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PubMedDate not supplied

[Effect of alkaloids from celandine on calcium accumulation and oxidative phosphorylation in mitochondria depending on their DNA intercalating properties].

The effect of principal alkaloids (sanguinarine, chelerythrine, coptisine, chelidonine) of greater celandine Chelidonium majus L., as well as the alkaloids from Colchicum autumnale L. (colchicine and colchamine) on calcium accumulation and oxidative phosphorylation in rat liver mitochondria has been studied. The obtained data were compared with DNA intercalating properties of alkaloids detected by the method of thermodenaturation (DNA melting curve plots). It was found that chelerythrine and sanguinarine blocked absorption and accumulation of calcium cations and inhibited oxidative phosphorylation, while the coptisine significantly diminished those indices. Chelidonine, colchicines and colchamine had no influence on the studied characteristics. The effect of alkaloids upon mitochondria functional state correlated tightly with their DNA intercalating properties: chelerythrine and sanguinarine were strong intercalators, while coptisine was a weak one, and chelidonine, colchicine and colchamine did not interact with DNA and caused no changes in its melting point. Correlation coefficient between the intercalating properties of alkaloids and their inhibition of calcium accumulation was 0.89, and with their oxidative phosphorylation inhibition - 0.93. It is suggested that the effect of studied alkaloids upon functional properties of mitochondria can be mediated by mtDNA.

Alkaloids↗
PubMed2006

Supramolecular structure of the mitochondrial oxidative phosphorylation system.

The protein complexes of the mitochondrial oxidative phosphorylation system were recently reported to form supramolecular assemblies termed respiratory supercomplexes or respirasomes. These supercomplexes are considered to be of great functional importance. Here we review new insights into supercomplex structure and physiology.

Animals↗
PubMed1993

Effects of dietary protein and fat level on oxidative phosphorylation in rat heart mitochondria.

The effect of dietary protein and fat levels on cardiac mitochondrial oxidative phosphorylation was assessed polarographically. Weanling rats were fed on semi-purified diets containing different protein levels (10, 30, 50 and 70%) on a gross energy basis (PGE) for 9, 23 and 58 d. Cardiac mitochondria isolated from rats fed on a 70% PGE diet for 23 d exhibited significantly reduced ADP:oxygen (ADP:O) values compared with mitochondria from rats fed on a low-protein diet. Feeding low-protein diets for 58 d increased the ADP: O value. When the dietary fat level was altered to provide (% PGE: % fat-energy): 30:14, 30:30, 70:14, 70:30, feeding 70% PGE diets reduced the ADP:O value compared with the 30% PGE level, but no difference was observed between low-fat and high-fat groups. These results indicate that the impaired ADP: O value for rats fed on very-high-protein diets was not due to the dietary fat level but that the level of dietary protein is an important determinant of oxidative phosphorylation in rat heart mitochondria.

Adenosine Diphosphate↗
PubMed1985

Non-local thermodynamic effects and efficiency of oxidative phosphorylation.

A non-equilibrium thermodynamic model of oxidative phosphorylation is formulated, which allows us to take into account some non-local effects. In this way, we compute the influence of the tangential resistivity of the inner mitochondrial membrane to proton current, as well as that of the distance between active sites, on the stoichiometry and efficiency of energy conversion.

Biological Transport↗
PubMed1964

DIHYDROSTREPTOMYCIN, VITAMIN K2-COUPLED TETRAZOLIUM REDUCTION, AND OXIDATIVE PHOSPHORYLATION IN ESCHERICHIA COLI.

Bragg, P. D. (University of British Columbia, Vancouver, B.C., Canada). Dihydrostreptomycin, vitamin K(2)-coupled tetrazolium reduction, and oxidative phosphorylation in Escherichia coli. J. Bacteriol. 88:1019-1023. 1964.-Dihydrostreptomycin inhibited the vitamin K(2)-coupled pyruvate-triphenyltetrazolium (TTC) reductase system in extracts from antibiotic-sensitive cells, but stimulated this reaction with extracts from a dependent mutant. The effects of nucleotides, phosphate, and uncoupling agents on the vitamin K(2)-TTC system are consistent with the linkage of reduction of the dye through intermediates of oxidative phosphorylation.

