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)

In the hermaphroditic pulmonate snail Lymnaea stagnalis a blood-gonad (blood-testis) barrier appears to exist. Septate junctions between Sertoli cells and epithelial cells of the neck areas of the gonadal acini constitute this barrier; they separate the male from the female compartment. Experiments with tracer substances (colloidal gold particles, lanthanum nitrate, tannic acid) showed that the basal lamina around the acini hardly forms a barrier; only the larger colloidal gold particles do not pass this lamina. Physiological, the blood-gonad barrier is apparent in studies on the composition of gonadal fluid, which differs considerably from that of haemolymph. The osmolarity and the concentration of protein and amino acids in gonadal fluid exceed those of haemolymph. As to the major ions, in the gonadal fluid Na+ is partly replaced by K+, and HCO-3 is almost totally replaced by Cl-. Such a distribution of HCO-3 and Cl- is indicative of metabolic acidosis. The cytochemical localization of carbonic anhydrase activity in cells lining the acinar lumen (Sertoli cells, epithelial cells) suggests that these cells are involved in the process of ion exchange. The metabolic acidosis in the gonad might result from the anaerobic production of lactate and succinate by Sertoli cells; these cells lack the enzymes cytochrome oxidase, lactate dehydrogenase, and succinate dehydrogenase. Spermatogenic cells, on the other hand, do possess these enzymes. This probably indicates that these cells metabolize lactate and succinate secreted by Sertoli cells.
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PMID:A morphological, enzyme-cytochemical, and physiological study of the blood-gonad barrier in the hermaphroditic snail Lymnaea stagnalis. 671 88

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

The energy metabolism of the English E-CMO strain of contagious equine metritis bacterium was studied in whole cells and cell extracts. This bacterium appears to have an active Krebs cycle and probably obtains energy by oxidative phosphorylation since glycolysis and the hexose monophosphate pathways appear to be absent. These conclusions are based on the findings that [U-14C]glucose incorporation by this bacterium is below the level of detection, and that respiration is stimulated by Krebs cycle intermediates (i.e., malate, citrate, and succinate), but not by glucose, fructose, maltose, or sucrose. Furthermore, support comes from the fact that enzymes generally associated with the Krebs cycle and electron transport (i.e., malate dehydrogenase, succinate dehydrogenase, isocitrate dehydrogenase, fumarate hydratase, malate dehydrogenase [decarboxylating], cytochrome oxidase, superoxide dismutase, NADH dehydrogenase, and catalase) were detected. Those enzymes normally associated with glycolysis and the hexose monophosphate pathways (i.e., hexokinase, glucose 6-phosphate dehydrogenase, fructose biphosphate aldolase, glycerol 3-phosphate dehydrogenase, phosphoenolpyruvate carboxykinase, pyruvate kinase, phosphate acetyl transferase, acetate kinase, alcohol dehydrogenase, and lactate dehydrogenase) were below the level of detection.
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PMID:Energy metabolism of the contagious equine metritis bacterium. 708 71

The effect of 11 weekly injections of nandrolone phenylpropionate (400 mg) on some skeletal muscle parameters was investigated in 6 Thoroughbred geldings undergoing training. Three muscles were sampled, the middle gluteal, the biceps femoris and the semitendinosus. Training alone produced increases in the percentage of fast twitch high oxidative fibres (FTH), glycogen content and the activities of citrate synthase, 3-hydroxyacl CoA dehydrogenase and cytochrome oxidase. In contrast the training programme did not alter water content, total protein content, the activities of lactate dehydrogenase, phosphofructokinase of beta glucuronidase, fibre area ratios or the number of capillaries per unit fibre area. Nandrolone phenylpropionate given in conjunction with the training programme only resulted in changes in 2 of these parameters. There was no increase in the percentage of FTH fibres in the biceps femoris with anaerobic training and the fibre area ratio increased significantly in this muscle.
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PMID:Effects of nandrolone phenylpropionate in the horse: (3) skeletal muscle composition in the exercising animal. 710 87

Energy metabolism has been examined in mouse LS cells growing under steady-state conditions in chemostat culture. The metabolic quotient of glucose oxidized (glucose consumed, but not fermented) remained constant, independent of growth rate between cell doubling times of 6 days and 1.2 days. Specific activities of cytochrome oxidase and malate dehydrogenase in the mitochondria remained constant at different growth rates, in accord with the constancy of the glucose oxidation rate. Cytosolic malate dehydrogenase activity was about fourfold greater than the mitochondrial isozyme. The steady-state rate of lactate production fluctuated because of technical limitations but correlated well with cytosolic lactate dehydrogenase activity.
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PMID:Glucose metabolism and dehydrogenase activities in the cytosol and mitochondria of mouse LS cells in chemostat culture. 721 34

The effect of the chronic intramuscular administration of some agents related to the S-adenosyl-L-methionine system on the hyperammonemia syndrome was evaluated. This experimental syndrome was induced in the rat by intraperitoneal administration of high doses of ammonium acetate (33, 100 and 300 mg/kg/day, 6 days a week for 80 days) followed by the assay of the activities of some cerebral enzymes involved in energy transduction. The enzymatic activities studied in the homogenate and in the mitochondrial fractions of brain tissue were: lactate dehydrogenase, citrate synthase, malate dehydrogenase, total NADH-cytochrome c reductase and cytochrome oxidase. All three doses of ammonium acetate induced significant modifications in the cerebral enzymatic activities. These doses reduced the activity of the total NADH-cytochrome c reductase both in the homogenate and in the mitochondrial fraction. On the other hand the activity of malate dehydrogenase was reduced limited to the two lower doses in the homogenate only. The simultaneous daily treatment (i.m.) with equimolar doses of substances involved in the S-adenosyl-L-methionine system (adenosine, methionine and S-adenosyl-L-methionine) did not cause any significant modification of the cerebral enzymatic activities associated with the administration of ammonium acetate at the three dose levels, thus confirming our previous results.
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PMID:Cerebral enzymatic activities during chronic hyperammonemia and treatment with S-adenosyl-L-methionine, adenosine and methionine in the rat. 725 Mar 59

