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

The impact of in vivo ischaemia and ischaemia-reperfusion (I-R) on mitochondrial respiratory function was investigated in hypertrophied (HP) hearts with aortic constriction compared with control hearts using an open-chest rat surgical model. Moreover, mitochondrial susceptibility to superoxide radicals (O2-.) in vitro was examined in HP and control hearts with or without I-R. With the site I substrates pyruvate-malate, mitochondrial state 4 (basal) respiration and the respiratory control index (RCI) were not affected by either ischaemia alone or I-R in both HP and control hearts. State 3 (ADP-stimulated) respiration was increased with I-R in control hearts, but showed a reduction after I-R in the HP hearts. Exposure of mitochondria to O2-. (20 nM hypoxanthine in the presence of 0.13 unit mL-1 xanthine oxidase) significantly increased state 4 respiration, whereas state 3 respiration and RCI were decreased in all treatment groups. I-R hearts in both HP and control showed greater increases in state 4 respiration with O2-. than either sham or ischaemic hearts. HP hearts exhibited a significantly lesser extent of inhibition in state 3 respiration and RCI by O2-. compared with control hearts. These changes in mitochondrial respiratory properties were not observed with the site II substrate succinate. Myocardial reduced vs. oxidized glutathione ratio was significantly decreased after I-R in both control and HP hearts. Malondialdehyde content showed an increase with I-R, but the increase was significant only in control hearts. These data indicate that short-term in vivo I-R does not impair heart mitochondrial respiratory function, but renders the organelles more vulnerable to imposed oxidative stress. Mitochondria from the HP hearts are more resistant to free radical damage under normal and ischaemic conditions; however, this advantage is severely compromised after reperfusion.
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PMID:Ischaemia-reperfusion induced alterations of mitochondrial function in hypertrophied rat heart. 886 86

Activities of adenosine deaminase, 5'-nucleotidase, xanthine oxidase, superoxide dismutase, glutathione peroxidase and catalase enzymes were measured in cancerous and non-cancerous adjacent colorectal tissues from 10 patients. Activities of DNA turn-over enzymes (ADA, 5'NT and XO) were found increased and those of free-radical metabolizing enzymes (SOD, GSH-Px and CAT) decreased in cancerous tissues compared with those of non-cancerous adjacent ones. Malondialdehyde (MDA) concentrations in cancerous tissues were also found higher than those of non-cancerous tissues, which indicated accelerated lipid peroxidation in the cancerous tissues. In the correlation analysis, disordered enzymatical relations were observed between the enzymes of both metabolic pathways. Results suggest that activities of purine metabolizing enzymes increase to cope with accelerated purine metabolism in cancerous tissues and, enzymatic antioxidant defense potential of cancerous tissues decreases due to carcinogenic processes in the tissues. Reduced antioxidant defense system makes the cancerous tissue more vulnerable to toxic effects of some free-radical species.
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PMID:Activities of the enzymes participating in purine and free-radical metabolism in cancerous human colorectal tissues. 992 74

Phospholipids located in the cellular membrane play a critical role in the fluid-mosaic model of membrane structure and membrane function. Evidence is mounting for the role of abnormal phospholipid metabolism in some neuropsychiatric disorders including schizophrenia. As an important essential fatty acid (EFA), omega-3 (omega-3) fatty acid series are found in large amounts in fish oil. The aim of this experimental study was to assess the changes of some of the oxidant and antioxidant parameters in the hypothalamus of rats fed with omega-3 EFA diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with omega-3 were decapitated under ether anesthesia, and hypothalamus was removed immediately. Malondialdehyde (MDA) and nitric oxide (NO) levels as well as superoxide dismutase (SOD) and xanthine oxidase (XO) enzyme activities in the hypothalamus were measured. SOD activity was significantly decreased in omega-3 EFA treated group compared to control group (p < 0.014). Tissue MDA and NO levels were also decreased in omega-3 EFA treated group compared to control rats (p < 0.0001). Xanthine oxidase activity was found to be increased in omega-3 EFA treated rats when compared to the control group (p < 0.0001). Taken together, this preliminary animal study provides strong support for a therapeutic effect of omega-3 EFA in some neuropsychiatric disorders in which reactive oxygen species (ROS) are recently accused to be an important physiopathogenetic factor.
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PMID:Hypothalamic superoxide dismutase, xanthine oxidase, nitric oxide, and malondialdehyde in rats fed with fish omega-3 fatty acids. 1527 95

