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At least 865 records · Page 48Linked to original sources
PubMed1990

Oxidative phosphorylation in mouse liver mitochondria during weaning.

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.

3-Hydroxybutyric Acid↗
PubMed1994

Steady state levels of mitochondrial and nuclear oxidative phosphorylation transcripts in Kearns-Sayre syndrome.

The steady state levels of both mitochondrial and nuclear transcripts were examined in a Kearns-Sayre syndrome patient harboring a heteroplasmic 7.7 kb mitochondrial DNA deletion. Transcripts originating from the genes located outside of the deletion were present in similar amounts to those of control samples, with the transcript levels of each tissue linked to its oxidative phosphorylation capacities. Transcripts originating from genes within the deletion were reduced according to the percentage of mtDNA deleted molecules in the tissue. The fusion transcript resulting from the rearranged genome is expressed in all the tissues tested and its level is related to the amount of the deleted mtDNA. The RNA levels from three nuclear genes encoding two of the Adenine Nucleotide Translocator isoforms (ANT1 and 2) and the beta subunit of the ATPsynthase (ATPsyn beta) were significantly induced in the different tissues independently of the percentage of deleted mtDNA molecules. In contrast, the ANT1 and ATPsyn beta levels were decreased in skeletal muscle. This result could be related to the different distribution of the deleted molecules in tissues.

Base Sequence↗
PubMed1991

Oxidative phosphorylation coupled to electron transfer in the filarial parasite Setaria digitata.

The filarial parasite of Bos indicus, Setaria digitata is reported to have many unique characteristics such as cyanide insensitivity and mitochondrial hydrogen peroxide production. The latter is more sensitive to the alternative oxidase inhibitor salicylhydroxamic acid (SHAM). Studies on the generation of ATP molecules through mitochondriae in the presence of different substrates and inhibitors showed that the oxidative phosphorylation coupled to electron transport occurs mainly at site I and involves the participation of quinone Q8. Based on the data, a scheme for the filarial electron transport system is proposed in which the quinones have a central role. Hence inhibitors at the quinone level might prove to be effective targets for chemotherapy.

Animals↗
PubMed2006

Association of 3-methylglutaconic aciduria with sensori-neural deafness, encephalopathy, and Leigh-like syndrome (MEGDEL association) in four patients with a disorder of the oxidative phosphorylation.

In this paper, we describe a distinct clinical subtype of 3-methylglutaconic aciduria. 3-Methylglutaconic aciduria is a group of different metabolic disorders biochemically characterized by increased urinary excretion of 3-methylglutaconic acid. We performed biochemical and genetic investigations, including urine organic acid analysis, NMR spectroscopy, measurement of 3-methylglutaconyl-CoA hydratase activity, cardiolipin levels, OPA3 gene analysis and measurement of the oxidative phosphorylation in four female patients with 3-methylglutaconic aciduria. 3-Methylglutaconic aciduria type I, Barth syndrome, and Costeff syndrome were excluded as the activity of 3-methylglutaconyl-CoA hydratase, the cardiolipin levels, and molecular analysis of the OPA3 gene, respectively, showed no abnormalities. The children presented with characteristic association of hearing loss and the neuro-radiological evidence of Leigh disease. They also had neonatal hypotonia, recurrent lactic acidemia, episodes with hypoglycemia and severe recurrent infections, feeding difficulties, failure to thrive, developmental delay, and progressive spasticity with extrapyramidal symptoms. Our patients were further biochemically characterized by a mitochondrial dysfunction and persistent urinary excretion of 3-methylglutaconic acid.

Adolescent↗
PubMed1975

Changes of the oxidative phosphorylation in mitchondria of rat skeletal muscle following strenous exercise.

The rate of oxygen consumption of mitochondria from rat muscles at pH 7.4 is elevated by 1-lactate. The respiratory control ratio and the ADP/O-ratio are decreased under these conditions. Acidification to pH 6.5 in the absence of 1-lactate does not change the interpreted mitochondrial functions. The experimental data are discussed as a partial uncoupling effect of 1-lactate on the oxidative phosphorylation. Similar changes in those mitochondrial functions are found after short-time intensive swimming exercise of rats. These variations might be a reason for the sometimes described reduced aerobic performance after intensive work.

