In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p<0.05). MDA levels in the ethanol+betaine group were significantly decreased compared to the ethanol group (p<0.05). ADA activity in the ethanol+betaine group decreased significantly when compared to the ethanol group (p<0.05). XO activities in ethanol-fed rats were decreased significantly compared to the control group (p<0.05). XO activity in the betaine group was increased significantly (p<0.05) compared to the ethanol group. SOD activity in the ethanol group decreased significantly compared to control group (p<0.001). SOD activity in the ethanol+betaine group decreased significantly (p<0.05) compared to the control group. We think that betaine, as a nutritional methylating agent, may be effective against ethanol-mediated oxidative stress in pancreatic tissue.
 ...
PMID:Betaine (trimethylglycine) as a nutritional agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats. 2010 9

Effects of vitamin E and selenium supplementation on aldehyde oxidase (AO) and xanthine oxidase (XO) activities and antioxidant status in liver, kidney, and heart of streptozotocin (STZ)-induced diabetic rats were examined. AO and XO activities increased significantly after induction of diabetes in rats. Following oral vitamin E (300 mg/kg) and sodium selenite (0.5 mg/kg) intake once a day for 4 weeks, XO activity decreased significantly. AO activity decreased significantly in liver, but remained unchanged in kidney and heart of vitamin E- and selenium-treated rats compared to the diabetic rats. Total antioxidants status, paraoxonase-1 (PON1) and erythrocyte superoxide dismutase activities significantly decreased in the diabetic rats compared to the controls, while a higher fasting plasma glucose level was observed in the diabetic animals. The glutathione peroxidase activity remained statistically unchanged. Malondialdehyde and oxidized low-density lipoprotein levels were higher in the diabetic animals; however, these values were significantly reduced following vitamin E and selenium supplementation. In summary, both AO and XO activities increase in STZ-induced diabetic rats, and vitamin E and selenium supplementation can reduce these activities. The results also indicate that administration of vitamin E and selenium has hypolipidemic, hypoglycemic, and antioxidative effects. It decreases tissue damages in diabetic rats, too.
 ...
PMID:Aldehyde and xanthine oxidase activities in tissues of streptozotocin-induced diabetic rats: effects of vitamin E and selenium supplementation. 2223 35

The study was aimed to evaluate the possible effects of dexamethasone on oxidant/antioxidant status in kidney tissues of rats administered mercuric chloride (HgCl2). Thirty male Wistar-albino rats were enrolled in this study. Rats were divided into 4 groups: G1 (n=7) underwent no therapy (control group), G2 (n=8) received HgCl2 + physiological saline, G3 (n=7) dexamethasone (DM) + physiological saline and G4 (n=8) received HgCl2 + DM. HgCl2 was injected subcutaneously into rats in the G2 and G4 on the first day of the study. Dexamethasone was injected intraperitoneally into rats in the G3 and G4 for 3 days. Malondialdehyde (MDA) levels, catalase (CAT), glutathione peroxidase (GSH-Px), xanthine oxidase (XO) and superoxide dismutase (SOD) activities were evaluated in the kidney tissues. Serum creatinine levels were also measured. Xanthine oxidase activity was increased in the G2 compared to the control group. Catalase activity in the control group was significantly higher compared to the other groups. In the histopathological examination of kidneys, there was a tubular degeneration in G2 and G4. It was concluded that HgCl2 administration may cause oxidative stress through increasing XO and decreasing CAT activities. Dexamethasone injection may partially protect the rat kidneys against oxidative reactions by preventing the increase in XO activity (Tab. 1, Ref. 33).
 ...
PMID:The effects of dexamethasone on oxidant/antioxidant status in kidneys of rats administered mercuric chloride. 2238 Apr 94

Accumulation of hydrophobic bile acids (BAs) during cholestasis plays an important role in apoptosis initiation as well as oxidative stress increase in liver cells. Ursodeoxycholic acid (UDCA) acts as a protector in BA-induced cell injury.The aim of the study was to evaluate the effect of UDCA on oxidative stress level and DNase I and II activity caused by liver injury in bile duct ligation (BDL) rats.Wistar rats were divided in four groups: group 1, control (sham-operated); group 2, sham-operated and injected with UDCA (30 mg/kg); group 3,animals with BDL; and group 4,UDCA-treatedcholestatic rats. Animals were sacrificed after 9 days. Malondialdehyde (MDA; lipid peroxidation end-product) level and protein-molecule oxidative modification (carbonyl group content) significantly increased in BDL rat liver. Catalase (CAT) activity in liver tissue was found to be decreased in BDL rats. In addition, xanthine oxidase (XO) activity, which is thought to be one of the key enzymes producing reactive oxygen species, was found to be increased in the cholestatic group. The apoptotic effect in cholestasis was probably triggered by the increased activation of DNase I and II. The protective effect of UDCA on liver tissue damage in BDL rats, in comparison to cholestatic liver, were 1) decrease of MDA levels, 2) increased CAT activity, 3) reduced XO activity, and 4) effect on terminal apoptotic reaction, shown as a decrease in DNase I and II activity.Therefore, UDCA may be useful in the preservation of liver function in cholestasis treatment.
 ...
PMID:The effect of ursodeoxycholic acid on oxidative stress level and DNase activity in rat liver after bile duct ligation. 2238 35

Increased evidence in role of oxidative stress and grape seed extract (GSE) in diabetes and its complication led us to investigate the changes of oxidative stress and anti-oxidant defence in liver tissue of diabetic rats and possible effects of GSE. Diabetes was induced by a single intraperitoneal injection of streptozotocin. Seven days after STZ injection four groups were formed: Control, GSE-supplemented control, diabetic and GSE-supplemented diabetic and GSE was given for 6 weeks. Malondialdehyde levels and xanthine oxidase activities were not different among the groups. However, nitric oxide (NO) levels were higher in diabetic and GSE supplemented groups compared with non-diabetic and non-supplemented groups, respectively. Total anti-oxidant activity (TAA) was lower in diabetic groups compared with their non-diabetic controls and it was not affected by GSE. In conclusion, GSE supplementation has limited protective effect in liver tissue of diabetic rats via affecting NO levels and was not affecting TAA.
 ...
PMID:Oxidative stress and anti-oxidant status in diabetic rat liver: effect of plant polyphenols. 2280 4


<< Previous 1 2 3 4 Next >>