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:1.9.3.1 (cytochrome oxidase)
8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown that high-altitude hypoxic hypoxia is associated with reduced ventilatory capacity that may be related to skeletal muscle weakness. In the present investigation, ascent to high altitude (4,000 m) was simulated experimentally by exposure of male rats (Sprague-Dawley, 250-350 g), anesthetized with thiopental sodium (25 mg/kg, i.p.), to a breathing gas mixture of 12% oxygen diluted in 88% nitrogen (FiO2 = 0.12). Determinations of oxygen saturation on microsamples (250 ul) of arterial and central venous blood were made spectrophotometrically. Neuromuscular conduction latency was measured following electrostimulation of the sciatic nerve (1-5 V, 0.5 msec duration, 1-40 Hz) and recording of the electromyogram from the gastrocnemius muscle. Experimental hypoxia (FiO2 = 0.12) produced a highly significant increase in conduction latency from a control value (mean +/- SEM) of 3.06 +/- 0.16 msec to 4.02 +/- 0.31 msec (n = 10, P less than 0.001). Conduction latency increased with decreasing arterial oxygen saturation from a control value of 92.9% +/- 0.18% to 83.2% +/- 0.76% (P less than 0.001) in the absence of statistically significant changes in central venous oxygen saturation, central venous pressure, arterial and central venous pH, and heart rate. A significant decrement in the mean arterial blood pressure from a control value of 85 +/- 1.5 mm Hg to 69 +/- 1.5 mm Hg suggests that local ischemia may be a component of this model. These responses were accompanied by marked reduction in uptake of 3,3'-diaminobenzidine (DAB) by gastrocnemius muscle mitochondria, suggesting decreased intracellular activity of cytochrome oxidase. It was concluded that exposure of rodents to hypoxic gas mixtures may provide a suitable model for studying the mechanism of skeletal muscle weakness associated with ascent to high altitude and of other conditions wherein the supply of oxygen to tissues is limited.
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PMID:Relationship between intracellular oxygenation and neuromuscular conduction during hypoxic hypoxia. 609 57

Evolutionary pressure induced by the release of O2 into the environment has necessitated the development of a group of mechanisms to deal with the toxic free radical byproducts of oxidative metabolism. The complete reduction of O2 to H2O2 involves the addition of four electrons which can occur univalently resulting in a series of toxic intermediates or quadrivalently by the mitochondrial cytochrome oxidase system, which avoids these reactive intermediates. Free radical mechanisms have been associated with a large number of disease states including inflammation, irradiation-induced injury and ischemia. The site of free radical generation, that is whether the generation of radical species is predominantly extracellular or intracellular, may determine to a degree, the types of macromolecular and cellular damage which result. A classification of diseases in which radical generating processes may play a role is presented in the hope that it may aid in the understanding and treatment of these diseases.
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PMID:An approach to free radicals in medicine and biology. 626 28

Changes in the maximal rate of some cerebral enzymatic activities related to 400ene transduction and neurotransmission (lactate dehydrogenase; citrate synthase and malate dehydrogenase; total NADH-cytochrome c reductase and cytochrome oxidase; glutamate dehydrogenase; acetylcholine esterase) were assayed both in the crude or purified mitochondrial fraction and in the crude synaptosomal fraction from rat whole brain or cerebral cortex. The evaluations were performed in rats before and after a postdecapitative normothermic ischemia of 5, 10, 20 and 40 min duration. Modification observed in some of these activities wer discussed for comparison with other experimental results from different researchers. At present no definite conclusions can be drawn, but certainly the observed modifications in activity of enzymes are not passive but expression of deranged metabolism of ischemic neurons.
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PMID:Brain enzymes and ischemia. 626 30

The effects of complete ischemia and of in vivo pharmacological treatment with trimetazidine were studied on some enzymatic activities related to energy transduction: lactate dehydrogenase for anaerobic glycolysis; citrate synthase and malate dehydrogenase for the Krebs' cycle; total NADH-cytochrome c reductase and cytochrome oxidase for the electron transport chain; glutamate dehydrogenase for amino acid metabolism and acetylcholine esterase for acetylcholine metabolism. These enzymatic activities were evaluated in brains of 10-day-old rats, at three different subcellular levels: homogenate in toto, purified mitochondrial fraction, crude, synaptosomal fraction. Complete normothermic post-decapitative ischemia of 30 min duration increased the activity of cytochrome oxidase in the homogenate in toto and increased the activities of citrate synthase and malate dehydrogenase in the purified mitochondrial fraction, the activities of the enzymes evaluated in the crude synaptosomal fraction being unaffected. The i.p. treatment with trimetazidine (at the dose level of 50 mg . kg-1) was without any significant effect on the tested enzymatic activities.
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PMID:Effects of ischemia and pharmacological treatment on subcellular fractions from neonatal rat brain. 628 22

