Antioxidants, Free Radicals Scavenging and Xanthine Oxidase Inhibitory Potentials of Ajuga iva L. Extracts.

2011 ◽  
Vol 1 (4) ◽  
pp. 21-30 ◽  
Author(s):  
Abderrahmane Baghiani ◽  
Sabah Boumerfeg ◽  
Moufida Adjadj ◽  
Djamila Ameni ◽  
Meriem Djermouni ◽  
...  
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Free Radicals Scavenging

Free radicals in hypoxic rat diaphragm contractility: no role for xanthine oxidase

2001 ◽  
Vol 281 (6) ◽  
pp. L1402-L1412 ◽  
Author(s):  
Leo M. A. Heunks ◽  
Herwin A. Machiels ◽  
Ronney de Abreu ◽  
Xiao Ping Zhu ◽  
Henricus F. M. van der Heijden ◽  
...  
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Power Output ◽  
Harmful Effect ◽  
Force Generation ◽  
Muscle Performance ◽  
Rat Diaphragm ◽  
Shortening Velocity ◽  
Contraction Pattern

Recent evidence indicates that hypoxia enhances the generation of oxidants. Little is known about the role of free radicals in contractility of the rat diaphragm during hypoxia. We hypothesized that antioxidants improve contractility of the hypoxic rat diaphragm and that xanthine oxidase (XO) is an important source of free radicals in the hypoxic diaphragm. The effects of N-acetylcysteine (NAC; 18 mM), Tiron (10 mM), and the XO inhibitor allopurinol (250 μM) were studied on isometric and isotonic force generation during hypoxia (Po 2 ∼7 kPa). NAC and Tiron decreased maximal force generation, slowed the shortening velocity, and decreased the power output. Fatigue rate was decreased in the presence of either NAC or Tiron. Allopurinol did not alter the contractility or fatigability of the diaphragm. During hyperoxia (Po 2 ∼85 kPa), neither NAC nor allopurinol affected the contractility or fatigability of the diaphragm. Thus free radicals play a significant role in diaphragm contractility during hypoxia. Whether antioxidants exert a beneficial or harmful effect on muscle performance depends on the contraction pattern of the muscle. Free radicals generated by XO do not play a role in diaphragm contractility during either hypoxia or hyperoxia.

Xanthine oxidase is not a major source of free radicals in focal cerebral ischemia

1991 ◽  
Vol 260 (2) ◽  
pp. H563-H568 ◽  
Author(s):  
A. L. Betz ◽  
J. Randall ◽  
D. Martz
Keyword(s):  
Uric Acid ◽  
Free Radicals ◽  
Cerebral Ischemia ◽  
Xanthine Oxidase ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Total Activity ◽  
Brain Regions ◽  
Free Radical Scavengers ◽  
Edema Formation

Xanthine oxidase (XO) has been proposed as an important source of free radicals during ischemia. This enzyme normally exists as a dehydrogenase (XD), but it is converted to XO in some ischemic tissues. Recently, treatment of animals with the XD and XO inhibitor allopurinol or with free radical scavengers before cerebral ischemia has been shown to reduce brain injury. Therefore, we studied conversion of XD to XO in three ischemic and nonischemic brain regions during focal cerebral ischemia resulting from permanent occlusion of the middle cerebral artery (MCAO) in anesthetized rats. In nonischemic brain, 16-22% of the enzyme was in the XO form. After 24 h of ischemia this value was not significantly different (10-15%). Neither the total activity of XO nor that of XD changed, indicating that there was no irreversible conversion of XD to XO. To further explore the possible role of XO, we examined the effect of various doses of allopurinol (5, 20, or 100 mg/kg given 1 h before MCAO or 100 mg/kg given 48, 24, and 1 h before MCAO) on uric acid accumulation, brain edema formation, and cerebral blood flow (CBF) 24 h after MCAO. All but the lowest dose of allopurinol greatly reduced the appearance of uric acid in the ischemic brain; however, only the highest dose of allopurinol had any beneficial effect on brain edema. This reduction in brain edema occurred without a significant improvement in CBF. Thus XO is probably not an important source of free radicals in this model of focal cerebral ischemia.

