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)

The protective effect of a new oligomeric derivative of prostaglandin B2, known as OC-5186, was evaluated using time-sharing spectrofluorometry in the cold-preserved rat liver. Experiments were divided into three groups: in group A, a 5000 ng dose of OC-5186 was administered via the peripheral vein, 1000 ng via the portal vein, and 200 ng/ml in University of Wisconsin (UW) solution; in group B, the OC-5186 dosage was ten times greater than that in group A; in group C (control group), liver procurement and storage were performed without OC-5186. At 0, 12, and 24 h after cold preservation at 4 degrees C, the liver was perfused for 30 min at 12 degrees C with oxygenized Krebs-Henseleit solution, after which the perfusate was switched to deoxygenized Krebs-Henseleit solution. Time sharing spectrofluorometry was used to follow NADH fluorescence at 450 nm with a 360-nm excitation wavelength, as well as the reflectance of cytochrome aa3 with 605 minus 620 nm from oxidation to reduction. Rate constants of NADH fluorescence and cytochrome aa3 reflectance were used as indices of integrity of the mitochondrial respiratory chain. In group C, the rate constant of NADH fluorescence decreased significantly (P < 0.05) from the control value of 8.31 +/- 0.21 x 10(-3) (sec-1) to 4.97 +/- 0.15 x 10(-3) and 5.58 +/- 0.16 x 10(-3) (mean +/- SEM) at 12 and 24 h after cold preservation, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of a prostaglandin oligomer on liver mitochondria in situ: time-shared measurements of fluorescence and reflectance in the cold-preserved rat liver. 141 8

Electromyographic detection of increased neuromuscular conduction latency that follows electrostimulation of spinal nerves has been used widely as a clinical tool for detection of ischemic muscle injury. We hypothesized that a biochemical marker for stagnant hypoxia provides more direct evidence for evaluating severity and monitoring resolution of ischemic muscle injury than the EMG. To detect intracellular changes in oxygen use during experimental ischemia, ultrathin sections of rat gastrocnemius muscle were treated with reducing agent, 3,3'-diaminobenzidine (DAB), a histochemical marker for intramitochondrial cytochrome oxidase activity. The observed decrease in mitochondrial uptake of DAB suggested that a decrease in cytochrome oxidase activity was associated with experimental ischemia. Neuromuscular conduction latency in rat gastrocnemius muscle was also quantitated after electrostimulation of the sciatic nerve. Ligation of the femoral artery produced ischemic tissue injury, during which recordings of the EMG showed that conduction latency increased [from a mean +/- SEM control value of 3.09 +/- 0.13 to 3.92 +/- 0.22 ms (N = 11, P less than 0.001).] The changes in both histochemically detectable cytochrome oxidase activity and neuromuscular conduction latency were reversed by reperfusion. Response of the rat tissue to arterial occlusion was thereby shown to be a physiologic model for skeletal muscle response to ischemia. In addition, histochemical detection of cytochrome oxidase activity was shown to be a sensitive intracellular marker for decreased oxygen use during ischemic muscle injury.
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PMID:Histochemical assessment of cytochrome oxidase activity for monitoring ischemic muscle injury. 298 23