The effect of a chronic (3 months) treatment with vincamine on the enzymatic activities related to energy transduction was studied on several areas of the cerebral cortex of dog brain. About enzymatic activities of the four different cortical areas, in controls, no difference was observed between the enzymatic activities evaluated in the crude mitochondrial fraction, with regard to both the tricarboxylic acid cycle (citrate synthase, malate dehydrogenase) and the electron transport chain (total NADH-cytochrome c reductase, cytochrome oxidase). On the contrary, in the homogenate, lactate dehydrogenase, malate dehydrogenase and acetylcholine esterase showed different maximal activities. In the crude mitochondrial fraction the intravenous treatment with the three different doses of vincamine failed to cause any significant change as compared to controls. On the contrary, with regard to the enzymatic activities evaluated in the homogenate in toto, the analysis of variance revealed an effect on cytochrome oxidase at the dose of 3 mg/kg intravenously.
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PMID:Effect of vincamine on some enzymatic activities from various areas of the beagle dog cerebral cortex. 729 73

Dose/action and time/action relationships relative to the effect of the in vivo treatment with some biological molecules (cytidine, uridine and glutamine) on several enzymatic activities connected with cerebral metabolism (lactate dehydrogenase, malate dehydrogenase, total NADH cytochrome c reductase, cytochrome oxidase and citrate synthase) were studied in the normal rat brain. While time/action curves were found to be in agreement with classical pharmacodynamic descriptions, dose/action curves exhibited a varying behavior according to the biological substrate tested (brain homogenate in toto or crude mitochondrial fraction from brain in toto). Often enzymatic activity changes as a function of dose failed to show linear correlations, a parabolic pattern being observed. At any rate, the changes affecting several cerebral enzymatic activities may account for some pharmacodynamic properties of the biological molecules tested.
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PMID:Dose/action and time/action relationships of some biological molecules evaluated on the cerebral enzymatic activities. 745 24

The changes induced by alphaxalone-alphadolone (3:1) in the cerebral enzymatic activities of the Kreb's cycle (citrate synthase, malate dehydrogenase) and electron transfer chain (total NADH-cytochrome c reductase and cytochrome oxidase) were studied. In addition, the activation of lactate dehydrogenase (for the glycolytic pathway) and of acetylcholine esterase (as indicative of transmission) were investigated. These enzymatic activities were evaluated in the homogenate in toto and/or in the crude mitochondrial fraction of rat brain, since these enzymes are variously located in the cytoplasm. Two relationships were studied: a) dose/action (0.5, 1. 2, 4, 8, 16 and 32 mg . kg-1) by measurements carried out 60 min after i.p. administration; b) time/action (16 mg . kg-1 i.p.; measurements 15, 30, 60, 120 and 240 min after administration). The results show that in both kinds of trials alphaxalone-adphadolone reduced only the activity of the enzyme cytochrome oxidase evaluated on the brain homogenate in toto. More specifically, with regard to the dose/action relationship, the effect occurred starting with the dose of 2 mg . kg-1 and did not take place linearly with the higher ones. As to the time/action relationship, the effect began 60 min after administration, the changes being observed also at the subsequent times. The data obtained are discussed with regard to the interactions between alphaxalone -alphadolone and mitochondrial enzymatic systems, and compared with the effects of phenobarbital on the same systems.
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PMID:Effect of alphaxalone-alphadolone on some enzymatic activities from rat brain. 745 57

The activities of nine enzymes in liver specimens obtained from four children who had died from Reye's syndrome were compared to the corresponding activities of a control group of four children who had died from unrelated causes. At the 95% significance level, the alterations could be classified into three groups. Five activities [lactate dehydrogenase, alanine aminotransferase, glucose 6-phosphatase, cytochrome oxidase, and malate dehydrogenase (mitochondrial plus cytosolic)] showed no change. Three enzymes [glutamate dehydrogenase, isocitrate dehydrogenase (NADP), and monoamine oxidase] were decreased. One activity (glucose 6-phosphate dehydrogenase) was increased. The malate dehydrogenase isozymes were resolved by electrophoresis, and the two bands were stained and measured. The ratio of cytosolic:mitochondrial enzyme was significantly greater in Reye's syndrome than in the control group. These results lend further support to the view that in Reye's syndrome the impairment of hepatic function is largely confined to the mitochondria. The lowered activity of monoamine oxidase means that the abnormalities extend to the outer mitochondrial membrane. Imbalances of the cytosolic:mitochondrial enzyme activities were evaluated in needle biopsy specimens from four other children under conditions where neurologic abnormalities were less severe. Two patients had elevated ratios of both glutamate:lactate dehydrogenase and cytosolic:mitochondrial malate dehydrogenase activities, and a third had only an abnormal malate dehydrogenase ratio. In contrast to these Reye's syndrome patients, a fourth case admitted with a provisional diagnosis of Reye's syndrome showed no abnormality in either ratio in stage IV coma.
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PMID:Comparison of cytosolic and mitochondrial hepatic enzyme alterations in Reye's syndrome. 745 35


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