The aims of this study were: (a) to assess whether the increased oxidative stress in otitis media with effusion (OME) induced in guinea pigs by histamine injection into the middle ear cavity is reflected by lipid peroxidation in erythrocytes, plasma, and middle ear effusion fluid; (b) to survey the alterations of oxidant and antioxidant enzyme activities in experimental OME; and (c) to determine the effects of melatonin and methylprednisolone on this oxidative stress. Malondialdehyde (MDA) level, erythrocyte total (enzymatic plus non-enzymatic) superoxide scavenger activity (TSSA), non-enzymatic superoxide scavenger activity (NSSA), superoxide dismutase (SOD), catalase (CAT), and xanthine oxidase (XO) activities were measured in 4 groups of 7 guinea pigs at 3 hr after injection of 0.1 ml of histamine (or saline) into the middle ear. Group I was the control group, Group II was an experimental group with OME induced by histamine, Group III was a melatonin-pretreated OME group, and Group IV was a methylprednisolone-pretreated OME group. In erythrocyte, plasma, and middle ear effusion samples, MDA levels were significantly increased in guinea pigs with OME (Group II), compared to controls (Group I); erythrocyte TSSA and SOD activities were lower and erythrocyte XO activity was increased in guinea pigs with OME (Group II) compared to controls (Group I). No significant differences were found in erythrocyte NSSA and CAT activities. In Group III, pretreatment of guinea pigs with i.p. melatonin at 1 hr prior to histamine induction of OME decreased the erythrocyte, plasma, and effusion MDA levels, compared to Group II; erythrocyte XO activity was diminished and erythrocyte TSSA, SOD, and CAT activities were increased in Group III compared to Group II. In Group IV, pretreatment of guinea pigs with i.p. methylprednisolone at 1 hr prior to histamine induction of OME decreased the plasma and effusion MDA levels and increased the erythrocyte TSSA and SOD activities, compared to Group II. These results suggest that reactive oxygen species (ROS) play a role in histamine-induced OME. Pretreatment with i.p. melatonin or methylprednisolone both decrease the ROS generated by experimental OME, but melatonin appears to be more effective than methylprednisolone.
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PMID:Protective effect of melatonin on experimental otitis media with effusion in guinea pigs. 1548 11

The role of oxygen-derived free radicals has been suggested in genesis of epilepsy and in the post seizure neuronal death. The aim of this study was to investigate whether erdosteine has a preventive effect against epilepsy and postepileptic oxidative stress. The mice (n=27) were divided into three groups: (i) PTZ-induced-epilepsy group (n=9); (ii) PTZ-induced-epilepsy+erdosteine group (n=9); (iii) control group (n=9). The animals were observed for a period of 30 min for latency to first seizure onset, total seizure duration, the number of seizure episodes. Then they were sacrificed and the brains were quickly removed, and frozen for biochemical analysis. Malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD) and xanthine oxidase (XO) activities were carried out in the brain tissue. The latent period between PTZ induction and seizure are longer in the PTZ+erdosteine group than in PTZ-induced-epilepsy group (P<0.05). Biochemical analyses of brain tissue, revealed a significant increase in the MDA, XO and NO levels in the PTZ group according to erdosteine group. SOD level did not change in this group. While MDA and XO levels are significantly lower, SOD level is significantly higher in the PTZ+erdosteine group compared to PTZ and control groups (P<0.01). The present study demonstrated that erdosteine treatment both may increase latent interval between seizures and may decrease oxidative stress, thus may ameliorate neuronal death in brain during seizures. It may be used as an adjunct therapy in epilepsy.
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PMID:Erdosteine ameliorates PTZ-induced oxidative stress in mice seizure model. 1586 21