The influence of plating cell density of an originally enriched myocardial cell population has been studied in neonatal rat heart cells in culture. Low density (LDM) is defined as a density (24 h after plating) of 209 +/- 44 cells/mm2 (mean +/- SEM) and is compared with high density (HDM), 419 +/- 67 cells/mm2. Cell growth is evaluated by the total cell number, the percentage of myocardial cells (M) in culture (PAS method) and the protein content per cell. Some differentiation parameters such as beating rates, glycogen concentration, enzymatic activities (cytochrome C oxidase and glycogen phosphorylase) are studied with time in culture (48, 96 and 192 hr). High density was designed to yield a complete confluency of the cells within 24 hr after plating and to minimize cell division of the non-muscle cells (F). At high density, cell division of F cells is effectively limited, thus leading to a more stable model regarding the cell density per plate and the percentage of M cells: 85.7 +/- 4% and 33.4 +/- 6% in LDM cultures compared with 86.5 +/- 4.7% and 51.7 +/- 9.8% in HDM cultures at 24 and 192 hr (mean +/- SEM). Heart cells increase similarly in size with age in culture in both groups. In HDM cultures the spontaneous contractions begin sooner (24 hr) than in LDM cultures and are more rapidly synchronized. The beating rate is higher in HDM cultures between 48 and 96 hr; however, after this time it falls in HDM and does not fall in LDM. Thus the overgrowth of muscle cells by non-muscle cells is not responsible for loss of beating with time in culture but more likely high density could be a limiting factor for isotonic contraction. There is more glycogen per myocyte in LDM than in HDM cultures. The cell density influences the enzymatic activities of cytochrome C oxidase and glycogen phosphorylase. The cytochrome oxidase activity is higher in HDM cultures than in LDM cultures at 96 hr whereas glycogen phosphorylase activity is higher in LDM cultures at time 96 and 192 hr. In LDM cultures, the ratio cytochrome C oxidase/glycogen phosphorylase decreases with time in culture from 1.685 +/- 0.680 at 48 hr to 0.780 +/- 0.290 at 192 hr but not in HDM cultures (2.13 +/- 0.36 and 1.64 +/- 0.34 respectively). Thus plating density influences properties of heart cell cultures with regard to the overgrowth of the F-cell population and the differentiated state of M cells.
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PMID:Influence of plating density on individual cell growth, cell division and differentiation of neonatal rat heart primary cultures. 301 Apr 99

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

Changes in the hepatic oxygenation state of rabbits during hemorrhage and subsequent epinephrine (n = 6) or dextran infusion (n = 6) were assessed by tissue near-infrared spectroscopy. Oxygen saturation of hemoglobin in the liver (hepatic SO2), and redox transition of cytochrome aa3 were analyzed by applying multicomponent analysis to the absorption spectrum of the liver. Hepatic SO2, representing extracellular oxygenation state, decreased from 62.4 +/- 2.7% (mean +/- SEM) to 21.1 +/- 7.3% after bleeding. It increased to 31.8 +/- 6.6% after epinephrine infusion, but returned to near-control levels after dextran infusion. Intracellular oxygenation state as assessed by the changes in the oxidized and reduced forms of cytochrome aa3 was impaired after bleeding, and remained as such even after epinephrine infusion. By contrast, it was normalized to near control levels after dextran infusion. Changes in the difference of hepatic SO2 and hepatic venous SO2 suggested that the intrahepatic blood flow was more heterogeneously distributed after bleeding, but that the heterogeneity of microcirculation was rather diminished after epinephrine infusion.
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PMID:Changes in the hepatic oxygenation state during hemorrhage and following epinephrine or dextran infusion as assessed by near-infrared spectroscopy. 750 28

Mitochondrial respiratory complexes such as cytochrome oxidase (CO) contain both mitochondrial- and nuclear-encoded subunits. To determine whether mitochondrial and nuclear gene expression are regulated proportionately in neurons, we analyzed CO subunit mRNA and mitochondrial DNA (mtDNA) levels by in situ hybridization and grain counting in the visual system of normal and monocular TTX-treated monkeys. We compared the regulation of these molecules with the regulation of CO activity and CO protein, analyzed by histochemistry and immunohistochemistry, respectively. In normal animals, CO activity was in general related more closely to mtDNA and CO subunit I (COI) (mitochondrial-encoded) mRNA levels than to COIV or COVIII (nuclear-encoded) mRNA levels. For example, puffs (also known as blobs) of high CO activity in striate cortex were enriched in mtDNA and COI mRNA, but not COIV or COVIII mRNA. In 3-7 d TTX-treated animals, proportionate decreases in CO activity and CO protein were observed in specific visual centers; these changes were accompanied by disproportionate decreases in COI, COIV, and COVIII mRNA levels. After 7 d of TTX, COI mRNA fell by 49 +/- 3% (mean +/- SEM) in LGN neurons, while COIV and COVIII mRNAs fell by only 18 +/- 3% and 29 +/- 3%, respectively. In comparison, CO activity decreased by 23 +/- 2%, and mtDNA by 26 +/- 4%. Qualitative observations in striate cortex also indicated that COI mRNA changed more than COIV mRNA, COVIII mRNA, mtDNA, or CO activity. Our results suggest that the local distribution of CO within neurons, and acute regulatory changes in CO activity occurring over periods of days are controlled mainly by regulation of the mitochondrial genes that encode the catalytic subunits of the enzyme.
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PMID:Mitochondrial and nuclear gene expression for cytochrome oxidase subunits are disproportionately regulated by functional activity in neurons. 838 52

