Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two groups (n = 5) of male weanling Wistar rats were housed individually and fed copper (Cu)-deficient (0.5 mg Cu/kg) diets either with or without methionine supplementation (18 g/kg) for 49 days. Plasma caeruloplasmin (EC 1.16.3.1) and erythrocyte superoxide dismutase (EC 1.15.1.1, CuSOD) activities were measured in blood. Tissue Cu levels and the activities of cytochrome c oxidase (EC 1.9.3.1, CCO) and CuSOD were measured in the heart and liver. Hepatic activities of the sulfhydryl-sensitive enzymes, creatine kinase (EC 2.7.3.2), fumarase (EC 4.2.1.2) glutathione S-transferase (EC 2.5.1.18) and lipoamide dehydrogenase (EC 1.6.4.3) were also measured. Apart from cardiac CCO activity all of the measured indices of Cu status were found to be significantly (p less than 0.05) decreased in the methionine supplemented rats. Although fumarase activity was significantly (p less than 0.05) decreased in the methionine-supplemented animals compared with controls, the activities of the other sulfhydryl-sensitive enzymes were not significantly decreased. These results suggest that some of the toxic effects of excess dietary methionine may be mediated through interference with copper metabolism rather than through the previously postulated inhibition of sulfhydryl-sensitive enzymes by metabolites of methionine.
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PMID:Excess dietary methionine decreases indices of copper status in the rat. 216 46

Chronic supraventricular tachycardia has been associated with ventricular dysfunction in humans and animals. However, this ventricular failure is poorly characterized, and the ultrastructural consequences of supraventricular tachycardia are unknown. We serially examined right and left ventricular function, endomyocardial ultrastructure, and creatine kinase activity in eight pigs at base line and again at 1, 2, and 3 wk following rapid atrial pacing. Left and right ventricular ejection fractions fell significantly from base line after 1 wk of chronic tachycardia. Three weeks of chronic pacing resulted in further deterioration in ejection fractions. Significant biventricular chamber dilatation developed and was associated with a reduction in end-diastolic wall thickness after 2 wk of tachycardia. Mitochondrial injury and diminished mitochondrial cytochrome oxidase staining of subendocardial myocytes were observed after 2 wk of tachycardia. Endomyocardial creatine kinase activity fell from control levels following 2 wk of pacing. Postmortem examination revealed a reduction in left ventricular wall thickness compared with 14 control animals. Fibrosis occurred along the subendocardial layer in paced animals, and glycogen content was also reduced. In summary, chronic supraventricular tachycardia resulted in severe biventricular pump dysfunction and chamber dilatation that were associated with ultrastructural alterations and reduced enzyme activity of the subendocardial myocytes. These ultrastructural and metabolic changes may be potential mechanisms responsible for the ventricular dysfunction and dilatation observed in this model.
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PMID:Chronic supraventricular tachycardia causes ventricular dysfunction and subendocardial injury in swine. 237 9

In chronic glucagon-treated ducklings (GT) showing thermogenic and hyperthermic responses without shivering to glucagon test injection and in control ducklings (TN; both aged 44 +/- 1 days and reared at thermoneutrality), subsarcolemmal (S) and intermyofibrillar (I) mitochondria from gastrocnemius muscle and mitochondria from liver were isolated. Respiration and cytochrome oxidase activity were determined in these isolated mitochondria by polarography and creatine kinase activity by spectrophotometry, both at 25 degrees C. In GT ducklings, the powerful thermogenesis observed in vivo after a glucagon test injection may be due to the uncoupling effect of released free fatty acids (FFA) in loose-coupled mitochondria because their respiration increased as a function of FFA concentration, and the loose coupling of these mitochondria was reversed by addition of albumin. In all types of mitochondria from GT ducklings, the increase in respiration because of FFA was about double that in mitochondria from controls. There was no change in creatine kinase activity from liver and I mitochondria, but a 16% decrease in this enzyme activity (expressed per mg mitochondrial protein) from S mitochondria was shown despite a strong increase in cytochrome oxidase activity from liver mitochondria (+114% if expressed per g tissue) and from muscle mitochondria (I, +53 or +48%; S, +41 or +97% if expressed per mg mitochondrial protein or per g tissue, respectively). These results support a coupling defect in liver and skeletal muscle mitochondria from the GT hyperthermic ducklings and an uncoupling reinforcement by FFA.
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PMID:Loose-coupled mitochondria in chronic glucagon-treated hyperthermic ducklings. 254 12

