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:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Free oxygen radicals (F.O.R.) belong to a very aggressive chemical species derived from molecular oxygen. Their role in inflammation is well established and Polymorphonuclear neutrophils (PMNS) make use of them as antibacterial weapons. Their role has been experimentally demonstrated in numerous ischemia-reperfusion models. Free radical scavengers such as the superoxide dismutase, allopurinol or desferrioxamine can prevent the occurrence of lesions. The essential role of PMNS in these models is demonstrated by the fact that previous depletion of the animal in PMNS also prevents such lesions. Histologically, in these ischemia-reperfusion models, PMNS infiltration may be quantified by assay of myeloperoxidase. In experimental models of inflammatory colitis (acetic acid, bacterial polysaccharides) intestinal wall infiltration by PMNS is a fundamental phenomenon and is also a characteristic of Crohn's disease and exacerbations of Ulcerative Colitis. Thus, it is probable in both disorders that F.O.R. play an important role since steroids inhibit their secretion by PMNS and 5-aminosalicylic acid has been shown to be a F.O.R. scavenger.
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PMID:[Oxygen free radicals and inflammatory diseases of intestines]. 254 36

To determine if inhibition of leukocyte adhesion and aggregation could improve postischemic ventricular dysfunction ("stunning"), a monoclonal antibody (904) that binds to the adhesion-promoting Mo1 glycoprotein on the cell surface of leukocytes was administered intravenously (0.5 mg/kg) to open-chest dogs before a 15-minute coronary occlusion. Ultrasonic crystals placed in ischemic and control myocardium were used to measure systolic wall thickening during a 15-minute occlusion of the left anterior descending artery and for 3 hours after reperfusion. Myocardial blood flow was measured with tracer-labeled microspheres before occlusion, after 10 minutes of occlusion, 3 minutes of reperfusion, and at 1 and 3 hours after reperfusion. Six animals receiving anti-Mo1 antibody had antibody excess demonstrated with immunofluorescence techniques at 5 minutes and 3 hours of reperfusion; this finding indicated saturation of binding sites. Five animals served as controls and received an antibody (murine immunoglobulin G) that does not influence neutrophils. The two groups did not differ hemodynamically during ischemia and reperfusion. Risk areas and myocardial blood flow were also not significantly different between the two groups. The main parameter used to define regional myocardial stunning, percentage systolic wall thickening in the ischemic/reperfused area, did not differ significantly between the two groups. Specimens from nonischemic myocardium were compared with ischemic specimens for myeloperoxidase content. There were no significant differences within or between groups. These data indicate that the anti-Mo1 monoclonal antibody (904) is not effective in improving the profound myocardial dysfunction that persists for 3 hours of reperfusion after 15 minutes of ischemia.
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PMID:F(ab')2 fragments of anti-Mo1 (904) monoclonal antibodies do not prevent myocardial stunning. 255 27

We have examined how a Ginkgo biloba extract influences the damaging effects of ischaemia in the small-intestinal mucosa. We used a rat experimental model in which a ligated loop of the distal ileum was subjected to ischaemia and revascularization, and the ensuing mucosal damage assessed by lysosomal enzyme release and intestinal permeability measurements. We also determined the mucosal content of malondialdehyde, a lipid peroxidation product, and the mucosal activity of myeloperoxidase, a neutrophil granulocyte marker. Ischaemia and revascularization alone caused increased mucosal permeability to sodium fluorescein, increased N-acetyl-beta-glucosaminidase release from the mucosa into the lumen, increased malondialdehyde content in the mucosa, and increased myeloperoxidase activity in the mucosa. Intravenous injection of G. biloba extract caused a dose-dependent attenuation of all these effects of ischaemia. It is suggested, therefore, that G. biloba extract may protect the intestinal mucosa against ischaemic damage by reducing neutrophil infiltration and lipid peroxidation.
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PMID:Ginkgo biloba extract prevents mucosal damage associated with small-intestinal ischaemia. 255 86

This study was designed to determine whether oxygen-derived free radicals play a role in the pathogenesis of gastric lesions produced by hemorrhagic shock in the rat. Allopurinol (Zyloric), an inhibitor of xanthine oxidase (responsible for the formation of superoxide radicals) and MTDQ-DA (Kontrad), a synthetic antioxidant of dihydroquinoline type were used. In the anesthetized rat 0.1 N HCl was instilled into the stomach and the rat was bled to reduce the blood pressure to 30 mmHg for 20 min. The blood shed was retransfused. Twenty min later the stomach was removed. The area of gastric mucosal lesions were measured, the activity of endogenous peroxidase was examined histochemically and a histological grading was made. Both allopurinol and MTDQ-DA significantly protected against hemorrhagic shock-induced gastric lesions and peroxidation. These results suggest that oxygen-derived free radicals play an important role in the formation of gastric lesions produced by ischemia plus 0.1 N HCl.
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PMID:Role of oxygen-derived free radicals in hemorrhagic shock-induced gastric lesions of rats. 259 23

