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 clinical formulation of the i.v. anaesthetic propofol contains both the substrate for and inhibitor of lipid peroxidation. In these in vitro experiments we have investigated the importance of this potential conflict in a system where haemoglobin was oxidized by reactive oxygen species generated by hypoxanthine and xanthine oxidase. The presence of lipid in the system accelerated the rate of haemoglobin oxidation. Propofol inhibited lipid-induced acceleration but not the underlying rate of reactive oxygen species-induced oxidation. The rate of conjugated diene production, measured semi-quantitatively by ultraviolet absorption at 234 nm, was not reduced by propofol. Propofol may act by preventing haemoglobin oxidation by lipid hydroperoxides.
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PMID:Effect of lipid and propofol on oxidation of haemoglobin by reactive oxygen species. 913 15

We have studied the ability of propofol and Intralipid to inhibit reactive oxygen species generated either by stimulated human leucocytes or cell-free systems using luminol chemiluminescence. Human leucocytes were stimulated by a chemotactic peptide, FMLP 1 mumol litre-1, or by a phorbol ester, PMA (protein kinase C activator) 0.1 mumol litre-1. In cell-free experiments, superoxide-hydrogen peroxide, hypochlorous acid or hydroxyl radical-induced chemiluminescence responses were initiated by xanthine 0.1 mmol litre-1 with xanthine oxidase 10 mu. ml-1, NaOCl 70 mumol litre-1 and FeSO4 3 mumol litre-1, respectively. Propofol with Intralipid, and to a lesser degree Intralipid alone, produced a concentration-dependent reduction in chemiluminescence from stimulated leucocytes. Similar attenuations were also observed using propofol with Intralipid on xanthine with xanthine oxidase-, HOCl- and ferrous iron-induced chemiluminescence. However, Intralipid produced a reduction only at high concentrations. Intralipid produced marked decreases in ferrous iron-induced chemiluminescence. This study suggests that propofol had a direct scavenging activity against HOCl, superoxide-hydrogen peroxide and hydroxyl radical in the concentrations used. These direct scavenging effects may contribute to the effect of propofol on human leucocyte chemiluminescence.
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PMID:Propofol and intralipid interact with reactive oxygen species: a chemiluminescence study. 969 71

Surgical operations often induce acute hyperglycemia, which is known to affect endothelial functions. In this study, we examined the effects of propofol, a commonly used general anaesthetic, on bovine aortic endothelial cell (BAEC) dysfunction induced by glucose overload. 2 D-glucose overload (23 mM) induced an accumulation of superoxide anion (O2-), assessed by MCLA chemiluminescence, to a similar extent as that generated by 233 microU ml(-1) xanthine oxidase (XO) and 100 micro M xanthine. Propofol inhibited this accumulation with an IC50 of 0.21 micro M, whereas much higher concentrations of propofol were required to scavenge O2- generated by 250 microU ml(-1) XO and 100 microM xanthine (IC50: 13.5 micro M). 3 D-glucose overload attenuated ATP-induced NO production which was detected using diaminofluorescence-2 (DAF-2). The inhibition was reversed by propofol with an EC50 of 0.60 microM. In contrast, inhibitions caused by xanthine/XO were not altered by propofol (1 microM). 4 D-glucose overload suppressed ATP-induced Ca2+ oscillations and capacitative Ca2+ entry (CCE), which were both restored by superoxide dismutase, indicating that O2- was responsible. Propofol restored these attenuated Ca2+ oscillations and CCE with EC50 of 0.31 and 1.0 microM, respectively. 5 D-glucose overload (23 mM) increased the intracellular glucose concentration 4 fold, compared with cells exposed to 5.75 mM glucose, and 1 micro M propofol reduced this increase to 2.8 fold. 6 We conclude from these results that anaesthetic concentrations of propofol prevent the impairment of Ca2+-dependent NO production in BAEC induced by glucose overload. This effect is mainly due to the reduction of O2- accumulation, and involves, at least in part, the inhibition of cellular glucose uptake.
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PMID:Propofol prevents endothelial dysfunction induced by glucose overload. 1238 82