Anti-Bacterial Agents↗
PubMed1978

Respiration and oxidative phosphorylation in Treponema pallidum.

Exogenous and endogenously generated reduced pyridine nucleotides caused marked stimulation of O(2) uptake when added to treponemal cell-free extracts, which indicated that terminal electron transport was coupled to the consumption of O(2). Oxidation of reduced nicotinamide adenine dinucleotide (NADH) was shown to correlate stoichiometrically with O(2) reduction, suggesting that NADH was being oxidized through a mainstream respiratory chain dehydrogenase. Oxygen evolution in treponemal extracts was observed after the completion of O(2) uptake which was stimulated by exogenous NADH and endogenously generated reduced NAD phosphate. Oxygen evolution was inhibited by both cyanide and pyruvate, which was consistent with O(2) release from H(2)O(2) by catalase. The addition of exogenous H(2)O(2) to treponemal extracts caused rapid O(2) evolution characteristic of a catalase reaction. A spectrophotometric assay was used to measure ATP formation in T. pallidum cell-free extracts that were stimulated with NADH. P/O ratios from 0.5 to 1.1 were calculated from the amounts of ATP formed versus NADH oxidized. Phosphorylating activity was dependent on P(i) concentration and was sensitive to cyanide, N, N'-dicyclohexylcarbodiimide, and carbonyl cyanide m-chlorophenyl hydrazone. Adenine nucleotide pools of T. pallidum were measured by the firefly luciferin-luciferase assay. Shifts in adenine nucleotide levels upon the addition of NADH to cell-free extracts were impossible to evaluate due to the presence of NAD(+) nucleosidase. However, when whole cells, previously incubated under an atmosphere of 95% N(2)-5% CO(2), were sparged with air, ATP and ADP levels increased, while AMP levels decreased. The shift was attributed to both oxidative phosphorylation and to the presence of an adenylate kinase activity. T. pallidum was also found to possess an Mg(2+) - and Ca(2+) -stimulated ATPase activity which was sensitive to N, N' -dicyclohexylcarbodiimide. These data indicated a capability for oxidative phosphorylation by T. pallidum.

Adenine Nucleotides↗
PubMed1999

Iron-dependent changes in cellular energy metabolism: influence on citric acid cycle and oxidative phosphorylation.

Iron modulates the expression of the critical citric acid cycle enzyme aconitase via a translational mechanism involving iron regulatory proteins. Thus, the present study was undertaken to investigate the consequences of iron perturbation on citric acid cycle activity, oxidative phosphorylation and mitochondrial respiration in the human cell line K-562. In agreement with previous data iron increases the activity of mitochondrial aconitase while it is reduced upon addition of the iron chelator desferrioxamine (DFO). Interestingly, iron also positively affects three other citric acid cycle enzymes, namely citrate synthase, isocitric dehydrogenase, and succinate dehydrogenase, while DFO decreases the activity of these enzymes. Consequently, iron supplementation results in increased formation of reducing equivalents (NADH) by the citric acid cycle, and thus in increased mitochondrial oxygen consumption and ATP formation via oxidative phosphorylation as shown herein. This in turn leads to downregulation of glucose utilization. In contrast, all these metabolic pathways are reduced upon iron depletion, and thus glycolysis and lactate formation are significantly increased in order to compensate for the decrease in ATP production via oxidative phosphorylation in the presence of DFO. Our results point to a complex interaction between iron homeostasis, oxygen supply and cellular energy metabolism in human cells.

Aconitate Hydratase↗
PubMed2005

The maternal age effect: a hypothesis based on oxidative phosphorylation.

The 'maternal age effect' in human reproduction, characterized by a negative relationship between maternal age and reproductive efficiency, remains a poorly understood phenomenon. Current data suggest that oocyte physiology determines this relationship. In this review, we present a hypothesis of a mitochondrial role in the physiology of ageing in human oocytes. We suggest that the efficiency of oxidative phosphorylation in the ageing human oocyte is degraded by free radical attack on the primordial oocytes residing in the ovary. Although deficiencies in oxidative phosphorylation can be accounted for in the short term by anaerobic respiration, we suggest that, in the long term, the level of oxidative phosphorylation strongly influences oocyte quality.

