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)

Many studies have shown increased affinity of hemoglobin for oxygen during metabolic alkalemia and dependence of intramitochondrial cytochrome oxidase activity on arterial oxyhemoglobin saturation. The present studies tested the hypothesis that metabolic alkalemia produces tissue hypoxia independent of arterial oxygen desaturation. Neuromuscular conduction latency was used as an indicator of functional impairment, and was measured following electrostimulation of the sciatic nerve and recording of the electromyogram from the gastrocnemius muscle of rats anesthetized with pentobarbital sodium. To increase the affinity of hemoglobin for oxygen, sodium bicarbonate was administered in graded doses every 15 min. Statistical significance of changes was estimated by the paired Student's t test. Arterial bicarbonate ion concentration increased from 25 +/- 1.3 to 39.0 +/- 3.0 mM while arterial pH increased from 7.30 +/- 0.02 to 7.50 +/- 0.03 (P less than 0.01). Neuromuscular conduction latency increased from 1.9 +/- 0.13 to 2.7 +/- 0.18 ms (P less than 0.01). Tissue hypoxia was suggested by a greater decrease in mass spectrometric determinations of gastrocnemius muscle oxygen tension (PO2) in separate groups of control (arterial pH 7.38 +/- 0.04) and experimental (arterial pH 7.48 +/- 0.03) rats. These changes were accompanied by markedly decreased uptake of 3.3'-diaminobenzidine (DAB) by gastrocnemius muscle mitochondria, suggesting decreased intracellular activity of cytochrome oxidase and intracellular oxygen availability to myocytes in the absence of arterial oxygen desaturation.
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PMID:Myocyte cytochrome oxidase activity and neuromuscular conduction associated with metabolic alkalemia. 302 9

Brain cytochrome oxidase activity was measured after the in vitro addition of potassium cyanide (KCN) or sodium nitroprusside (SNP). Activity of cytochrome oxidase was sensitive to KCN; however, this activity was unaffected by SNP. In SNP- and KCN-treated animals brain cytochrome oxidase activities were measured. At 3 min after SNP injection, inhibition of the enzymatic activity was the same as 1 min after KCN injection. Time to death for SNP-treated animals was longer than for KCN-treated animals. These data suggest that cyanide was released in vivo from SNP and that time was necessary for this release to occur.
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PMID:In vivo release of cyanide from sodium nitroprusside. 303 Mar 85

Purified epithelial basolateral membrane vesicles were prepared from lobster hepatopancreas by sorbitol gradient centrifugation. Na+-K+-adenosinetriphosphatase, alkaline phosphatase, and cytochrome-c oxidase enzyme activities in the final membrane preparation were enriched 9.6-, 1.4-, and 0.4-fold, respectively, compared with their activities in the original tissue homogenate. Vesicle osmotic reactivity was demonstrated using 60-min equilibrium 36Cl uptake experiments at a variety of transmembrane osmotic gradients. 36Cl uptake into vesicles preloaded with HCO3 was significantly greater than into vesicles lacking HCO3. This exchange process was stimulated by a transmembrane proton gradient (internal pH greater than external pH). Proton-gradient-dependent Cl-HCO3 exchange was potential sensitive and stimulated by an electrically negative vesicle interior. 36Cl influx (4-s exposures) into HCO3-loaded vesicles occurred by the combination of 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid sensitive, carrier-mediated transfer and "apparent diffusion." 36Cl influx was a hyperbolic function of both internal [HCO3] and internal [Cl]. The two internal anions displayed a 100-fold difference in apparent affinity constants with HCO3 being strongly preferred. 36Cl influx was stimulated more by preloaded monovalent than by divalent anions. Na was an inhibitor of proton-dependent anion antiport, whereas K had no effect. A model for HCl-HCO3 antiport is suggested that employs combined transmembrane concentration gradients of Cl and HCO3 to power anion exchange and transfer protons against a concentration gradient.
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PMID:Proton-stimulated Cl-HCO3 antiport by basolateral membrane vesicles of lobster hepatopancreas. 303 81