Testicular torsion and detorsion are important clinical problems for infertile man and oxidative stress may have a role in this clinical situation. The aim of this study was to investigate the protective role of erdosteine, an antioxidant, on unilateral testicular reperfusion injury in rats. The rats were divided into four groups including seven rats in each group: control, torsion, torsion/detorsion and torsion/detorsion+erdosteine. Rats, except the sham operation group, were subjected to left unilateral torsion (720( composite function) rotation in the clockwise direction) without including the epididymis. The experiments were finished after sham operation time for control, 120 min torsion for torsion group and 120 min torsion and 240 min detorsion for torsion/detorsion groups. Bilateral orchiectomy was performed for all groups of rats. The ipsilateral and controlateral testis were divided into two pieces to analyse biochemical parameters and to investigate the light microscopic view. Malondialdehyde level of ipsilateral testis was increased in torsion and torsion/detorsion groups in comparison with the other groups (p < 0.05). Erdosteine treatment ameliorated lipid peroxidation after torsion/detorsion in ipsilateral testis (p < 0.05). Also, xanthine oxidase activity of ipsilateral testis was increased in torsion/detorsion group in comparison with the others (p < 0.05). Nitric oxide (NO) level of ipsilateral testis was higher in all experimental groups than sham operated control group (p < 0.05). Also, NO level of torsion group was increased in comparison with detorsion groups (p < 0.05). Erdosteine treatment caused increased glutathione peroxidase activity in comparison with torsion and torsion/detorsion groups and catalase activity in comparison with the other groups in ipsilateral testis (p < 0.05). Superoxide dismutase activity of ipsilateral testis was higher in torsion/detorsion and torsion/detorsion+erdosteine groups than control and torsion groups (p < 0.05). The biochemical parameters were not affected in controlateral testis in all groups. Torsion, torsion/detorsion and torsion/detorsion+erdosteine groups showed ipsilateral testicular damage in the histological examination, but the specimens from torsion/detorsion had a significantly greater histological injury than those from the other groups (p < 0.05). Control rats showed normal seminiferous tubule morphology. Rats in torsion group had slight-to-moderate disruption of the seminiferous epithelium. Rats in torsion/detorsion group displayed moderate-to-severe disruption of the seminiferous epithelium. In all animals from torsion/detorsion+erdosteine group, the testicular tissues were affected with slight-to-moderate degenerative changes of the seminiferous epithelium. Administration of erdosteine resulted in a significantly reduced histological damage associated with torsion of the spermatic cord compared with torsion/detorsion. In all groups, the contralateral testes were histologically normal. In conclusion, the results clearly displayed that erdosteine treatment may have a protective role on testicular torsion/detorsion injury.
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PMID:The protective role of erdosteine on testicular tissue after testicular torsion and detorsion. 1631 23

1. Increased oxidative stress has an important role in the pathogenesis of diabetic nephropathy. The aim of the present study was to evaluate diabetic nephropathy by determining markers of oxidative stress and the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), albumin and to investigate the possible protective effects of in vivo melatonin on renal tubular oxidative damage in diabetic rats. 2. Twenty-six rats were randomly divided into three groups: (i) group I, control, non-diabetic rats (n = 9); (ii) group II, untreated diabetic rats (n = 8); and (iii) group III, melatonin-treated diabetic rats (n = 9). In groups II and III, diabetes developed 3 days after administration of a single dose of streptozotocin (35 mg/kg, i.p.). Thereafter, whereas the rats in group II received no treatment, rats in group III began to receive 10 mg/kg per day, i.p., melatonin for 8 weeks. Malondialdehyde (MDA), an index of lipid peroxidation, NAG and microalbumin in the urine, markers of renal tubular damage, were the parameters used for oxidative stress-induced renal injury. Superoxide dismutase (SOD), xanthine oxidase (XO) and glutathione peroxidase (GSH-Px) activities were determined to evaluate changes in the anti-oxidant status of kidney tissue. 3. In untreated diabetic rats, urinary NAG, albumin and renal MDA levels were markedly increased compared with control rats (P < 0.0001). However, these parameters were reduced in diabetic rats by melatonin treatment (P < 0.0001). Urinary excretion of NAG was positively correlated with the microalbuminuria and renal MDA levels (r = 0.8; P < 0.0001). The SOD and XO activities in the untreated diabetic group were found to be significantly higher than those of the control group (P < 0.0001). Superoxide dismutase and XO activities decreased in melatonin-treated rats compared with untreated diabetic rats (P < 0.002 and P < 0.023, respectively). However, the decrease did reach levels seen in control rats. There were no significant differences in GSH-Px activity between the three groups. 4. Therefore, on the basis of these data, we suggest that urinary NAG, albumin excretion, XO activity and MDA levels are more valuable parameters showing the degree of renal tubular injury than classical markers of oxidative stress, including SOD and GSH-Px, in diabetic rat kidneys. Melatonin has an ameliorating effect on oxidative stress-induced renal tubular damage via its anti-oxidant properties. Thus, it may be suggested that urinary NAG excretion and microalbuminuria may be important markers showing the degree of renal changes and the success of long-term treatment of renal impairment with melatonin.
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PMID:Melatonin reduces urinary excretion of N-acetyl-beta-D-glucosaminidase, albumin and renal oxidative markers in diabetic rats. 1644 6