Propofol, which is widely used as an intravenous anesthetic, has been shown to have an antioxidant activity on several tissues. This study was designed to investigate the prevention of reperfusion injury with propofol after testicular torsion. Five groups of rats (seven in each group) were used. Animals in the control group (group I) did not received any treatment, while animals in the sham group (group II) underwent scrotal incision and testicular fixation only. After 2 h of 720 degrees left testicular torsion in groups III, IV and V, subsequent detorsion was done for 2 h in groups IV and V. Propofol (50 mg/kg) was injected transperitoneally 30 min prior to detorsion in group V. Both testicles in all rats were retrieved and tissue malondialdeyhde (MDA) level, which is a measure of the amount of free oxygen radicals, and enzymatic activity of xanthine oxidase (XO), which converts hypoxanthine to xanthine and uric acid were studied. In addition, tissue catalase (CAT) and glutathione peroxidase (GSH-Px) activities, which are endogenous scavenger enzymes, protecting tissues against free radicals, were studied. Additionally, histological evaluations were performed after hematoxylin and eosin staining. Testicular MDA levels, and XO and CAT activities were higher in the torsion group compared to sham control group (P<0.05). Detorsion caused a further increase in MDA levels, contrasting with a decrease in the levels of XO activity, while CAT activity was not changed. Pretreatment with propofol prevented a further increase in MDA levels and significantly decreased CAT activity following detorsion. GSH-Px activities were not effected either by torsion/detorsion or propofol pretreatment. Histologically, torsion caused some separation between germinal cells in the seminiferous tubules, which became much more prominent in the detorsion group and attenuated with propofol pretreatment. There was no significant change in any of the above-mentioned enzymatic activities nor were there histopathological changes in the contralateral testicle in any groups. It is concluded that biochemically and histologically reperfusion injury occurs in the ipsilateral testis following detorsion up to 2 h. Preference of propofol for anaesthesia during the detorsion procedure may attenuate such reperfusion injury.
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PMID:Propofol attenuates reperfusion injury after testicular torsion and detorsion. 1558 May 8

Reactive oxygen species play a role during brain injury due to closed head trauma. Enzymatic or nonenzymatic antioxidants may protect brain tissue against oxidative damage. The present study was performed to assess the changes of endogenous indices of oxidative stress in serum from rats subjected to head trauma and whether treatment with propofol and/or erythropoietin (EPO) modifies the levels of endogenous indices of oxidative stress. For these purposes, female Wistar Albino rats were divided into five groups: non-traumatic sham group, trauma performed control, trauma with propofol (i.p.), trauma with EPO (i.p.) and trauma with propofol and EPO performed study groups. At the end of the experimental procedure, blood was taken by cardiac puncture to determine superoxide dismutase (SOD) and xanthine oxidase (XO) activities as well as malondialdehyde (MDA) and nitric oxide (NO) levels in serum. Serum MDA level of control traumatic brain injury (TBI) group was significantly higher than sham operation group (p<0.012). Serum MDA levels in propofol, EPO and propofol+EPO groups were found to be decreased in comparison with control group (p<0.039, p<0.030 and p<0.018, respectively). Serum NO level was found to be increased in TBI group, but difference was not statistically significant when compared to sham-operated group (p=0.092). Propofol, EPO and propofol+EPO administration efficiently reduced serum NO levels to reach sham-operated group (p<0.002, p<0.001 and p<0.015, respectively). These results suggested that acute administration of both propofol and EPO altered the indices of oxidative stress similarly against brain injury due to trauma.
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PMID:Antioxidant properties of propofol and erythropoietin after closed head injury in rats. 1597 43

So far, several treatment modalities have been attempted to brain protection in cases such as brain trauma, stroke or brain hemorrhage. However, a treatment method that the effect begins immediately and definitely helpful has not been discovered yet. In this study, we aimed to compare the effects of propofol and erythropoietin (Epo) on brain injury caused by oxidative stress and antioxidant properties of these agents after closed head injury (CHI) in rats. For this study, female Wistar Albino rats were divided into five groups: non-traumatic control group, trauma performed group CHI, trauma with propofol (100 mg/kg) intraperitoneally (i.p.), trauma with Epo (5000 U/kg) i.p. and trauma with propofol and Epo performed study groups. Twenty-four hours after CHI, rats were sacrificed and the brains were removed. Superoxide dismutase (SOD), catalase (CAT), xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA) levels were measured in brain tissue. MDA and NO levels were decreased significantly in Groups Epo, Propofol and Epo+Propofol than Group CHI (p<0.01). XO activity was significantly lower in Group Epo than Group CHI (p<0.05). Epo and propofol decreased oxidative stress by decreasing MDA and NO level in brain tissue after CHI. However, combination of Epo and propofol has no significant beneficial advantage than Epo or propofol alone.
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PMID:Propofol and erythropoietin antioxidant properties in rat brain injured tissue. 1776 98