Polarographic measurements show that activity of cytochrome oxidase (CO), assayed as ascorbate plus TMPD oxidase, is decreased in the mitochondria (M) from postischemic areas of rabbit heart 1, 6, and 9 days after temporary (1-hr) coronary artery occlusion (CAO). This effect is observable only in the absence of added cytochrome c. Cytochrome oxidase activity in the cytochrome c-containing medium was not different from the control level. Levels of cytochromes c + c1 and a were substantially lower in tissue from postischemic areas and elevated in the intact tissue 1 and 6 days after temporary CAO as compared with control hearts. Stoichiometry of the cytochromes was not changed. After 1 or 4 hr of permanent CAO, CO activity (plus cytochrome c) of ischemic M was equal to that of M from intact area; CO activity (with or without cytochrome c) was reduced after 0.5 and 1 hr but elevated after 3 or 4 hr of in vitro ischemia as compared with control. The changes of CO activity in infarcted human heart M were similar to those in rabbits after temporary CAO; CO activity was restored after addition of cytochrome c. The data suggest that leakage of cytochrome c occurs during isolation of M and is more pronounced in ischemia-damaged M.
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PMID:Cytochrome oxidase activity of mitochondria from ischemic and reperfused myocardium. 630 31

Cerebral blood volume, hemoglobin saturation and the cytochrome a, a3 redox state were monitored simultaneously by using three wavelengths of light in the near infrared portion of the spectrum for transillumination of the intact skull of rats. The changes in these parameters following incomplete cerebral ischemia were assessed in Wistar and Long-Evans rats submitted to carotid ligation. Another group of Wistar rats was submitted to vertebral + carotid occlusion. The experiments, performed under N2O/O2 anesthesia, showed that in all three groups carotid occlusion induced a decrease in blood volume, Hb saturation and a reduction of cyt. a, a3. However, the cytochrome redox state tended to normalize during ischemia as a consequence of higher O2 extraction from blood. The primary finding of this study was the marked hyperoxidation of cyt. a, a3 which occurred after reestablishing of the carotid blood supply, in spite of a secondary post-ischemic hypoperfusion of the brain. Although uncoupling of oxidative phosphorylation cannot be excluded the dissociation between blood supply and metabolism could well be due to ischemia-induced hypermetabolism of the central nervous tissue. In view of the marked oxidation of cyt. a, a3 during the reperfusion period as compared with the small extent of its reduction during the ischemic episode, the data also support the hypothesis that under steady state conditions in vivo, cytochrome oxidase is mainly reduced.
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PMID:Incomplete cerebral ischemia in the rat: vascular and metabolic changes as measured by infrared transillumination in vivo. 631 78

The maximal rate of some cerebral enzymatic activities related to energy transduction (hexokinase; phosphofructokinase; lactate dehydrogenase; citrate synthase; malate dehydrogenase; total NADH-cytochrome c reductase; cytochrome oxidase), amino acid metabolism (glutamate decarboxylase; glutamate dehydrogenase) and cholinergic metabolism (acetylcholine esterase) were tested in the cerebral cortex and in sub-cortical area of rats. The evaluations were performed both in the homogenate in toto and in the crude mitochondrial fraction, before and after a postdecapitative normothermic ischemia of 5, 10, 20, and 40 min duration. The results are discussed also with respect to the pharmacological pretreatment with two biological substances which may modulate amino acid (L-alanine) and phospholipid metabolism (CDP-choline). The analysis of the present data suggests the occurrence in brain tissue of a variety of interrelated factors implicated in the ischemia-induced changes of the maximal rate of the enzymatic activities related to the energy transduction. These include: (a) rearrangement of the enzymatic activities because of the changed metabolic and chemico-physical condition; (b) decrease in the activity of enzymes related to the electron transfer chain and glycolysis; (c) changes in enzymes related to mitochondrial membranes. The effects of in vivo administration of alanine or CDP-choline, even if significant, are not consistent throughout the time period studied.
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PMID:Changes induced by ischemia on some cerebral enzymatic activities related to energy transduction and amino acid metabolism. 685 30