Blockade of platelet-mediated relaxation in rat aortic rings exposed to xanthine-xanthine oxidase

1994 ◽  
Vol 266 (6) ◽  
pp. H2212-H2219 ◽  
Author(s):  
B. C. Yang ◽  
S. Khan ◽  
J. L. Mehta
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Hydroxyl Radicals ◽  
Vascular Tone ◽  
Oxygen Free Radicals ◽  
Ischemia Reperfusion ◽  
Arterial Occlusion ◽  
Superoxide Anions ◽  
Vascular Tissues ◽  
Hydroxyl Radical Scavengers

Platelet-induced relaxation of endothelium-intact vascular tissues, mediated via release of endothelium-derived relaxing factor (EDRF), is diminished or lost after ischemia and reperfusion. Release of oxygen free radicals during ischemia-reperfusion may degrade EDRF and influence response of vascular tissues to platelets. To determine platelet modulation of tone of blood vessels treated with oxygen free radicals, rat aortic rings with intact endothelium were exposed to xanthine (X) plus xanthine oxidase (XO) 5 min before contraction with norepinephrine followed by exposure of rings to platelets. Treatment of aortic rings with X+XO caused a modest contraction, potentiated norepinephrine-mediated contraction, and inhibited platelet-mediated vasorelaxation. Exposure of aortic rings to X+XO also decreased ADP- as well as acetylcholine-mediated relaxation. Pretreatment of rings with superoxide dismutase or catalase did not change X+XO-induced inhibition of platelet-mediated relaxation, but it abolished the X+XO-induced contraction of rings as well as subsequent potentiation of norepinephrine-mediated contraction. Pretreatment of rings with hydroxyl radical scavengers dimethyl-2-thiourea, dimethyl sulfoxide, mannitol, or histidine attenuated the X+XO-induced inhibition of platelet-mediated relaxation, although these agents did not affect X+XO-induced contraction of rings. This study indicates that the vasoconstriction on exposure of aortic rings to X+XO is due to generation of superoxide anions, whereas inhibition of platelet-mediated relaxation after exposure of vessels to X+XO is due, at least in part, to release of hydroxyl radicals. Release of superoxide anions and hydroxyl radicals after temporary arterial occlusion may be the basis of subsequent modulation of vascular tone.

scholarly journals The superoxide-dependent transfer of iron from ferritin to transferrin and lactoferrin

1988 ◽  
Vol 256 (3) ◽  
pp. 923-928 ◽  
Author(s):  
H P Monteiro ◽  
C C Winterbourn
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Xanthine Oxidase ◽  
Binding Protein ◽  
Gel Filtration ◽  
Iron Binding ◽  
Oxidase System ◽  
Oxidative Reactions ◽  
Phospholipid Liposomes ◽  
Iron Binding Protein

By the use of gel filtration and [59Fe]ferritin, apotransferrin and apolactoferrin were shown to take up iron released from ferritin by superoxide generated by hypoxanthine and xanthine oxidase. Apotransferrin also inhibited uptake of released iron by ferrozine. Ferritin and the xanthine oxidase system induced lipid peroxidation in phospholipid liposomes. This peroxidation was inhibited by apotransferrin or apolactoferrin. Thus, although superoxide and other free radicals can release iron from ferritin, either iron-binding protein, if present, should take up this iron and prevent its catalysing subsequent oxidative reactions.

Modification of cardiac adrenergic receptors by oxygen free radicals

1991 ◽  
Vol 260 (3) ◽  
pp. H821-H826 ◽  
Author(s):  
M. Kaneko ◽  
D. C. Chapman ◽  
P. K. Ganguly ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Oxygen Free Radicals ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Cgp 12177 ◽  
Number Of Binding Sites

To examine the effects of oxygen free radicals on alpha- and beta-adrenergic receptors, rat heart crude membranes were incubated with xanthine plus xanthine oxidase, H2O2, or H2O2 plus Fe2+. The assay of beta-adrenergic receptors involving [3H]dihydroalprenolol (DHA) binding revealed that the maximal number of binding sites (Bmax) and dissociation constant (Kd) were increased by xanthine plus xanthine oxidase. H2O2 increased the Kd value for [3H]DHA binding. When a hydrophilic ligand, [3H]CGP-12177, was used for the beta-adrenergic receptor assay, an increase in Kd value without any changes in Bmax value was evident on treating the membranes with xanthine plus xanthine oxidase. The assay of alpha-adrenergic receptors involving [3H]prazosin binding showed a decrease in the number of binding sites and an increase in Kd value only after a prolonged period of incubation. Both H2O2 and H2O2 plus Fe2+ increased the Kd value for [3H]prazosin without changes in Bmax. Changes in both alpha- and beta-adrenergic receptors similar to those with crude membranes were also seen by employing the purified heart sarcolemmal membranes. These data indicate that adrenergic receptors in the sarcolemmal membranes are modified by oxygen free radicals.

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