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)

Previous studies have shown that most neuronal ATP is produced by oxidative metabolism, and consumed by Na+,K(+)-ATPase. We hypothesized that the distribution of Na+,K(+)-ATPase in brain would correlate with that of the energy-producing enzyme, cytochrome oxidase (CO). We localized these enzymes in monkey hippocampus and striate cortex by histochemistry and immunohistochemistry. Their distributions were generally similar, although some differences were observed. We also studied regulation of enzyme levels, using monocular impulse blockage with tetrodotoxin (TTX) to alter neuronal activity in the visual system. Parallel changes in CO and Na+,K(+)-ATPase activity were induced in striate cortex. These results provide further evidence that neuronal energy demands regulate CO levels and distribution.
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PMID:Coordination of ATP production and consumption in brain: parallel regulation of cytochrome oxidase and Na+, K(+)-ATPase. 132 57

Electron microscopic enzyme cytochemical reactions of Entamoeba histolytica trophozoite showed that acid phosphatase (ACP) and cytidine monophosphatase (CMPase) were located in the lysosomes. The lysosome containing enzymes were distributed in the endoplasm and beneath the plasmalemma, and the releasing enzymes by lysosomes excreted outside of the plasmalemma and caused the injury to host cells. The cytochemical positive reactions of catalase and glucose-6-phosphatase (G-6-Pase) showed that E. histolytica contains microbodies and endoplasmic reticulum. The reactive products of peroxidase (POase) were seen in the lysosome-like structure. The reactions of cytochrome oxidase (COase) and succinate dehydrogenase (SDH) were both negative, indicating that E. histolytica lacked mitochondria. The reactions of thiamine pyrophosphatase (TPPase) and nicotinamide adenine dinucleotide phosphatase (NADPase) were both negative, indicating that E. histolytica lacked Golgi body. The reactions of Na(+)-K(+)-ATPase were located on plasmalemma.
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PMID:[Electron microscopic enzyme cytochemistry of Entamoeba histolytica trophozoite]. 133 24

Thymomodulin and Thymolymphotropin, biologically active thymus derivative peptides exert recovery effects on the functionality of some membrane bound, mitochondrial and lysosomal enzymes (monoamine oxidase, ATPase, phosphatases, cytochrome oxidase, succinate oxidase) affected by gamma-irradiation. These drugs exert antistress effect by re-establishing the function of hypothalamus-pituitary-adrenal axis and that of lymphoid organs.
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PMID:The effects of thymomodulin and thymolymphotropin on the stress response of neuroendocrine system by gamma-irradiated Wistar rat. 134 4

The mitochondrial import and assembly of the F1ATPase subunits requires, respectively, the participation of the molecular chaperones hsp70SSA1 and hsp70SSC1 and other components operating on opposite sides of the mitochondrial membrane. In previous studies, both the homology and the assembly properties of the F1ATPase alpha-subunit (ATP1p) compared to the groEL homologue, hsp60, have led to the proposal that this subunit could exhibit chaperone-like activity. In this report the extent to which this subunit participates in protein transport has been determined by comparing import into mitochondria that lack the F1ATPase alpha-subunit (delta ATP1) versus mitochondria that lack the other major catalytic subunit, the F1ATPase beta-subunit (delta ATP2). Yeast mutants lacking the alpha-subunit but not the beta-subunit grow much more slowly than expected on fermentable carbon sources and exhibit delayed kinetics of protein import for several mitochondrial precursors such as the F1 beta subunit, hsp60MIF4 and subunits 4 and 5 of the cytochrome oxidase. In vitro and in vivo the F1 beta-subunit precursor accumulates as a translocation intermediate in absence of the F1 alpha-subunit. In the absence of both the ATPase subunits yeast grows at the same rate as a strain lacking only the beta-subunit, and import of mitochondrial precursors is restored to that of wild type. These data indicate that the F1 alpha-subunit likely functions as an "assembly partner" to influence protein import rather than functioning directly as a chaperone. These data are discussed in light of the relationship between the import and assembly of proteins in mitochondria.
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PMID:The mitochondrial F1ATPase alpha-subunit is necessary for efficient import of mitochondrial precursors. 138 80

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.
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PMID:In vitro and in vivo effect of methyl isocyanate on rat liver mitochondrial respiration. 147 Nov 48

Incubation of normal mitochondria at 45 degrees C results in increases of respiration and of total apparent proton conductance (TAPC, respiration/proton motive force) and in an upward shift of the flow-force relationships. Similar effects are observed during operation of the redox proton pumps at different sites of the respiratory chain. These effects are accompanied by an almost equivalent increase of the passive proton conductance (PPC, proton leakage/proton motive force). In mitochondria from 3,3,5-triiodo-L-thyronine (T3)-treated rats there are also increases of respiration and of TAPC and an upward shift of flow-force relationships, more pronounced at the level of the cytochrome oxidase proton pump. However, at variance from the incubation at 45 degrees C, in mitochondria from T3-treated rats there is only a slight increase of PPC. Addition of bovine serum albumin to normal mitochondria incubated at 45 degrees C results in a marked depression of TAPC in the nonlinear range of the flow-force relationships. An equivalent effect is not observed in mitochondria from T3-treated rats. The experimental results have been compared with computer simulations obtained on the basis of a chemiosmotic model of energy transduction. The increase of TAPC following incubation at high temperature is apparently due to changes of the proton conductance mainly at the level of PPC, while the increase of TAPC following T3 administration is rather due to changes presumably at the level of the redox or ATPase proton pumps.
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PMID:Mechanism of loss of thermodynamic control in mitochondria due to hyperthyroidism and temperature. 163 81