The mechanism of cyanide intoxication has been attributed to the inhibition of cytochrome oxidase, thereby decreasing the tissue utilization of oxygen. One mechanism of cyanide antagonism is by sequestering cyanide with methaemoglobin to form cyanmethaemoglobin and another mechanism is detoxifying with a sulphur donor to thiocyanate. Questions have been raised with regard to these classical mechanisms. Oxygen with nitrite-thiosulphate antagonizes the lethal effects of cyanide. Theoretically, increased oxygen should serve no useful purpose, as it is the tissue utilization of oxygen which is inhibited. In the nitrite-thiosulphate antidotal combination, the proposal is made that the predominate antidotal action of nitrite is a vasogenic action, rather than methaemoglobin formation, because when methaemoglobin formation is inhibited by methylene blue the protective action of sodium nitrite persists. This suggests that methaemoglobin formation plays only a small part, if any, in the therapeutic antagonism of the lethal effects of cyanide. The roles and implications of sodium thiosulphate and non-rhodanese substrates in the detoxification mechanism are compared. Lastly, a new approach to cyanide antagonism has been initiated which involves the erythrocyte encapsulation of thiosulphate and sulphurtransferase as an antidote and prophylaxis against cyanide.
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PMID:The mechanism of cyanide intoxication and its antagonism. 307 59

The pathophysiology, clinical features, and management of cyanide toxicity are reviewed and sources of cyanide are listed. Cyanide is a deadly poison that is found in many foods and household and industrial products, including some that are readily available. Cyanide binds with cytochrome oxidase, the enzyme responsible for oxidative phosphorylation, and paralyzes cellular respiration. Because the tissues cannot use oxygen that is delivered, aerobic metabolism ceases. The signs and symptoms of cyanide poisoning reflect the extent of cellular hypoxia. Manifestations may include respiratory abnormalities (progressing from tachypnea and dyspnea to respiratory depression and apnea), hemodynamic instability, metabolic acidosis, and, possibly, local irritant effects after oral ingestion of cyanide. The mainstays of therapy are 100% oxygen and specific antidotes to cyanide. Sequential treatment with amyl nitrite by inhalation, intravenous sodium nitrite 3%, and intravenous sodium thiosulfate 25% is directed toward decreasing the amount of cyanide available for cellular binding. Nitrites convert hemoglobin to methemoglobin, which reacts with cyanide to form cyanomethemoglobin. Sodium thiosulfate serves as a source of sulfur groups, which are needed for conversion of cyanide to thiocyanate, a compound that is relatively less toxic and is excreted renally. Supportive care also is important. Cobalt EDTA, hydroxocobalamin, and aminophenols have also been used but are not considered standard treatments. Cyanide poisoning is a medical emergency that requires prompt recognition and immediate and aggressive treatment.
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PMID:Clinical features and management of cyanide poisoning. 353 Jun 15

Protein and lipid analyses were conducted on isolated erythrocyte and lymphocyte plasma membranes from 7-wk-old male C57BL copper-deficient and copper-supplemented mice to investigate mechanisms for the altered immunity that accompanies dietary copper deficiency. Beginning at parturition, dams were fed a diet low in copper (0.5 mg/kg) and the offspring were weaned to this diet. Half the dams and their respective offspring received supplemental copper (20 mg/L) in the drinking water (+Cu) and served as controls. Unsupplemented offspring (-Cu) had lower activity of cuproenzymes serum ceruloplasmin, spleen and thymus cytochrome-c oxidase and copper, zinc-superoxide dismutase. The -Cu mice exhibited anemia, splenomegaly and thymic atrophy. Based on the marker enzyme alkaline phosphodiesterase I (APDE-I), lymphocyte plasma membranes were enriched 7- to 10-fold for spleen and thymus, respectively, after discontinuous sucrose density centrifugation. The activity of APDE-I was higher in spleen and thymus samples from -Cu mice than from those of +Cu mice for both crude homogenates and purified plasma membranes. Proteins were fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by silver staining. A yellow-appearing band, Mr 74,000, present in all splenic membrane samples from +Cu mice was not evident in the samples from -Cu mice. Fatty acid methyl esters (FAME) were quantified by gas chromatography. Compared to splenic membranes from +Cu mice, the samples from -Cu mice demonstrated significant changes in all FAME (lower 16:0, 18:0 and 20:3n-6 and higher 18:1n-9, 18:2n-6 and 20:4n-6), including a higher unsaturation index. FAME composition of erythrocyte ghosts from -Cu mice demonstrated similar changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary copper deficiency alters protein and lipid composition of murine lymphocyte plasma membranes. 359 18