Regional changes in myocardial function and oxidative metabolism during acute coronary artery occlusion were recorded spectrophotometrically by incorporating fiber optics in the isolated rat heart perfused by Langendorff's procedure. Oxygen saturation of myoglobin, reduction of cytochrome aa3, and the dynamic wall thickness of the left ventricle were continuously and concurrently measured from absorbancy increments at 581-592 nm, 605-630 nm, and 568-592 nm, respectively. In contrast to a gradual decrease in the extent of systolic wall thickening in anoxia, observed decreases in both the extent and the duration of systolic wall thickening and the appearance of a late systolic bulge occurred within 5 s after the onset of regional ischemia. After 10 s of both anoxia and regional ischemia, oxygen saturation of myoglobin decreased by 50%, but fluorescence of nicotinamide adenine dinucleotide remained at aerobic level which indicated that mitochondrial oxidative energy production might still be maintained. Thus early and pronounced dysfunction of the ischemic region appeared to precede a substantial loss of ATP production.
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PMID:Regional myocardial function and metabolism during acute coronary artery occlusion. 709 58

The objective of this study was to assess the relationship between the changes in the redox state of cytochrome oxidase (Cyt. ox.) and those of spontaneous EEG activity and cellular energy state during cerebral ischemia and recirculation. We induced 5-min forebrain ischemia by occluding the bilateral common carotid arteries in anesthetized gerbils. Redox changes of Cyt. ox. were monitored with near-infrared spectroscopy (NIRS) through the experiments. Cortical energy metabolites, ATP, ADP, and AMP, were also measured with high performance liquid chromatography (HPLC) during ischemia and recirculation. Ischemia immediately caused a rapid reduction of Cyt. ox., which paralleled to deterioration of spontaneous EEG activity and preceded significant changes in cellular energy state. Re-oxygenation of Cyt. ox. was observed just after recirculation, and paralleled to the recovery of cellular energy state. Spontaneous EEG activity did not recover even when all other NIRS parameters almost recovered during recirculation after 5-min ischemia. During clamping of the carotid artery, NIRS findings also correlated with those of somatosensory evoked potential (SEP). We concluded that, by means of monitoring redox changes of Cyt. ox., NIRS can detect non-invasively critical neuronal hypoxia prior to a significant impariment of cellular energy state caused by cerebral ischemia, and that NIRS can also detect recovery of oxidative phosphorylation during recirculation, which cannot be observed on EEG.
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PMID:[Near-infrared monitoring of cerebral oxygenation during cerebral ischemia]. 759 May 92

The survival of infants with congenital heart disease has improved dramatically. However, the incidence of neurological injury in infants surviving cardiac surgery remains considerable. These neurological sequelae are attributable at least in part to hypoxia-ischemia/reperfusion, which inevitably accompanies infant heart surgery with deep hypothermia, cardiopulmonary bypass, and circulatory arrest. To begin to identify mechanisms of brain injury during infant cardiac surgery, we used near-infrared spectroscopy to study the relationship between cerebral intravascular (hemoglobin) and mitochondrial (cytochrome aa3) oxygenation in 63 infants (aged 1 day to 9 months) undergoing deep hypothermic repair of congenital heart defects, throughout the intraoperative period. Moreover, we assessed the effect of postnatal age on these changes. The cerebral concentration of oxidized cytochrome aa3 decreased from the onset of deep hypothermic cardiopulmonary bypass, despite apparent abundant intravascular oxygenation manifested by a simultaneous increase in the cerebral concentration of oxyhemoglobin. During this interval infants older than 2 weeks had a greater decrease in oxidized cytochrome aa3 than did infants 2 weeks old or younger. During deep hypothermic circulatory arrest, cerebral levels of oxidized cytochrome aa3 remained depressed while those of oxyhemoglobin declined. With reperfusion following circulatory arrest, the recovery of oxidized cytochrome aa3 was delayed, despite a rapid recovery of intravascular oxygenation (HbO2). After rewarming and 60 minutes of reperfusion, only 46% of infants recovered to the baseline level of cerebral oxidized cytochrome aa3. These findings demonstrate a paradoxical dissociation of changes in intravascular and mitochondrial oxygenation during hypothermic cardiopulmonary bypass; a pronounced decrease of mitochondrial oxygenation is established during induction of hypothermia and a delay in recovery of mitochondrial oxygenation occurs following circulatory arrest. These effects were more pronounced in infants older than 2 weeks than in younger infants. The data suggest potentially deleterious impairments of intrinsic mitochondrial function or of delivery of intravascular oxygen to the mitochondrion or both, effects previously undetected and apparently influenced by cerebral maturation.
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PMID:Cerebral oxygen supply and utilization during infant cardiac surgery. 771 85


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