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)

In liver mitochondria of control animals and of animals subjected to swimming for three hours experiments are made to determine the activities of rotenone-insensitive NAD.H-cytochrome c-oxireductase, succinate-cytochrome c-oxireductase, MDH, SDH, ATP-ase and cytochrome oxidase, as well as oxygen uptake, respiratory control index and ADP/O ratio upon oxidation of succinate and glutamate + malate. Decrease of the ADP/O ratio and of the respiratory control index, as well as increased ATP-ase activity, are established after swimming. The e--transport rate decreases. The activity of the remaining enzymes is unchanged. The activities of MDH, SDH, NAD.H-cytochrome c- and succinate-cytochrome c-oxireductases decrease 22 hours after exhaustive swimming. The activities of the cytochrome oxidase and the ATP-ase are unchanged compared with the controls. A single exhaustive loading results in changes in the capacity of phosphorylation in the liver mitochondria and the changes in the activities of the enzymes studied are established 22 hours later.
 ...
PMID:Effect of exhaustive swimming on the oxidative phosphorylation and the activity of some enzymes in rat liver mitochondria. 101 5

The object of the study was the investigation of the occurrence and distribution of some oxidative enzymes in the sporocyst of Fasciola hepatica L. The samples were examined for the presence of cytochrome oxidase, peroxidase, NADH and NADPH tetrazolium reductases, as well as succinate, isocitrate, malate, lactate, alpha-glycerophosphate, glyceraldehyde-3-phosphate, glucose-6-phosphate, beta-hydroxybutyrate, L-glutamate and alcohol dehydrogenases. All of them save cytochrome oxidase were found to occur in the sporocyst. The presence and localization of these enzymes were examined by histochemical methods in various stages of development of the sporocyst. These investigations permitted it to be established that glycolytic processes are the principal way of release of energy for all developmental groups of this larva. Moreover, the functions of the tricarboxyl acid and pentose-phosphate cycles were detected and found to play a less important part in processes of energy production in the sporocyst. In addition, the functioning and metabolism of each larval organ in various stages of its development were discussed in so far as was possible on the basis of the analysis of the above-mentioned oxidative enzymes.
 ...
PMID:Oxidative enzymes in the development of Fasciola hepatica L. III. The activities of oxidases and dehydrogenases in the sporocyst. 119 74

Quantitative histochemistry (scanning microphotometry) was used to determine the activities of the mitochondrial enzymes NAD-linked isocitrate dehydrogenase (EC 1.1.1.41), L-glutamate dehydrogenase (EC 1.4.1.3) and GABA transaminase (EC 2.6.1.19) in various layers of the hippocampus (middle one third) of young (3-4 months old) and memory-impaired aged rats (28-30 months old). For comparison, determinations of cytochrome c oxidase (EC 1.9.3.1) as a marker for mitochondria and energy metabolism were also performed. The study showed that there was a layered reaction pattern in the hippocampus and that the cellular distribution and the levels of enzyme activity were different. However, the activities of the different enzymes (excepting GABA transaminase and cytochrome c oxidase) were significantly correlated in the hippocampus in both age groups. Age-dependent changes were only observed for NAD-linked isocitrate dehydrogenase and GABA transaminase (significant increases of activities in some layers of the hippocampus, preferentially in the terminal field of the perforant path). From the present study it is concluded that, 1. the enzymatic complement of mitochondria in neurons and glia depends upon layer specific metabolic processes of the hippocampus (also with respect to glutamatergic and GABAergic terminal fields) indicating a layer specific interaction of the enzymes studied to produce or catabolize glutamate and GABA, and 2. the age dependent changes of the studied enzymes are very restricted.
 ...
PMID:Mitochondrial enzymes related to glutamate and GABA metabolism in the hippocampus of young and aged rats: a quantitative histochemical study. 134 64

In a model of autoimmune myocarditis in guinea piga, the authors studied energy producing processes in mitochondria and the role of oxygen free radical generation in tissue injury. A significant decrease in the capacity of oxidative phosphorylation was detected in parameters QO2 (S3) on the basis of glutamate + malate (p < 0.005) and pyruvate (p < 0.05) measurements. Other parameters studied were however only insignificantly reduced in myocarditic heart mitochondria as compared to controls. The activity of mitochondrial cytochrome oxidase was also insignificantly reduced in animals with myocarditis. Generation of oxygen free radicals was in the presence of the inflammatory infiltrate in this model not significantly higher than in the intact myocardial tissue.
 ...
PMID:[The role of mitochondrial energy metabolism and oxygen free radicals in the pathogenesis of experimental autoimmune myocarditis]. 139 34