Adenosine Diphosphate↗
PubMed1999

Functional brain imaging in the resting state and during activation in Alzheimer's disease. Implications for disease mechanisms involving oxidative phosphorylation.

In vivo brain imaging of patients with Alzheimer's disease (AD) using positron emission tomography (PET) demonstrates progressive reductions in resting-state brain glucose metabolism and blood flow in relation to dementia severity, more so in association than primary cortical regions. During cognitive or psychophysical stimulation, blood flow and metabolism in the affected regions can increase to the same extent in mildly demented AD patients as in age-matched controls, suggesting that energy delivery is not rate limiting. Activation declines with dementia severity, and is markedly reduced in severely demented patients. These results suggest that there is an initial "normal" functionally-responsive stage in AD, followed by a late less responsive stage. Studies of biopsied and postmortem brain indicate that the initial stage is accompanied by selective and potentially reversible down-regulation of the brain enzymes, including cytochrome oxidase, which mediate mitochondrial oxidative-phosphorylation.

Alzheimer Disease↗
PubMed2001

Control of oxidative phosphorylation in skeletal muscle.

The classical concept of ATP-demand control of energy metabolism in skeletal muscle has to be modified on the basis of studies showing the influence of additional controlling parameters (reducing equivalent supply, oxygen availability, proton leak, diffusion restrictions and the creatine kinase system) and on the basis of applications of metabolic control analysis showing very clearly multistep control. This concept of multistep control allows to quantify the individual influence of any parameter on mitochondrial oxidative phosphorylation and is extremely helpful to analyze the metabolic consequences of enzyme deficiencies in skeletal muscle occurring in mitochondrial myopathies.

Adenosine Diphosphate↗
PubMed1975

Quantitative structure-activity relationships for dicoumarol antivitamins K in the uncoupling of mitochondrial oxidative phosphorylation.

The dynamic structure of dicoumarols substituted on the methylene bridge has been studied by nuclear magnetic resonance (nmr) spectroscopy. These molecules may be considered as dimers with restricted rotation around the methylene bridge, held by intramolecular hydrogen bonds; the presence of the substituent R modifies this dynamic process, mainly the facility of exchange of the two hydroxyl protons. These compounds have been compared in respect to their potency in uncoupling oxidative phosphorylation in pig heart mitochondria; the data have been correlated with constants used to characterize the substituent R; to make a potent uncoupler, R should be as small and as hydrophilic as possible. These results are discussed in consonance with the postulated mechanisms of action of the uncouplers, but no simple conclusion can be drawn, especially concerning the role of the dissociable protons.

Animals↗
PubMed1983

Effects of glucagon on basal metabolic rate and oxidative phosphorylation of rat liver mitochondria.

Glucagon produced fast but transient stimulation of respiration rates in state 3 and state 4 rat liver mitochondria when either succinate or beta-hydroxybutyrate was used as substrate. Stimulation was already detectable 7.5 minutes after glucagon injection. Glucagon also clearly activated basal metabolic rate, and its effects on oxygen consumption rates reached their maximum 20 to 30 minutes after injection. Pretreatment with cycloheximide blocked most activation by glucagon of both oxidative phosphorylation and basal metabolic rate, but did not affect its enhancement of glycaemia. The rise in basal metabolic rate was the direct result of glucagon's effect on mitochondria, which was secondary to nucleocytoplasmic protein synthesis.

Animals↗
PubMed1975

Mechanism of action of agents which uncouple oxidative phosphorylation: direct correlation between proton-carrying and respiratory-releasing properties using rat liver mitochondria.

The proton-carrying properties of uncoupling agents were investigated by measuring passive mitochondrial swelling under conditions where electrogenic proton transport was rate limiting. The ability of uncoupling agents to transport protons into mitochondria, measured in this way, was compared with respiratory stimulation. The results show that with the single exception of arsenate, all agents tested which uncouple oxidative phosphorylation demonstrate a very close correlation between release of respiration and proton transport. These findings are in support of Mitchell's original proposal that uncoupling agents act by promoting electrogenic hydrogen ion transport across the mitochondrial inner membrane.

Animals↗
PubMed2005

Does AMP-activated protein kinase couple inhibition of mitochondrial oxidative phosphorylation by hypoxia to calcium signaling in O2-sensing cells?

