Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.17.3.2 (xanthine oxidase)
8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have evaluated the abilities of ferulic acid, (+/-) catechin, (+) catechin and (-) epicatechin to scavenge the reactive oxygen species hydroxyl radical (OH.), hypochlorous acid (HOCl) and peroxyl radicals (RO2.). Ferulic acid tested at concentrations up to 5 mM inhibited the peroxidation of phospholipid liposomes. Both (+/-) and (+) catechin and (-) epicatechin were much more effective. All the compounds tested reacted with trichloromethyl peroxyl radical (CCl3 O2.) with rate constants > 1 x 10(6) M-1 s-1. A mixture of FeCl3-EDTA, hydrogen peroxide (H2O2) and ascorbic acid at pH 7.4, has often been used to generate hydroxyl radicals (OH.) which are detected by their ability to cause damage to the sugar deoxyribose. Ferulic acid, (+) and (+/-) catechin and (-) epicatechin inhibited deoxyribose damage by reacting with OH. with rate constants of 4.5 x 10(9)M-1 s-1, 3.65 x 10(9) M-1 s-1, 2.36 x 10(9) M-1 s-1 and 2.84 x 10(9) M-1 s-1 respectively. (-) Epicatechin, ferulic acid and the (+) and (+/-) catechins exerted pro-oxidant action, accelerating damage to DNA in the presence of a bleomycin-iron complex. On a molar basis, ferulic acid was less effective in causing damage to DNA compared with the catechins. A mixture of hypoxanthine and xanthine oxidase generates O2-. which reduces cytochrome c to ferrocytochrome c. (+) Catechin and (-) epicatechin inhibited the reduction of cytochrome c in a concentration dependent manner. Ferulic acid and (+/-) catechin had only weak effects. All the compounds tested were able to scavenge hypochlorous acid at a rate sufficient to protect alpha-1-antiproteinase against inactivation. Our results show that catechins and ferulic acid possess antioxidant properties. This may become important given the current search for "natural" replacements for synthetic antioxidant food additives.
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PMID:Evaluation of the antioxidant actions of ferulic acid and catechins. 750 56

The free radical scavenging effect of "beta catechin", an antioxidant preparation containing green tea extract, ascorbic acid, sunflower seed extract, dunaliella carotene and natural vitamin E, was evaluated. Two techniques were used: electron spin resonance (ESR) spectrometry to measure radical-scavenging activity, and measurement of its effect on iron-induced lipid peroxidation in brain. A 0.05% solution of "beta catechin" completely scavenged 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals (6.1 x 10(15)spins/ml). A 10% solution of "beta catechin" completely scavenged superoxide (4.2 x 10(15) spins/ml) generated by the hypoxanthine-xanthine oxidase system. An undiluted solution of "beta catechin" scavenged about 90% of hydroxyl radicals (3.5 x 10(15) spins/ml) generated by the Fenton reaction. "beta catechin"s effect on the accumulation of thiobarbituric acid-reactive substances (TBARS) was evaluated from tissue obtained from the ipsilateral cortex of FeCl3-induced epileptic rats. Oral administration of "beta catechin" (1 or 2ml/kg body weight) both inhibited TBARS formation and increased the activity of superoxide dismutase (SOD) in the ipsilateral cortex 30 min after iron-salt injection into the left sensory motor cortex. These data suggest that "beta catechin" has an antioxidant effect and may have a prophylactic effect against aging and other neurological diseases related to free radical mechanisms.
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PMID:Antioxidant effects of "beta catechin". 754 42

Intracortical injection of iron ions has been used as a model of posttraumatic epilepsy. Oxidation of lipids in neural membranes by reactive oxygen species, especially hydroxyl radicals (OH), is involved in the mechanisms responsible for iron-induced seizures. We examined the scavenging effects of adenosine (Ado) and 2-chloroadenosine (Cl-Ado) on OH radicals and superoxide (O2.-) using an electron spin resonance (ESR) spectrometer, and the occurrence of epileptic discharges in electrocorticogram (ECoG) induced by FeCl3 injection into the sensorimotor cortex of rats. Though DMPO-O2.- spin adducts generated by the hypoxanthine-xanthine oxidase system were not quenched by Ado or Cl-Ado, 5 mM of each showed a quenching effect on DMPO-OH spin adducts (5.3 x 10(16) spins/ml) generated by the Fenton reagent. In ECoG of rats, spike discharges appeared 15-45 min after FeCl3 injection (500 nmol) into the sensorimotor cortex, and polyspikes and/or ictal patterns were observed 70-90 min after the injection. Cl-Ado (1 mg/kg) or Ado (5 mg/kg) injected intraperitoneally 30 min prior to the FeCl3 injection suppressed or delayed the occurrence of epileptic discharges induced by FeCl3. Cl-Ado and Ado may suppress the occurrence of epileptic discharges by scavenging OH and by their anticonvulsant effect.
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PMID:Adenosines scavenged hydroxyl radicals and prevented posttraumatic epilepsy. 759 Mar 96