Small mesenteric arteries supplying partially isolated jejunal segments were totally occluded for 5 minutes and then released. With video microscopy, blood flow was calculated from measurements of submucosal arteriolar diameter and red blood cell velocity. For the first 30 minutes of reperfusion, the serosa was superfused with a Ringer's vehicle containing either adenosine (ADO; 10(-4) M), acetylcholine (ACh; 10(-5) M), or prostacyclin (PGI2; 3 x 10(-7) M). Thereafter, the substances were removed from the suffusate, and superfusion continued with vehicle alone for an additional 10-30 minutes. These concentrations were equieffective for causing vasodilation. During the first minute of reperfusion, blood flow increased more than 300% of baseline in all groups. Within the subsequent 30 minutes, blood flow fell to 45 +/- 3% of baseline with vehicle alone, which demonstrates the no-reflow phenomenon. While either ADO, ACh, or PGI2 was in the suffusate, vasodilation was persistent. After washout of these substances, the postocclusion blood flows were significantly higher with each treatment than with vehicle alone, which shows that each substance had a positive action. However, with ADO, blood flow was 121 +/- 7% of baseline after washout, whereas with ACh or PGI2, it was 64 +/- 10% or 69 +/- 5% of baseline after washout. This property of ADO was observed if the mucosa was superfused with a Ringer's solution or with a bile salt solution, which suggests that ADO might have similar properties in situ. After 60 minutes of reperfusion, the intestinal villi were short, thick, and edematous with epithelial necrosis and crypt degeneration. ADO attenuated most of these histological changes to a greater extent than either PGI2 or ACh. Furthermore, ADO reduced a biochemical index of neutrophil infiltration; tissue myeloperoxidase concentration was increased to 169 +/- 14% of baseline with vehicle but was increased to 120 +/- 8% with ADO. Overall, these observations suggest that ADO protects the intestine from ischemia-reperfusion injury by causing vasodilation and by inhibiting neutrophil function. The vasodilatory effect probably is a minor component because other vasodilators (ACh and PGI2) had minimal protective effects in these conditions.
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PMID:Attenuation of no-reflow phenomenon, neutrophil activation, and reperfusion injury in intestinal microcirculation by topical adenosine. 266 71

Previous studies showed the beneficial effects of superoxide dismutase +/- catalase in perfusion-preserved rabbit kidneys but failed to show benefit in flush-cooled organs. The current studies undertook to evaluate scavengers, xanthine oxidase inhibitors, and agents that prevent the release of myeloperoxidase in 3 systems: kidneys preserved by perfusion or by flush cooling for 24 hr, studied immediately, and warm ischemia-injured kidneys evaluated after a 24-hr recovery period. In none of these groups could we demonstrate any protective effects against preservational or warm ischemic injury by the above modalities. Even though biochemical and other evidence from previous studies suggested free radical-induced injury to occur in preserved rabbit kidneys, these studies using renal function as the indicator did not do so.
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PMID:Lack of effect of oxygen-radical scavenging systems in the preserved reperfused rabbit kidney. 267 97

Intestinal ischemia-reperfusion injury is a common and important clinical event associated with the activation of an endogenous inflammatory response. Some of the mediators of this response may be involved in the pathogenesis of multiple organ system failure. The purpose of this study was to determine whether remote organ dysfunction--specifically, acute lung injury--occurs after intestinal ischemia-reperfusion injury. After an ischemia-reperfusion event in rat intestine, whole lungs were obtained for measurement of tissue adenosine triphosphate (ATP) and myeloperoxidase values, and evaluation of histologic condition. In addition, lung microvascular permeability was assessed by determination of the rate at which iodine 125-labeled bovine serum albumin sequestration in the extravascular compartment occurred. Lung tissue ATP levels were no different in sham-operated animals than in those that had undergone 120 minutes of intestinal ischemia. Within 15 minutes of gut reperfusion, however, lung ATP decreased from 3.82 +/- 0.27 to 1.53 +/- 0.90 x 10(-7) moles/50 mg tissue, p less than 0.05. Neutrophil accumulation in the lungs, estimated by tissue myeloperoxidase determination, increased sevenfold (0.13 +/- 0.02 to 0.97 +/- 0.25 units/gm, p less than 0.05) after 120 minutes of ischemia and 15 minutes of reperfusion. Lung microvascular permeability increased threefold after 120 minutes of intestinal ischemia and 120 minutes of reperfusion (0.10 +/- 0.01 vs. 0.35 +/- 0.05 [lung/blood counts per minute], p less than 0.05). Intestinal ischemia followed by reperfusion is associated with acute lung injury characterized by increased microvascular permeability, histologic evidence of alveolar capillary endothelial cell injury, reduced lung tissue ATP levels, and the pulmonary sequestration of neutrophils. These data confirm an acute lung injury associated with intestinal ischemia-reperfusion and suggest a possible pathogenic role for the neutrophil.
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PMID:Evidence for neutrophil-related acute lung injury after intestinal ischemia-reperfusion. 276 27