Specialized O2-sensing cells exhibit a particularly low threshold to regulation by O2 supply and function to maintain arterial pO2 within physiological limits. For example, hypoxic pulmonary vasoconstriction optimizes ventilation-perfusion matching in the lung, whereas carotid body excitation elicits corrective cardio-respiratory reflexes. It is generally accepted that relatively mild hypoxia inhibits mitochondrial oxidative phosphorylation in O2-sensing cells, thereby mediating, in part, cell activation. However, the mechanism by which this process couples to Ca2+ signaling mechanisms remains elusive, and investigation of previous hypotheses has generated contrary data and failed to unite the field. We propose that a rise in the cellular AMP/ATP ratio activates AMP-activated protein kinase and thereby evokes Ca2+ signals in O2-sensing cells. Co-immunoprecipitation identified three possible AMP-activated protein kinase subunit isoform combinations in pulmonary arterial myocytes, with alpha1 beta2 gamma1 predominant. Furthermore, their tissue-specific distribution suggested that the AMP-activated protein kinase-alpha1 catalytic isoform may contribute, via amplification of the metabolic signal, to the pulmonary selectivity required for hypoxic pulmonary vasoconstriction. Immunocytochemistry showed AMP-activated protein kinase-alpha1 to be located throughout the cytoplasm of pulmonary arterial myocytes. In contrast, it was targeted to the plasma membrane in carotid body glomus cells. Consistent with these observations and the effects of hypoxia, stimulation of AMP-activated protein kinase by phenformin or 5-aminoimidazole-4-carboxamide-riboside elicited discrete Ca2+ signaling mechanisms in each cell type, namely cyclic ADP-ribose-dependent Ca2+ mobilization from the sarcoplasmic reticulum via ryanodine receptors in pulmonary arterial myocytes and transmembrane Ca2+ influx into carotid body glomus cells. Thus, metabolic sensing by AMP-activated protein kinase may mediate chemotransduction by hypoxia.

AMP-Activated Protein Kinases↗
PubMed1977

The influence of growth substrate and capacity for oxidative phosphorylation on respiratory oscillations in synchronous cultures of Escherichia coli K12.

Fluctuations in cell volume during exponential growth of Escherichia coli K12 changed the effectiveness of the continuous-flow centrifugation method for preparing synchronous cultures. Rates of oxygen uptake in synchronous cultures were measured using an electrode system open to the atmosphere. In synchronous cultures of both the parental strain and an adenosine triphosphatase-deficient mutant, which was incapable of oxidative phosphorylation, respiration rates doubled during the cell cycle but oscillated with a periodicity of approximately half a cycle. Synchronous cultures of the parental strain growing on glycerol and Casamino acids showed a stepwise pattern of oxygen consumption. Continuous flow centrifugation did not markedly affect the increases in the numbers and respiration rates of cells in syndhronous cultures. Respiratory oscillations also occurred on inoculation of a late-stationary phase culture into fresh medium, although synchronous division was not observed. The possible mechanisms underlying respiratory fluctuations under different growth conditions are discussed.

Amino Acids↗
PubMed1975

Dependence of platelet adenyl cyclase system on oxidative phosphorylation.

The radioactive adenosine 3',5'-monophosphate (cyclic AMP) level derived from 8-14C adenine in intact rabbit platelets decreased in the presence of mitochondrial inhibitor (potassium cyanide) or uncoupler (sodium azide), and markedly increased by the addition of NaF, monoiodoacetic acid (MIA), or 2-deoxy-D-glucose. The stimulative effect of the glycolytic inhibitors was distinctly enhanced by the simultaneous addition of sodium succinate. MIA did neither directly stimulate the adenyl cyclase activity nor inhibit the phosphodiesterase activity. These results suggest that cyclic AMP synthesis in platelets is closely linked to mitochondrial oxidative phosphorylation.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Oxidative phosphorylation linked to the dissimilatory reduction of elemental sulphur by Desulfovibrio.

