Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.10.3.3 (ascorbate oxidase)
 778 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo measurement of the rapid changes in the extracellular concentrations of L-glutamic acid in the mammalian brain during normal neuronal activity or following excessive release due to episodes of anoxia or ischemia has not been possible to this date. Current techniques for the measurement of the release of endogenous glutamate into the extracellular space of the central nervous system are relatively slow and do not measure the actual concentration of free glutamate in the extracellular space. An enzyme-based electrode with rapid response times (about 1 s) and high degree of sensitivity (less than 2 microM) and selectivity for L-glutamic acid is described in this paper. This electrode has both L-glutamate and ascorbate oxidase immobilized on its surface. The latter enzyme removes almost completely any interferences produced by the high levels of extracellular ascorbate present in brain tissue. The response of the electrode to glutamate and other potentially interfering substances was fully characterized in vitro and its selectivity, sensitivity and rapidity in responding to a rise in extracellular glutamate concentrations was also demonstrated in vivo. Placement of the electrode in the dentate gyrus of the hippocampus led to the detection of both KCl-induced release of L-glutamic acid and the release induced by stimulation of the axons in the perforant pathway. The development of this selective, sensitive and rapidly responding glutamate sensor should make it now possible to measure the dynamic events associated with glutamate neurotransmission in the central nervous system.
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PMID:Direct measurement of glutamate release in the brain using a dual enzyme-based electrochemical sensor. 782 Jun 52

We performed experimental and clinical studies with measurement of electrical character in the skeletal muscle to assess ischemic damage and reperfusion injury in lower limbs. In 14 dogs, the bilateral hind limbs were squeezed at the inguinal region to make ischemia and they were reperfused after various intervals. Conductivity (G) of the skeletal muscles in hind limbs was measured with an LCR meter, which is an impedance analyzer. Change of G from 0 to 3 h of reperfusion (Delta3G) was calculated. G was decreased during ischemia and increased after reperfusion. In those whose Delta3G as more than 2.1 mS/cm, serum creatine kinase and aldolase at 10 h after reperfusion were correlated significantly (P < 0.01) to Delta3G. In patients with an abdominal aortic aneurysm (N = 3), arteriosclerosis obliterans (N = 1), or acute arterial occlusion (AAO, N = 1), G of lower extremities was measured from arterial clamp to declamp. Conductivity markedly increased after reperfusion and serum creatine kinase was the highest in the patient with AAO. We suggested that measurement of G may provide monitoring of ischemic and reperfused phase injury in the skeletal muscle and may be applicable to prediction of the skeletal muscular reperfusion injury.
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PMID:Evaluation of ischemic damage in the skeletal muscle with the use of electrical properties. 987 23

Apart from its physiological role as a major antioxidant, ascorbate is highly concentrated in neuropils and ascorbate-mediated protection from excitotoxins has been demonstrated in vitro. Therefore, extracellular release of ascorbate during the early stage of ischemia-reperfusion was measured using a microdialysis electrode technique. One or two probes of the microdialysis biosensor were inserted into the rat striatum. One probe (n=16) was perfused with phosphate-buffered saline (PBS) for continuous oxidative signal recording. A second electropolymerised probe inserted into the other side of the striatum was perfused with PBS containing ascorbate oxidase in six rats. Forebrain ischemia-reperfusion was performed for 10min, followed by reperfusion for 60min. Ascorbate increased transiently during ischemia, and markedly to a maximum of 247.5+/-55. 8 microM from the baseline of 68.5+/-25.3 microM after reperfusion. The marked increase of extracellular ascorbate may be a marker of the early stage of reperfusion.
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PMID:Continuous real-time measurement of extracellular ascorbate release in the rat striatum in vivo during forebrain ischemia-reperfusion. 1102 49

Distribution of ascorbate into tissues is an essential process in ascorbate antioxidant defense. Hibernating animals are studied as a model of tolerance to ischemia-reperfusion because of their tolerance to fluctuations in blood flow associated with prolonged torpor and periodic arousal episodes. Throughout hibernation, plasma ascorbate concentration ([Asc](p)) repetitively increases during torpor, then falls during periodic arousal bouts. We previously proposed that high [Asc](p) provides a ready source of antioxidant protection for distribution to the central nervous system and peripheral tissues during arousal. Here we tested whether deliberate oxidation of plasma ascorbate by intravenous administration of ascorbate oxidase (AO), prior to arousal, compromised tissue levels of ascorbate or the other water-soluble antioxidants, glutathione (GSH) and urate. Although AO decreased [Asc](p) to below the level of detection during torpor and after arousal, ascorbate oxidation did not decrease post-arousal tissue levels of reduced ascorbate, glutathione, or urate in any tissue examined, except liver. The data imply that ascorbate is taken up equally well into brain and other tissues as either ascorbate or its oxidized product dehydroascorbate, with subsequent intracellular reduction of dehydroascorbate. Lack of effect of ascorbate oxidation on tissue levels of GSH or urate indicates that dehydroascorbate uptake and reduction do not compromise tissue concentrations of these other water-soluble antioxidants. Thus, we show equal availability of reduced and oxidized plasma ascorbate during metabolically demanding thermogenesis and reperfusion associated with arousal from hibernation.
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PMID:Ascorbate distribution during hibernation is independent of ascorbate redox state. 1525 22

Real-time monitoring of L-glutamate release from various neuronal regions of mouse hippocampal slices under ischemia (a glucose-free hypoxia condition) is described. A glass capillary microelectrode with a tip size of approximately 10 microm containing a very small volume ( approximately 2 microL) of a solution of glutamate oxidase (GluOx) and ascorbate oxidase was used. First, the amperometric response behavior of the electrode at 0 V versus Ag/AgCl was characterized with a standard glutamate solution in terms of continuous measurements, effect of oxygen, viscosity of solution and concentration dependence. The electrode was applied to the real-time monitoring of L-glutamate released from different neuronal regions of acute hippocampal slices submerged in a hypoxia solution. The time-resolved amounts of L-glutamate released at various neuronal regions (CA1, CA3 and DG) of mouse hippocampal slices were quantified and compared with the reported L-glutamate fluxes using difference-image analysis during ischemia.
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PMID:Real-time monitoring of L-glutamate release from mouse brain slices under ischemia with a glass capillary-based enzyme electrode. 1615 99