Female↗
PubMed1983

Reversible uncoupling of oxidative phosphorylation at low oxygen tension.

The stoichiometry of oxidative phosphorylation at low oxygen tension (less than 3 torr; O2 less than 5 microM) has been measured in rat liver mitochondria. In a steady-state model in which respiration rate was experimentally controlled by either oxygen or substrate (succinate) limitation, flux-dependent variation in the phosphorylation efficiency (P/O ratio) of stimulated mitochondrial respiration was evaluated. P/O ratio remained constant over a wide range of respiration rates in mitochondria limited only by substrate availability. In contrast, oxygen-limited mitochondria demonstrated a continuous decline in P/O ratio as respiration was increasingly restricted. Significant differences in the two test conditions were demonstrated throughout the range of analysis. The effect of oxygen limitation on phosphorylation efficiency was shown to be completely reversed by restoring zero-order kinetics associated with high oxygen tension. These findings are discussed in regard to a proposed uncoupling of mitochondrial coupling site II at low oxygen tension arising as a consequence of energy-dissipating electron flux through the ubiquinone-cytochrome b-c1 region of the respiratory chain (complex III).

Adenosine Diphosphate↗
PubMed1996

Theoretical studies on control of oxidative phosphorylation in muscle mitochondria at different energy demands and oxygen concentrations.

The mathematical dynamic model of oxidative phosphorylation in muscle mitochondria developed previously was used to calculate the flux control coefficients of particular steps of this process in isolated mitochondria at different amounts of hexokinase and oxygen concentrations. The pattern of control was completely different under different conditions. For normoxic concentration, the main controlling steps in state 4, state 3.5 and state 3 were proton leak, ATP usage (hexokinase) and complex III, respectively. The pattern of control in state 4 was not changed at hypoxic oxygen concentration, while in state 3.5 and state 3 much of the control was shifted from other steps to cytochrome oxidase. The implications of the theoretical results obtained for the regulation of oxidative phosphorylation in intact muscle are discussed.

Adenosine Triphosphate↗
PubMed1983

Involvement of intramitochondrial adenine nucleotides and inorganic phosphate in oxidative phosphorylation of extramitochondrially added adenosine-5'-diphosphate.

Possible direct, product/substrate mediated interactions between the phosphate carrier and/or the adenine nucleotide translocator and the mitochondrial H+-ATPase were investigated by tracer flux experiments. For this purpose the specific radioactivity of ATP synthesized was measured and compared with those of intra- and extramitochondrial precursors. Two experimental strategies were applied: 1) preloading of mitochondria with [32P]Pi before starting oxidative phosphorylation of external ADP; 2) simultaneous addition of tracer amounts of [3H]ADP and [32P]Pi to phosphorylating mitochondria under steady-state conditions. The observed participation of the intramitochondrial Pi pool in oxidative phosphorylation excludes a directly functional interaction between Pi carrier and H+-ATPase. At 5 degrees C an at least partial compartmentation of intramitochondrial ADP during oxidative phosphorylation was found, whereas at 25 degrees C a complete equilibrium of intra- and extramitochondrial [32P]Pi and [3H]ADP could be observed, excluding a functionally important compartmentation of these species in the intramitochondrial space under physiological conditions.

Adenine Nucleotides↗
PubMed2000

Histoenzymology of oxidases and dehydrogenases in peripheral blood lymphocytes and monocytes for the study of mitochondrial oxidative phosphorylation.

Histoenzymological methods usually performed on muscle fibres have been adapted to assess the functioning of oxidative phosphorylation in human circulating blood lymphocytes and monocytes. Oxidases and dehydrogenases were analysed in lymphocyte/monocyte smears. The specificity of each histoenzymological reaction was tested using a specific respiratory chain inhibitor: rotenone for NADH diaphorase, thenoyltrifluoroacetone for succinate dehydrogenase, potassium cyanide for cytochrome c oxidase and oligomycin for ATPase. Complex I activity was detected, but inhibition with rotenone was incomplete. Complexes II, IV and V were almost completely inhibited. These observations indicate that histoenzymology is a valuable method for detecting the activity of these oxidative phosphorylation enzymes in lymphocytes and monocytes. The histoenzymology tests performed on fresh peripheral blood cells resembled those used for muscle biopsies. They could be useful for the diagnosis of respiratory chain disorders in patients.