Lipid peroxidation (LPO) is the oxidative deterioration of polyunsaturated fatty acids (PUFA) with the production of lipid hydroperoxides, cyclic peroxides, cyclic endoperoxides, and finally fragmentation to ketones and aldehydes (including malonaldehyde, MDA). Estimation of LPO through MDA formation measured by assaying thiobarbituric acid (TBA) reactive products remains the method of choice to study the development of oxidative stress in tissues. However, MDA estimation by TBA reactive products is non-specific and often gives erroneous results. In this report we describe a method using high-performance liquid chromatographic separation to estimate MDA, formaldehyde (FDA), acetaldehyde (ADA), acetone, and propionaldehyde (PDA), the degradation products of oxygen-derived free radicals (ODFR) and PUFA, as presumptive markers for LPO. Oxidative stress was induced in the tissue by perfusing an isolated rat heart with hydroxyl radical generating system (xanthine + xanthine oxidase + FeCl3 + EDTA). The coronary effluents were collected, derivatized with 2,4-dinitrophenylhydrazine (DNPH), and extracted with pentane. Aliquots of 25 microliters in acetonitrile were injected onto a Beckman Ultrasphere C18 (3 microns) column. The products were eluted isocratically with a mobile phase containing acetonitrile-water-acetic acid (40:60:0.1, v/v/v), measured at three different wavelengths (307, 325 and 356 nm) using a Waters M-490 multichannel UV detector and collected for gas chromatography-mass spectrometry (GC-MS) analysis. The peaks were identified by cochromatography with DNPH derivatives of authentic standards, peak addition, UV pattern of absorption at the three wavelengths, and by GC-MS. The retention items of MDA, FDA, ADA, acetone, and PDA were 5.3, 6.6, 10.3, 16.5, and 20.5 min, respectively. The results of our study indicated progressive increase of all five lipid metabolites as a function of the duration of ODFR perfusion. Hydroxyl radical scavengers, superoxide dismutase plus catalase, completely inhibited the formation of these lipid metabolites, demonstrating that the release of lipid metabolites from the isolated heart was indeed in response to oxidative stress. Since MDA, FDA, ADA, acetone, and PDA are the products of ODFR-PUFA interactions, this method allows proper estimation of LPO which monitors the oxidative stress developed during the reperfusion of ischemic myocardium.
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PMID:High-performance liquid chromatographic method for the simultaneous detection of malonaldehyde, acetaldehyde, formaldehyde, acetone and propionaldehyde to monitor the oxidative stress in heart. 813 6

Previous studies have shown that myocardial membranes, isolated from ischemic myocardial tissue, showed marked changes in microviscosity. To evaluate the contribution of free radical production and concomitant lipid peroxidation to these changes in microviscosity, the in vitro effects of two radical producing systems (H2O2/FeCl2 and xanthine oxidase/hypoxanthine/FeCl3) were investigated separately on the microviscosity of sarcolemmal, mitochondrial and sarcoplasmic reticulum membranes. In all three membranes both these free radical producing systems caused formation of malondialdehyde as quantitated by the thiobarbituric acid test. The sensitivity of the membranes to free radical damage differed: the sarcolemma was more sensitive to H2O2 damage, while mitochondrial malondialdehyde production was highest with xanthine oxidase. H2O2/FeCl2 caused a reduction in microviscosity (i.e. increased fluidity) of all three membranes, whereas the xanthine oxidase system increased mitochondrial and sarcolemmal microviscosity and reduced that of the sarcoplasmic reticulum. The similarity between ischemia-induced membrane microviscosity changes and those induced in vitro by xanthine oxidase, indicate a possible causal role for superoxide and hydroxyl free radicals produced during ischemia.
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PMID:Free radical effects on myocardial membrane microviscosity. 829 62