Excessive accumulation of hydrogen ions in the brain may play a pivotal role in initiating the necrosis seen in infarction and following hyperglycemic augmentation of ischemic brain damage. To examine possible mechanisms involved in hydrogen ion-induced necrosis, sequential structural changes in rat brain were examined following intracortical injection of sodium lactate solution (pH 4.5), as compared with injections at pH 7.3. Following pH 7.3 injection, neuronal swelling developed between 1 and 6 h, but only a needle track wound surrounded by a thin rim of necrotic neurons and vacuolated neuropil was present 24 h after injection. In contrast, pH 4.5 injection produced neuronal necrosis as soon as 1 h after injection, followed by necrosis of astrocytes and intravascular thrombi at 3 and 6 h. Alterations common to both groups included vascular permeability to horseradish peroxidase, dilation of extracellular spaces, astrocyte swelling, capillary compression, and vascular stasis. These data suggest that neurons, astrocytes, and endothelia can be directly damaged by increased acid in the interstitial space. Lethal injury initially appeared to affect neurons, while subsequent astrocyte necrosis and vascular occlusion may damage tissue by secondary ischemia.
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PMID:Light and electron microscopic evaluation of hydrogen ion-induced brain necrosis. 282 Oct 31

The hydroxyl radical is one of the most damaging oxygen metabolites that are thought to be produced during ischemia and reperfusion of cardiac tissue. Therefore, we used the isolated, isovolumetric, buffer-perfused rat heart preparation of cardioplegic arrest to assess the effects of interventions targeted at inhibiting production of the hydroxyl radical by decreasing either the availability of one of its precursors (hydrogen peroxide) or that of the metal catalyst (ferric iron) involved in the radical formation. Sixty hearts were studied and, except for nonischemic controls, were subjected to 3 hr of hypothermic (15 degrees to 18 degrees C) cardioplegic arrest, followed by 45 min of reperfusion. The following interventions were tested: pretreatment with peroxidase, a scavenger of hydrogen peroxide, pretreatment with a combination of peroxidase and the iron chelator deferoxamine, pretreatment with peroxidase followed by supplementation of the cardioplegic solution with deferoxamine, and supplementation of the cardioplegic solution with deferoxamine without preischemic enzymatic treatment. Based on comparisons of postreperfusion pressure development, maximal ventricular dP/dt, left ventricular compliance, and coronary flow, deferoxamine-containing cardioplegic solution alone afforded the best myocardial protection. This may be due to the ability of deferoxamine to act both as an iron chelator and as a direct scavenger of superoxide anion, an activated oxygen species that participates in hydroxyl radical formation. This study confirms that an important component of the cardiac damage sustained during global ischemia and reperfusion may involve injury caused by the hydroxyl radical. Furthermore, our results point out the potential therapeutic usefulness of deferoxamine in the context of cardioplegic protection during open-heart procedures.
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PMID:Prevention of hydroxyl radical formation: a critical concept for improving cardioplegia. Protective effects of deferoxamine. 282 88

Some publications have pointed out that oxygen free radicals can induce injury of vessel wall and increase platelet aggregation and clotting, which can suppose a dependent relationship with arteriosclerotic process. We therefore studied the hypothesis of a possible abnormal platelet antioxidant enzymatic equipment in arteriopathic patients. A control group of 20 healthy subjects and an other one of 40 non diabetic patients with peripheral arterial disease were investigated, and the following tests were performed: measure of transcutaneous oxygen tension (PTCO2), determination of activity of platelet superoxide dismutase (SOD), glutathione-peroxidase (G-Px) and catalase (CAT). A significant decrease of SOD and G-Px is observed in platelets of arteriopathic patients. This decrease seems to be correlated with the severity of ischemia. The pathological reduction of platelet antioxidant equipment can be one factor enhancing thrombotic complications in chronic arterial disease.
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PMID:[Platelet antioxidant enzyme activities in arteriopathy]. 282 99


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