1. The non-invasive method of near-infrared spectroscopy was used to measure myocardial oxygenation and haemodynamics in response to left anterior descending coronary artery occlusion in a porcine model. 2. Near-infrared spectroscopy measures changes in haemoglobin (and myoglobin) oxygenation and blood volume to yield information on tissue perfusion and flow. It also measures the redox state of cytochrome aa3, thus providing information about intracellular oxygen utilization. 3. Left anterior descending coronary artery occlusion was induced to produce periods of ischaemia lasting between 24s and 13.5 min (n = 13). The changes in deoxyhaemoglobin, oxyhaemoglobin and cytochrome aa3 measured during occlusion were all highly significant compared with baseline variation. In all occlusions (n = 13) a rapid decrease in oxyhaemoglobin concentration (-75.83 +/- 3.27 mumol/l, mean +/- SEM) with a simultaneous increase in deoxyhaemoglobin of 9.27 +/- 1.69 mumol/l was measured. The total haemoglobin concentration also fell by -71.3 +/- 5.32 mumol/l. Cytochrome aa3 was also reduced during occlusion (-8.35 +/- 1.044) mumol/l. 4. Over the range 24-60s occlusion, the magnitude of the fall in total haemoglobin and oxyhaemoglobin correlated with the duration of occlusion (P < 0.003 and 0.013 respectively). For total haemoglobin only the magnitude of the fall correlated with the increase upon release of occlusion (r = 0.89, P < 0.003). 5. Release of occlusion (n = 8) resulted in an immediate increase in the concentration of deoxyhaemoglobin at 9.88 +/- 1.06s, then total haemoglobin at 13.62 +/- 1.23s and finally oxyhaemoglobin at 29.75 +/- 5.96s. The difference between the timing of the maxima after reperfusion is significant (P < 0.002 and P < 0.007 respectively). Moreover, the time for the deoxyhaemoglobin signal to reach maximum values was found to correlate with the duration of occlusion (P < 0.04). This could be indicative of the PO2 of the ischaemic tissues and an immediate off-loading of oxygen from oxyhaemoglobin. The results are reliable, reproducible and sensitive enough to detect the kinetics of haemoglobin oxygenation from a beating heart in situ.
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PMID:Non-invasive measurement of cardiac oxygenation and haemodynamics during transient episodes of coronary artery occlusion and reperfusion in the pig. 877 60

The study investigated the hypothesis that delayed cerebral injury after transient cerebral ischemia is associated with vasoconstriction and decreased cerebral oxygenation. Eight chronically instrumented, late gestation fetal sheep were subjected to 30 min of cerebral ischemia in utero. Cortical impedance (CI) and electrocorticogram (ECoG) were recorded to determine the time course of cellular dysfunction. Histologic outcome was assessed 4 d postischemia. Changes in cerebral vascular tone and oxygenation were observed during and for 4 d after the insult using near infrared spectroscopy to measure changes in total cerebral Hb ([tHb]), oxyhemoglobin ([Hbo2]), and oxidized cytochrome aa3 ([Cyto2]). Results are expressed as mean +/- SEM. CI increased transiently during ischemia; then a delayed increase commenced 17.5 +/- 2.3 h postischemia and peaked at 42.3 +/- 2.4 h. ECoG was depressed during and after the insult. Seizures started 13.6 +/- 3.0 h postinsult and persisted for 25.4 +/- 3.2 h. Increases in [tHb] indicated two periods of cerebral vasodilation: immediately after early reperfusion, lasting 2.3 +/- 0.4 h and peaking to 20 +/- 2.0 mumol.L-1; and a later phase, commencing 12.8 +/- 2.0 h postischemia, peaking to 43 +/- 4.0 mumol.L-1 and lasting 43.1 +/- 5.2 h. [Hbo2] was relatively elevated (18 +/- 3.0 mumol.L-1) during d 4 postischemia, demonstrating a delayed increase in mean cerebral oxygen saturation. [Cyto2] fell during the insult (-0.7 +/- 0.2 mumol.L-1); and, commencing at 28-30 h postischemia, fell progressively to reach a minimum of -5.0 +/- 2.8 mumol.L-1 at 78-80 h postischemia. A greater fall in [Cyto2] was related to worse cerebral injury (p < 0.05). Delayed cerebral injury is accompanied by vasodilation and increased mean cerebral oxygen saturation, although a progressive fall in [Cyto2] might indicate a fall in mitochondrial oxygenation, cell loss, or changes in tissue optical characteristics.
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PMID:Delayed vasodilation and altered oxygenation after cerebral ischemia in fetal sheep. 882 85