Significant levels of mitochondrial uncoupling protein were demonstrated on neonatal dog mitochondria prepared from perirenal, bladder and subcutaneous adipose tissue sites. The protein was not detected in homogenates of adipose tissue samples from the same sites in adult, control dogs. However, chronic treatment of adult dogs with a beta-stimulant (LY 79730) led to the appearance of detectable amounts of uncoupling protein in perirenal and bladder but not subcutaneous adipose tissue depots. Decreases in mean cell diameter, increases in the frequency of multilocular cells and of cytochrome oxidase and creatine kinase were also associated with the effects of treatment on dog adipose tissue. The results demonstrate the age-related decline in dog brown adipose tissue and its reversal by chronic treatment with beta-stimulant.
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PMID:Immunological, histological and biochemical assessment of brown adipose tissue activity in neonatal, control and beta-stimulant-treated adult dogs. 288 91

Oxidized dialdehyde analogs of ADP or ATP (oADP and oATP) were shown to inhibit irreversibly adenine nucleotide translocator (T) and creatine kinase (CK) in heart mitochondria. Inactivation of T and CK was parallel with carboxyatractyloside - sensitive and (ADP + phosphocreatine) - sensitive incorporation of o[3H]ADP into mitochondria, respectively. o[3H]ADP incorporation sensitive to CAT or ADP+phosphocreatine was used to determine T and CK contents in mitochondria. T content in cardiac mitochondria from rat, rabbit, dog, and chicken was calculated to be 2.6 - 2.9 moles/mole cyt.aa3. The same value of T/cyt.aa3 ratio was found in liver mitochondria with lower cytochrome aa3 content. In all types of cardiac mitochondria CK content was found to be 2.4 - 2.6 moles/mole cyt.aa3. The data show that T and CK are present in molar ratio 1:1 in all types of cardiac mitochondria.
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PMID:Affinity modification of creatine kinase and ATP-ADP translocase in heart mitochondria: determination of their molar stoichiometry. 300 38

The stoichiometry and dissociation constant for the binding of homogeneous chicken heart mitochondrial creatine kinase (MiMi-CK) to mitoplasts was examined under a variety of conditions. Salts and substrates release MiMi-CK from mitoplasts in a manner that suggests an ionic interaction. The binding of MiMi-CK to mitoplasts is competitively inhibited by Adriamycin, suggesting that they compete for the same binding site. Fluorescence measurements also show that Adriamycin binds to MiMi-CK so that the effect of Adriamycin on the binding of MiMi-CK to mitoplasts is not simple. Titrating mitoplasts with homogeneous MiMi-CK at different pH values shows a pH-dependent equilibrium involving a group(s) on either the membrane or the enzyme with a pKa = 6. Extrapolating these titrations to infinite MiMi-CK concentration gives 14.6 IU bound/nmol cytochrome aa3 corresponding to 1.12 mol MiMi-CK/mol cytochrome aa3. Chicken heart mitochondria contain, after isolation, 2.86 +/- 0.42 IU/nmol cytochrome aa3. Titrating respiring mitoplasts with carboxyatractyloside gives at saturation 3.3 mol ADP/ATP translocase/mol cytochrome aa3. Therefore, chicken heart mitoplasts can maximally bind about 1 mol of MiMi-CK per 3 mol translocase; in normal chicken heart mitochondria about 1 mol of MiMi-CK is present per 13 mol translocase.
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PMID:Association of chicken mitochondrial creatine kinase with the inner mitochondrial membrane. 381 58

It has been demonstrated in experiments on 134 cats that during acute blood loss (24 +/- 0.8 ml/kg), hyperbaric oxygen therapy (3039 hPa, 60 min) stimulates cytochrome oxidase, eliminates compensatory activation of mitochondrial creatine kinase and maintains the hyperactivity of cytoplasmic creatine kinase in the diencephalon, stabilizes the elevated AMP content at the level of blood loss compensation stage, prevents the fall in pO2 and in the ATP level as well as that in the energy charge and creatine phosphate content in the sensomotor cortex and subcortex, that is typical for the decompensation stage. Besides, hyperbaric oxygen therapy also averts the development of the terminal state that supervenes in the majority of untreated animals.
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PMID:[Bioenergetic processes in the cerebral cortex and diensephalon during hyperbaric oxygenation therapy of acute blood loss]. 613 71