This study was carried out to determine if Ginkgo Biloba Extract (GBE or Egb 761) exerts a beneficial effect against cisplatin-induced renal failure in rats. Sprague Dawley rats were divided into four groups. The first group (control) received orally 1 mL/kg/day of 0.9% saline by an oral carrier vehicle on days 1 to 10. The second group was injected with 7 mg/kg cisplatin intraperitoneally (i.p.) on the fourth day, once only. The third group (vit E+cisplatin) was administered 10 mg/kg/day i.p. vit E on 1 to 10 days with one dose of i.p. cisplatin (7 mg/kg) injection on the fourth day. The fourth group (GBE+cisplatin) was given GBE orally at 100 mg/mL/kg started on the first day up to the tenth day with one dose of cisplatin (7 mg/kg) injection on the fourth day. Cisplatin was found to lead a statistically significant increase in plasma BUN and creatinine levels, as well as urine micro total protein (MTP) levels, leading to acute renal failure (ARF) in rats. Renal xanthine oxidase (XO) activities increased in all groups (statistically significant in cisplatin + GBE-treated rats; P < 0.001). Adenosine deaminase (AD) activities were increased in cisplatin-treated rats, and decreased in cisplatin+GBE-treated (P < 0.041) and cisplatin+vit E-treated (P < 0.005) rats, compared to controls. Malondialdehyde (MDA), nitric oxide (NO) levels and myeloperoxidase (MPO) activities were increased in the kidney tissue of cisplatin-treated rats. Vit E improved plasma creatinine and urine MTP levels, together with tissue MDA, NO levels, and MPO activities. But GBE had no statistically significant effect on those parameters. These results indicate that increased XO, AD and MPO activities, as well as MDA and NO levels play a critical role in cisplatin nephrotoxicity. GBE has been shown to protect against cisplatin-induced nephrotoxicity.
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PMID:The effects of ginkgo biloba extract on tissue adenosine deaminase, xanthine oxidase, myeloperoxidase, malondialdehyde, and nitric oxide in cisplatin-induced nephrotoxicity. 1671 42

Reperfusion injury causes oxidative stress thereby resulting in an imbalance between oxidant-antioxidant systems. In the present communication, the effect of ascorbic acid supplementation has been studied on certain oxidant and antioxidant parameters in the blood of the patients with myocardial infarction before and after thrombolysis. In patients after thrombolysis, the activity of antioxidant enzyme, superoxide dismutase, in the blood was found to be significantly reduced where as the activity of the oxidant enzyme, xanthine oxidase, was found to be significantly increased. Malondialdehyde levels, the index of free radical mediated damage, was also found to be significantly elevated in thrombolysed patients compared to the patients before thrombolysis. Supplementation of vitamin C to the post reperfusion patients restored these parameters back to normal or near normal levels.
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PMID:Effect of ascorbic acid supplementation on certain oxidative stress parameters in the post reperfusion patients of myocardial infarction. 1671 65

Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused by Escherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24 h, PYN 48 h, PYN 72 h, CAPE 24 h, CAPE 48 h and CAPE 72 h. E. coli (1 x 10(9) c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten microM/kg-body weight CAPE was injected to the rats in all CAPE groups 24 h before E. coli infection, and injections were repeated at 24-h intervals. Rats were sacrificed 24 h, 48 h and 72 h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated by E. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced by E. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy.
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PMID:Caffeic acid phenethyl ester suppresses oxidative stress in Escherichia coli-induced pyelonephritis in rats. 1705 18


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