The maximal rates (Vmax) of some mitochondrial enzyme activities related to energy transduction (citrate synthase, succinate dehydrogenase, malate dehydrogenase, NADH-cytochrome c reductase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase, glutamate-pyruvate- and glutamate-oxaloacetate- transaminases) were evaluated in non-synaptic ("free") and intrasynaptic "light" and "heavy" mitochondria from hippocampus of Macaca fascicularis (Cynomolgus monkey). The different mitochondrial populations were isolated from the hippocampus of monkeys treated p.o. with dihydroergocryptine at a dose of 12 mg/kg/day before and during the induction of a Parkinson's-like syndrome by MPTP administration (i.v., 0.3 mg/kg/day for 5 days). The MPTP administration modified the activity of some enzymes related to the metabolism of glutamate and the activity of succinate dehydrogenase on selected types of mitochondria. Pharmacological treatment by dihydroergocryptine promoted return to the steady-state levels of most enzymes, demonstrating a protective effect on these biochemical parameters.
 ...
PMID:Mitochondrial factors involved in Parkinson's disease by MPTP toxicity in Macaca fascicularis and drug effect. 146 62

Previous work has shown that irrespective of the route of exposure methyl isocyanate (MIC) caused acute lactic acidosis in rats (Jeevaratnam et al., Arch. Environ. Contam. Toxicol. 19, 314-319, 1990) and the hypoxia was of stagnant type due to tissue hypoperfusion resulting from hypovolemic hypotension in rabbits administered MIC subcutaneously (Jeevarathinam et al., Toxicology 51, 223-240, 1988). The present study was designed to investigate whether MIC could induce histotoxic hyperoxia through its effects on mitochondrial respiration. Male Wistar rats were used for liver mitochondrial and submitochondrial particle (SMP) preparation. Addition of MIC to tightly coupled mitochondria in vitro resulted in stimulation of state 4 respiration, abolition of respiratory control, decrease in ADP/O ratio, and inhibition of state 3 oxidation. The oxidation of NAD(+)-linked substrates (glutamate + malate) was more sensitive (five- to sixfold) to the inhibitory action of MIC than succinate while cytochrome oxidase remained unaffected. MIC induced twofold delay in the onset of anerobiosis, and cytochrome b reduction in SMP with NADH in vitro confirms inhibition of electron transport at complex I region. MIC also stimulated the ATPase activity in tightly coupled mitochondria while lipid peroxidation remained unaffected. As its hydrolysis products, methylamine and N,N'-dimethylurea failed to elicit any change in vitro; these effects reveal that MIC per se acts as an inhibitor of electron transport and a weak uncoupler. Administration of MIC sc at lethal dose caused a similar change only with NAD(+)-linked substrates, reflecting impairment of mitochondrial respiration at complex I region and thereby induction of histotoxic hypoxia in vivo.
 ...
PMID:In vitro and in vivo effect of methyl isocyanate on rat liver mitochondrial respiration. 147 Nov 48

The maximal rate (Vmax) of some mitochondrial enzyme activities related to energy transduction (citrate synthase, alpha-ketoglutarate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, NADH-cytochrome c reductase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase, glutamate-pyruvate transaminase and glutamate-oxaloacetate transaminase) are evaluated in non synaptic ("free") and intrasynaptic mitochondria from brain hippocampus. The different mitochondrial populations were isolated from rat subjected to single i.p. treatment with saline solution, almitrine (30 mg/kg) and delta-yohimbine (10 mg/kg). In control rats, the mitochondrial populations exhibit different enzymatic patterns. Acute treatment with almitrine decreases cytochrome oxidase activity in intra-synaptic mitochondria, while acute treatment with delta-yohimbine decreases succinate dehydrogenase activity in both types of free and intra-synaptic mitochondria. NADH-cytochrome c reductase activity is also decreased by acute treatment with almitrine ("free" and "synaptic" mitochondria) and delta-yohimbine (synaptic mitochondria only).
 ...
PMID:Factors involved in drug interference on enzyme activities of three mitochondrial populations from rat hippocampus. 180 34