The mRNA levels of ATPase beta, ATPase 6, cytochrome oxidase (COX) VIb and COX I subunits were found to be 2.4-13.8-fold higher in brown adipose tissue (BAT) than in heart, skeletal muscle, brain and liver of mice. The comparison with tissue contents of ATPase and COX revealed that the selective, 5-11-fold reduction of ATPase in BAT is not caused by decreased transcription of ATPase genes. Likewise, the ATPase beta and COX VIb mRNA levels in cultured brown adipocytes were also not influenced by norepinephrine, which activated the expression of the UCP gene by two orders of magnitude. The results indicate that the biosynthesis of mitochondrial ATPase in BAT is post-transcriptionally regulated.
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PMID:Low content of mitochondrial ATPase in brown adipose tissue is the result of post-transcriptional regulation. 166 83

The objective of this study was to characterize mechanisms which maintain intracellular calcium homeostasis in bloodstream forms of Trypanosoma brucei. The identification of homeostatic pathways is required to understand signal transduction in these organisms. The fluorescent probes Fura-2, 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein, and bisoxonal were used to measure intracellular calcium ([Ca2+]i), intracellular pH (pHi), and membrane potential, respectively. Homeostatic pathways maintained [Ca2+]i at 98 +/- 12 nM in the presence of 1.8 mM extracellular calcium despite a steady leak of calcium into the cell. The addition of 2.7 microM nigericin acidified the cytosol, depolarized the plasma membrane, and induced an approximate 3-fold increase in [Ca2+]i. The rise in [Ca2+]i could not be induced with valinomycin or gramicidin D under conditions where membrane depolarization occurred. By contrast, the proton ionophore, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, elevated [Ca2+]i in a manner that was not additive with nigericin. Changes in pHi appeared to regulate [Ca2+]i since: 1) stepwise addition of K+ to nigericin-treated cells generated and incremental increase in pHi and concomitant decrease in [Ca]i; 2) addition of serum to nigericin-treated cells allowed simultaneous recovery of pHi and [Ca2+]i; and 3) addition of NH4Cl to untreated cells resulted in a biphasic change in pHi with corresponding biphasic change in [Ca2+]i. The rise in [Ca2+]i was derived from an intracellular pool which was not dependent on functional cytochrome oxidase, mitochondrial alternative oxidase, or the F0F1-ATPase. These data demonstrate that large quantities of calcium are reversibly stored in a non-mitochondrial pH-sensitive intracellular pool in T. brucei. We conclude that changes in pHi can serve to trigger calcium signals in these organisms.
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PMID:Calcium homeostasis in Trypanosoma brucei. Identification of a pH-sensitive non-mitochondrial calcium pool. 172 3

In vivo administration of testosterone significantly stimulated the activities of cytochrome oxidase, alpha-glycerophosphate dehydrogenase (alpha-GPDH), succinate dehydrogenase (SDH) and adenosine triphosphatase (Mg2+ ATPase), in mitochondria isolated from the liver of G. carnosus. Administration of dehydroepiandrosterone and androstenedione while significantly stimulated the activities of cytochrome oxidase and alpha-GPDH, did not change that of SDH and Mg2+ ATPase. Simultaneous injections of testosterone and actinomycin D or chloramphenicol prevented the testosterone-stimulated activities of all the oxidative enzymes studied. The results clearly document the important stimulatory role of androgens in the regulation of hepatic mitochondrial metabolism in G. carnosus.
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PMID:Androgenic control of hepatic mitochondrial metabolism in an apoda, Gegenophis carnosus (Beddome). 181 79

Addition of bovine serum albumin to state 4 mitochondria results in a depression of the proton leak and of the resting respiration of 70 and 25%, respectively. The conductance membrane potential diagram, both in the ohmic and in the non-ohmic region, shows that in the presence of bovine serum albumin the level of ohmic conductance is lowered while that of non-ohmic conductance is increased toward higher delta psi values. The same effect is observed during operation of the different proton pumps. Addition of chloroform affects the conductance membrane potential diagram in the following manner: there is no effect in the ohmic region with all pumps, while there is an effect in the non-ohmic region either at site III or at sites II plus III but not at site II. This suggests a possible effect of chloroform at the level of the cytochrome oxidase proton pump. During titration with oligomycin of the ATPase proton pump the conductance potential diagram shows a region of non-ohmicity only in the presence but not in the absence of an ATP-regenerating system. Protonophoric uncouplers such as carbonyl cyanide p(trifluoromethoxy)phenylhydrazone and intrinsic uncouplers such as chloroform have different effects on the relationship between rates of charge translocation and of oxygen consumption, and thus on the pump stoichiometries, in that the slope of the diagram is modified by the latter but not by the former. The differential effects of protonophores and of intrinsic uncouplers on the stoichiometries have been analyzed by computer simulations and represent an additional criterion to distinguish between extrinsic and intrinsic mechanisms of uncoupling.
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PMID:Flux ratios and pump stoichiometries at sites II and III in liver mitochondria. Effect of slips and leaks. 184 85


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