In order to test the effect of aerobic training on blood pressure, and to examine the putative mechanisms involved, stroke-prone spontaneously hypertensive rats (SHR-SP), borderline hypertensive rats (BHR), and Wistar-Kyoto control rats (WKY) were swim-trained for up to 1.5 h twice-daily for 22 weeks. The BHR were F1 back-cross SHR-SP, WKY. A training effect was observed in the trained rats compared to controls, as demonstrated by slower heart rates, heavier hearts and increased cytochrome oxidase activity in their skeletal muscle. Trained SHR-SP and BHR had significantly lower blood pressures at the end of the intervention period (approximately 10 mmHg) compared to controls. Acute increases in blood pressure with swimming were less in trained than in untrained rats. Trained rats had higher extracellular sodium values than untrained rats. Further, trained SHR-SP and BHR had lower intra-erythrocyte sodium values than controls. Increases in corticosterone, epinephrine and norepinephrine with swimming were less in trained rats than in controls. We conclude that exercise conditioning ameliorates hypertension in rats. The mechanism may involve an effect on cation transmembrane transport, as well as decreased, adrenosympathetic tone. Moreover, these effects may be related.
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PMID:Blood pressure, electrolyte and adrenal responses in swim-trained hypertensive rats. 361 73

The development of protein bodies in proteinoplasts of tobacco (Nicotiana tabacum L. var. Wis. 38) roots was investigated with TEM, HVEM, and enzyme cytochemistry. These plastids contain a three-dimensional network of fenestrated tubules which originate from invaginations of the inner membrane of the plastid envelope. Elaboration of the network occurs in parallel with cell differentiation: slender tubules common to plastids in meristematic cells undergo dilation as protein accumulates during cell differentiation; proteinoplasts of vacuolate and root cap cells usually contain a large protein body. The contents of the peripheral tubules, originating from the inner membrane, are less electron dense than the tubules making up the central network. Localized dilations within the tubular network result in the formation of dense spheroidal structures, protein bodies, apparently as a result of continued protein accumulation via tubules connecting to the central network. Protein might be imported from segments of rough ER attached to or apposed to the outer membrane of the proteinoplast envelope. The presence of catalase (E.C. 1.11.1.6), peroxidase (E.C. 1.11.1.7), and cytochrome oxidase (E.C. 1.9.3.1) was demonstrated by cytochemistry with diaminobenzidine (DAB) as substrate. Oxidized DAB was found in protein bodies after incubation in each of the specific reaction media. While aminotriazole and sodium azide inhibited oxidation of DAB by catalase and peroxidase, respectively, only potassium cyanide completely inhibited oxidation of DAB in protein bodies. We conclude that protein bodies of proteinoplasts in tobacco roots are not sites for storage of protein, rather protein bodies contain heme protein(s) with strong oxidase activity that may convey a specific function to proteinoplasts.
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PMID:Development and enzyme activity of protein bodies in proteinoplasts of tobacco root cells. 404 99

beta-Granules were prepared from micro-dissected pancreatic islets of obese-hyperglycaemic mice. This fraction contained 60% of the insulin, 30% of the cytochrome oxidase, 16% of the acid phosphatase activity and 20% of the protein present in whole islets. The isolated granules retained a heavy metal during fractionation. Optimum conditions for granule stability were low ionic strength and pH6, the granules being unexpectedly fragile at pH7.4. The stability of the granules was unaffected by sucrose in the concentration range 50-320mm, but 1% (w/v) sodium deoxycholate released all insulin. A solubilizing effect was also noted with ATP and citrate. Spinning through 1.6m-sucrose yielded a further purification in relation to mitochondria and acid-phosphatase-carrying particles but virtually no purification in relation to protein. Electron microscopy revealed that the major contaminants were rough-surfaced vesicles and membranes. A separation of granules from acid phosphatase was achieved by phase distribution in polyethylene glycol and dextran. The location of the enzyme to the interphase was so pronounced in systems buffered with lithium phosphate that the technique may be used for future purification of acid-phosphatase-carrying particles from the beta-cells.
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PMID:Physicochemical characteristics of insulin secretion granules. 488 94

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


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