Basal dendritic field areas of layer III pyramidal neurons were compared between the first (V1), second (V2), dorsolateral (DL) and fundus of the superior temporal (FST) areas in marmoset monkey visual cortex. These areas correspond to early stages of visual processing (V1, V2) and to areas specialized for the analysis of shape (DL) and motion (FST). Neurons in fixed tangential cortical slices (250 microns) were injected with Lucifer Yellow and immunohistochemically processed for a diaminobenzidine reaction product. Dendritic field areas were calculated for layer III pyramidal cells whose complete basal projection was judged to be within the section (n = 189). Borders between different visual areas were established based on cytochrome oxidase immunohistochemistry and myelin patterns in the experimental hemisphere, and electrophysiological recordings in the contralateral hemisphere. Pyramidal neurons in V1 had a mean basal dendritic field area of 1.84 x 10(4) microns2 (SEM = 2.04 x 10(3) microns2; n = 21). Layer III pyramidal cells in V2 had a mean basal dendritic field 1.26 times larger (mean = 2.32 x 10(4) +/- 1.78 x 10(3) microns2; n = 42) than that of V1 neurons. The mean dendritic field area of layer III pyramidal cells in DL (n = 76) was 1.5 times larger than that in V1 (mean = 2.75 x 10(4) +/- 1.59 x 10(3) microns2), and that in FST (n = 50) was 2.3 times larger (mean = 4.26 x 10(4) +/- 2.79 x 10(3) microns2). Our results show that there is a correlation between tangential dendritic field area of basal dendrites of layer III pyramidal neurons and modality of visual processing. The increase in basal dendritic field area of layer III pyramidal cells may allow more extensive sampling of inputs as required by higher-order processing of visual information.
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PMID:Comparison of dendritic fields of layer III pyramidal neurons in striate and extrastriate visual areas of the marmoset: a Lucifer yellow intracellular injection. 892 37

The concentrations of manganese, copper, and zinc in cerebrospinal fluid (CSF) from patients with multiple sclerosis (MS) and patients with no known neurological disease (control group) were measured. Manganese and copper levels were determined by two different analytical methods: atomic absorption spectrometry (AAS) and high-resolution inductively coupled plasma-mass spectrometry (HR-ICP-MS), whereas zinc levels were determined by HR-ICP-MS only. Manganese levels (mean+/-SEM) were significantly decreased in the CSF of MS patients (1.07+/-0.13 microg/L, ICP-MS; 1.08+/-0.11 microg/L, AAS) compared to the levels in the control group (1.78+/-0.26 microg/L, ICP-MS; 1.51+/-0.17 microg/L, AAS). Copper levels were significantly elevated in the CSF of MS patients (10.90+/-1.11 microg/L; ICP-MS, 11.53+/-0.83 microg/L, AAS) compared to the levels in the control group (8.67+/-0.49 microg/L, ICP-MS; 9.10+/-0.62 microg/L, AAS). There were no significant differences between the CSF zinc levels of MS and control patients. The physiological basis for the differences in manganese and copper concentrations between MS patients and controls is unknown, but could be related to alterations in the manganese- containing enzyme glutamine synthetase and the copper-containing enzyme cytochrome oxidase.
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PMID:Manganese, copper, and zinc in cerebrospinal fluid from patients with multiple sclerosis. 1283 84


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