Hydrogenase and cytochrome c3 purified from Desulfovibrio gigas and D. desulfuricans strain Norway form a soluble complex which is capable of transferring electrons from molecular hydrogen to colloidal sulphur (S0). In this reaction, sulphur is reduced to hydrogen sulphide. Since both strains are capable of growth using elemental sulphur as terminal electron acceptor, it was of interest to check for oxidative phosphorylation in this sulphur reduction sytem. Membranes isolated from D. gigas or D. desulfuricans strain Norway contain hydrogenase and c-type cytochromes and catalyse the H2 leads to S0 reaction. With D. gigas, esterification of orthophosphate is coupled to the membrane-mediated transfer of electrons from H2 to S0. A P/2e ratio of 0.1 was observed and this value could be reduced by the addition of colloidal sulphur with c2 may be more than a purely chemical reaction. Since whole cells can use sulphur flower while cell-free extracts react only with colloidal sulphur, it is evident that cells handle sulphur in a way which is not yet fully understood.

Adenosine Triphosphate↗
PubMed2003

PGC-1alpha-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes.

DNA microarrays can be used to identify gene expression changes characteristic of human disease. This is challenging, however, when relevant differences are subtle at the level of individual genes. We introduce an analytical strategy, Gene Set Enrichment Analysis, designed to detect modest but coordinate changes in the expression of groups of functionally related genes. Using this approach, we identify a set of genes involved in oxidative phosphorylation whose expression is coordinately decreased in human diabetic muscle. Expression of these genes is high at sites of insulin-mediated glucose disposal, activated by PGC-1alpha and correlated with total-body aerobic capacity. Our results associate this gene set with clinically important variation in human metabolism and illustrate the value of pathway relationships in the analysis of genomic profiling experiments.

Animals↗
PubMed1997

L-carnitine stimulation of mitochondrial oxidative phosphorylation rate in isolated rat skeletal muscle mitochondria.

L-carnitine effects on mitochondrial adenosine triphosphate (ATP) production rate were investigated in mitochondria isolated from rat extensor digitorum longus (EDL) muscle. Kinetic parameters, apparent Michaelis constant for free adenosine diphosphate (ADP) (K(m)) and apparent maximal ATP production rate (Vmax), were determined in absence and presence of L-carnitine. Although the K(m) remained unchanged in response to L-carnitine addition when pyruvate + malate was oxidized, the affinity of isolated mitochondria towards ADP was decreased when pyruvate + palmitoylcarnitine + malate was used as substrate. As a result of L-carnitine addition, a slight non-significant (P < 0.07) increase in Vmax was observed with pyruvate + malate while the increase reached the level of significance with pyruvate + palmitoylcarnitine + malate. Moreover, a positive correlation was obtained when mitochondrial ATP production rate was plotted against the difference between values measured with and without L-carnitine. Our data suggest that addition of L-carnitine to isolated rat skeletal muscle mitochondria can stimulate mitochondrial oxidative phosphorylation rate under conditions where the inhibitory effect of acetyl-CoA accumulation on pyruvate dehydrogenase complex activity is optimized. A change in the control of mitochondrial ATP flux by pyruvate dehydrogenase (PDH) complex might also occur with increasing mitochondrial ATP production rate, reinforcing the L-carnitine effects.

Adenosine Triphosphate↗
PubMed1982

Mechanism of polymeric prostaglandin PGBx for in vitro stabilization of rat liver mitochondrial oxidative phosphorylation.

The mechanism of the in vitro PGBx effect on mitochondria was studied by determining the specific requirements of the assay system composition. These studies showed that (a) rat liver mitochondria must first be exposed to hypotonic media containing PGBx under aerobic conditions, (b) oxygen, Pi, Mg++, phosphate acceptor (nucleotides), and some oxidizable substrates are essential components to yield optimal phosphorylation values. KCl and bovine serum albumin are non-essential components. With regard to nucleotide acceptor specificity, the AMP, ADP, and glucose-ADP-hexokinase systems were satisfactory. With regard to substrate specificity, only beta-hydroxybutyrate and externally reduced NAD+ were unsatisfactory. The requirement for oxygen was twofold: (a) as an absolute requirement for oxidative phosphorylation, and (b) as a requirement for the hypotonic degradation of mitochondria. These results suggest that PGBx reacts with mitochondria to "protect" against degradation during aerobic hypotonic exposure.

Anaerobiosis↗