Citrinin (CTN), a mycotoxin produced by several species of Penicillium and Aspergillus, causes renal proximal tubule (RPT) cell injury and death by an unknown mechanism of action. Using suspensions of rat RPT, the cellular events preceding CTN-induced cytotoxicity were investigated. Tubule viability decreased in a concentration- and time-dependent manner after CTN exposure, with cell death beginning 1, 2, and 4 hr after exposure to 500, 125-250, and 63 microM, respectively. Basal oxygen consumption (QO2) of RPT increased from 41 to 53 nmol O2.mg protein-1.min-1 30 min after exposure to 250 microM CTN and returned to control values 1 hr after exposure. A similar concentration- and time-dependent transitory rise in basal QO2 occurred at all concentrations of CTN tested (63-500 microM). Nystatin-stimulated QO2, an indirect measure of mitochondrial state 3 respiration in RPT, decreased 11% at 0.5 and 1 hr after exposure to 500 and 250 microM CTN, respectively, but was not affected after exposure to 63 and 125 microM CTN. Adenosine triphosphate content declined 22% to 48% in RPT at 0.5 and 1.5 hr after exposure to 500 and 125-250 microM CTN, respectively. Although lipid peroxidation occurred concurrently with RPT cell death, iron-mediated oxidative stress was not a causative factor in the development of toxicity since pretreatment with 1 mM deferoxamine prevented iron-mediated lipid peroxidation but did not protect RPT from CTN-induced cell death. Further studies using RPT and isolated renal cortical mitochondria (RCM) showed that CTN had multiple effects on mitochondrial function. Direct probing of mitochondrial function within RPT showed that a 1-hr exposure to 250 microM CTN increased spontaneous respiration 55% in RPT respiring on the site I respiratory substrates glutamate/malate while state 3 respiration decreased 34%. CTN also decreased succinate supported respiration but had no effect on cytochrome c-cytochrome oxidase. With isolated RCM, a 3-min exposure to 125 and 250 microM CTN increased state 4 respiration in the absence of a phosphate acceptor 27 and 67%, respectively, while 250 microM CTN decreased state 3 respiration 23%. Respiration in the presence of a known uncoupler was reduced after CTN exposure (63-250 microM) in a concentration-dependent manner. These results indicate that CTN has multiple effects on mitochondrial function in RPT and isolated RCM which may contribute to the development of cell death in rat RPT.
 ...
PMID:The role of altered mitochondrial function in citrinin-induced toxicity to rat renal proximal tubule suspensions. 185 44

Oxidative energy metabolism in mouse liver mitochondria was examined during weaning using different substrates. During the post-natal development, from suckling to weanling stage, the respiration rates showed a temporary decrease. These altered levels recovered in the adults. Respiration rates with the three substrates studied namely, glutamate, beta-hydroxybutyrate and succinate showed the same pattern. However, the levels of primary dehydrogenase as well as that of basal adenosine triphosphatase were not significantly altered during weaning. The content of cytochromes aa3 and b significantly decreased during this period. The results indicate that cytochrome aa3 may be of primary importance in the restoration of full respiratory function in mitochondria after the weaning period.
 ...
PMID:Oxidative phosphorylation in mouse liver mitochondria during weaning. 197 70

Male rats, aged 17 weeks at the end of experiments, were divided into four groups. Two groups lived in normal cage conditions with or without extra load (20% of the body weight) and two groups were trained by running with or without extra load for 8 weeks. Oxidation rates of succinate, glutamate + malate, palmitoylcarnitine, and pyruvate, and the activities of lactate dehydrogenase, citrate synthase, isocitrate dehydrogenase and cytochrome oxidase were measured in homogenates of the right ventricle and in those of the subendocardial and subepicardial layers of the left ventricle. Oxidation rates of succinate and palmitoylcarnitine tended to be higher in the subendocardium than in the subepicardium of sedentary control animals (p less than 0.1 and p less than 0.05, respectively). Transmural differences of succinate and palmitoylcarnitine oxidation rates were even more clear after running training (p less than 0.01 and p less than 0.05, respectively), after carrying extra load (p less than 0.001 and p less than 0.001, respectively) and after training carrying extra load (p less than 0.001 and p less than 0.05, respectively). Training also enhanced pyruvate oxidation rate in the subendocardium. Oxidation rates of all substrates were lower in the right ventricle than in the left ventricle. In control animals there were no regional differences in the myocardial enzyme activities and the training- or extra-load-induced changes were modest compared with the changes in the oxidation rates. The most significant change was the training-induced enhancement in the lactate dehydrogenase activity of the subendocardium (p less than 0.001 vs subepicardium). These results show greater subendocardial than subepicardial oxidation rates of certain substrates in the normal heart. These results also suggest that the myocardium adapts to increased work by increasing the subendocardial oxidation rate of some but not all substrates, indicating further that there may be qualitative mitochondrial differences in the different regions of the heart.
 ...
PMID:Regional differences of substrate oxidation capacity in rat hearts: effects of extra load and endurance training. 207 98


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>