We have screened a number of plants from the Indian soil for potential antioxidant properties out of which fifteen extracts were found to be positive. Leaves/bulk from the plants were crushed and extracted with organic solvents by three different ways. The first group of plants were extracted with CHCL3:CH3OH (2:1), evaporated, partitioned between petroleum ether and methanol (9:1), aqueous methanolic part re-partitioned between methanol:H2O (4:1) and dichloromethane. Methanol was evaporated from the aqueous methanolic part and extracted with n-butanol. The second group of plants were extracted with methanol followed by partitioning between petroleum ether and CH3OH. The rest of the extraction procedure was the same as above. A third extraction procedure was used for Ocimum sanctum which after extraction with CHCL3:CH3OH (2:1), partitioned between CCL4 and CH3OH:H2O (9:1). Aqueous methanolic part was repartitioned between CH3OH:H2O (4:1) and CHCl3 and CHCl3 soluble part was used for the study. Free radical scavenging activities of the plant extracts were examined by chemiluminescence method. Peroxyl radical was generated from 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH), superoxide radical (O2-) from xanthine/xanthine oxidase (XO) and hydroxyl radical (OH) from Xanthine/XO/FeCl3/ EDTA. In addition, O2- and OH. scavenging activities were also determined by cytochrome C reduction and deoxyribose oxidation methods, respectively. The results of this study demonstrate that these plant extracts possess potent antioxidant activities.
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PMID:Evaluation of antioxidant effectiveness of a few herbal plants. 935 Apr 26

We have previously shown that surfactant protein A (SP-A) mediates in vitro killing of mycoplasmas by alveolar macrophages (AMs) from resistant C57BL/6 mice through a nitric oxide (.NO)-dependent mechanism. Herein, SP-A-deficient [SP-A(-/-)] and inducible.NO synthase-deficient [iNOS(-/-)] mice were infected intranasally with 10(5) or 10(7) colony-forming units of Mycoplasma pulmonis. SP-A(-/-) mice were as susceptible to mycoplasmal infection as highly susceptible C3H/He mice, and far more susceptible than resistant C57BL/6 mice. iNOS(-/-) mice had significantly greater numbers of mycoplasmas and severity of lung lesions than iNOS(+/+) controls. In vitro, AMs isolated from C57BL/6 mice, activated with IFN-gamma, incubated with SP-A (25 micrograms/ml), and infected with 10(10) colony-forming units of M. pulmonis, killed mycoplasmas within 6 h. Mycoplasmal killing was abrogated by 1,000 units/ml of copper-zinc superoxide dismutase. In the absence of AMs, incubation of M. pulmonis with the peroxynitrite generator 3-morpholinosynodiomine.HCl (SIN-1) effected complete killing of mycoplasmas by 90 min in a dose-dependent manner. Addition of copper-zinc superoxide dismutase (3,000 units/ml), which converts SIN-1 to a.NO donor, prevented this killing. Neither of the reactive oxygen species generated by xanthine oxidase (10 milliunits/ml, plus 500 microM xanthine and 100 microM FeCl3), nor.NO generated by 1-propanamine-3-(2-hydroxy-2-nitroso-1-propylhydrazine (PAPA NONOate) (100 microM) killed mycoplasmas. These data establish that peroxynitrite generation by AMs is necessary for the killing of a pathogen in vitro and in vivo.
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PMID:Surfactant protein A mediates mycoplasmacidal activity of alveolar macrophages by production of peroxynitrite. 1022 Apr

Formocresol has long been used for pulpotomy of primary teeth and as an intracanal medicament. Little is known, however, about the pharmacological effect of tricresols. This study showed that three cresol isomers, o-cresol, m-cresol and p-cresol, are H2O2 scavengers with a 50% inhibitory concentration (IC50) of 502, 6.7 and 10.16 microM, respectively. o-, m- and p-cresol were also shown to be effective scavengers of superoxide radicals generated by xanthine/xanthine oxidase with an IC50 of 282, 153 and > 4000 microM, respectively, as analyzed by luminometer. o-, m- and p-cresol showed protective effects on the DNA breaks generated by H2O2/FeCl2 and FeCl3/ascorbate/H2O2 systems at concentrations ranging from 70 microM to 1.43 mM, o-, m- and p-cresol also showed differential protective effects against DNA breaks induced by 0.17% NaOCl with 100% inhibitory concentration (IC100) of about 10, 1 and 10 mM, respectively. In addition, reaction with 3% H2O2 and 0.17% NaOCl completely prevented NaOCl-induced DNA breaks. The results indicate that the three cresol isomers are effective ROS scavengers and may prevent ROS induced damage when used as pulpotomy agents or as intracanal medicaments. Owing to the difference in the position of the functional hydroxyl group in the three cresol isomers, m-cresol is the most effective ROS scavenger. Concomitant use of H2O2 for root canal irrigation may diminish both the tissue dissolving capacity of NaOCl and NaOCl-induced DNA damage.
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PMID:Scavenging property of three cresol isomers against H2O2, hypochlorite, superoxide and hydroxyl radicals. 1238 2


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