ATP-dependent calcium sequestration was previously localized in vesicles of mitotic apparatus isolated from sea urchins. We now demonstrate that the mitotic apparatus contains an ATP-regenerative system characterized as creatine kinase (EC 2.7.3.2). Mitotic apparatus isolated with vesicles intact converted ADP to ATP if phosphocreatine was present. Omission of ADP or phosphocreatine gave negligible ATP. When mitotic apparatus were washed with detergent-containing buffer to remove vesicles, their ability to produce ATP from ADP and phosphocreatine was reduced. Assays of creatine kinase activity using NADP+:glucose-6-phosphate dehydrogenase indicated that 70% of the creatine kinase activity was extractable with 0.5% Triton X-100. The insoluble residue containing the skeleton of the mitotic apparatus had the rest of the activity. Experiments with a luciferin/luciferase assay showed that Triton removed above 82% of the activity. Preparations of intact mitotic apparatus were free of cytochrome c oxidase (EC 1.9.3.1) activity and therefore free of mitochondria. About 10(8) mitotic apparatus (total volume about 1 liter) could produce 17 mmol of ATP/min when substrates were not limiting. The creatine kinase enzyme activity described herein and the previously described membrane vesicular calcium sequestration system are nonmitochondrial, integral constituents of the sea urchin mitotic apparatus.
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PMID:Identification of nonmitochondrial creatine kinase enzymatic activity in isolated sea urchin mitotic apparatus. 631 91

The purpose of the study was to verify the influence of several weeks of chronic low-frequency electrical stimulation (LFES) on the metabolic profile and functional capacity of human skeletal muscle. Knee extensor muscles (KEM) of eight subjects were electrically stimulated at 8 Hz for 8 h/day and 6 days/wk. Vastus lateralis muscle samples were taken before, after 4 wk, and after 8 wk of LFES, and activities of anaerobic (creatine kinase, phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase) and aerobic-oxidative (citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, cytochrome-c oxidase) enzyme markers were determined. KEM dynamic performance was also assessed before, after 4 wk, and after 8 wk of LFES. Activity levels of anaerobic enzymes were not altered, whereas the activity levels of citrate synthase (29%),3-hydroxyacyl-CoA dehydrogenase (22%), and cytochrome-c oxidase (25%) were significantly increased after 4 wk of LFES but were not further increased after 4 additional wk of LFES. KEM performance was also improved (P < 0.05) but leveled off after 4 wk of LFES. Although significant changes were observed, the results of the present study suggest that the muscle characteristics investigated in the current study have a limited capacity of adaptation in response to this form of chronic LFES.
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PMID:Human skeletal muscle adaptation in response to chronic low-frequency electrical stimulation. 783 13

Mice were treated for 7-12 wk with the creatine analogue beta-guanidinopropionic acid (beta-GPA). Treatment reduced total creatine to approximately 5% of control values in soleus (SOL) and extensor digitorum longus (EDL) muscles. In both muscles from treated mice, phosphorylated beta-GPA accumulated and resting [ATP] decreased by approximately 50%. Relative to controls, cytochrome oxidase and citrate synthase activities increased significantly in EDL from treated mice, but not in SOL; creatine kinase activity decreased significantly in SOL, but not in EDL. Measurements of poststimulation energy metabolism show that the energy cost to maintain tension in SOL and EDL from treated mice was approximately 50% of that in control muscle. Relative to controls, first-order rate constants of poststimulation O2 demand were 2- and 3.6-fold greater in SOL and EDL, respectively, from treated mice. Increased economy of SOL and EDL from treated mice is consistent with previously reported changes in myosin isoenzymes. Increases in rate constants of O2 utilization in creatine-depleted muscle are inconsistent with the hypothesis that cytoplasmic or mitochondrial creatine kinase is rate limiting for cellular respiration.
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PMID:Contractile economy and aerobic recovery metabolism in skeletal muscle adapted to creatine depletion. 804 75


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