Adolescent↗
PubMed1975

Mitochondria from the lamprey (Lampetra fluviatilis). Oxidative phosphorylation and related processes.

1. High efficiency of oxidative phosphorylation and a good respiratory control in liver, heart and somatic muscle mitochondria of the lamprey (Lampetra fluviatilis) were observed when the particles were isolated in a complex sucrose medium containing EDTA, heparin and nicotinamide. The coupling properties of these mitochondria were further improved by including serum albumin in the incubation medium. 2. The content of total adenine nucleotides in lamprey mitochondria was between 4 and 6 nmoles/mg protein. The translocation of these nucleotides across mitochondrial membrane was stimulated by serum albumin. 3. Lamprey mitochondrial phospholipids contain a large proportion (64-72%) of polyunsaturated fatty acids. 4. Electron micrographs of mitochondria from lamprey liver, heart and somatic muscle are presented.

Animals↗
PubMed1979

Studies on Chinese hamster ovary mutants showing multiple cross-resistance to oxidative phosphorylation inhibitors.

Several stable Chinese hamster ovary (CHO) mutants were selected after ethylmethane sulfonate mutagenesis for resistance to oligomycin, ruatmycin, venturicidin, or antimycin. These mutants shared a number of common properties. They exhibited cross-resistance to those drugs which act on oxidative phosphorylation, irrespective of the structure and site of action of the drug. All the mutants showed a reduced ability to grow in suspension and to reach high saturation densities. They were also unable to use galactose as a carbon source. The short lag period required for selection (10-15 days), the similarity of the mutation rates for resistance to each of the four drugs, the high variance/mean ratios in fluctuation tests, and the recessive behavior of the resistance marker in hybrids suggest that the mutations responsible for resistance to oxidative phosphorylation inhibitors in CHO cells are coded by nuclear DNA. Segregation experiments indicated no linkage between the oligomycin-resistant marker (OLG) AND Thg (thioguanine resistance). Oxidative phosphorylation, as measured by the rate of respiration coupled to phosphorylation in whole cells remained as sensitive to the drugs in the mutants as in the parental cell line. Glucose transport and the overall Krebs' cycle activities also appeared similar in the mutants and the wild type. All the mutants had an increased rate of lactic acid production (up to twofold), associated with increased specific activities for several glycolytic enzymes when assayed in cell-free extracts.

Animals↗
PubMed2005

Regional selectivity of amyloid mRNA expression and neurotrophins on repetitive inhibition of oxidative phosphorylation.

Previously we showed that repetitive inhibition of oxidative phosphorylation impairs synaptic transmission and induces overexpression of amyloid precursor protein mRNA (APP-mRNA) in the hippocampus (Hellweg et al., 2003). Here we show that APP-mRNA remains alike in murine frontal cortex and cerebellum on repetitive treatment with 3-nitropropionate. However, nerve growth factor and brain-derived neurotrophic factor decreased by 28 to 38% in frontal cortex. Taken together, the pattern of change resembles genetic models of Alzheimer's disease with less susceptibility for overexpression of amyloid mRNA in frontal cortex than in hippocampus and reduced neurotrophin levels in frontal cortex. Given the similarity of this pattern to the one observed in human Alzheimer's disease the present model in future may give further insight into the pathophysiology of sporadic Alzheimer's disease.

Alzheimer Disease↗
PubMed1990

Control processes in oxidative phosphorylation: kinetic constraints and stoichiometry.

Control processes in oxidative phosphorylation have been studied in three experimental models. (1) In isolated yeast mitochondria, external ATP is a regulatory effector of cytochrome-c oxidase activity. In phosphorylating or uncoupling states, the relationships between respiratory rate and delta mu H+, and the respiratory rate and cytochrome-c oxidase reduction level are dependent on this kinetic regulation. (2) In rat liver mitochondria, the response of the respiratory rate to uncoupler addition is age-dependent: liver mitochondria isolated from young rats maintain a greater delta mu H+ than liver mitochondria isolated from adults, with the same respiratory rate obtained with the same concentration of uncoupler. This behaviour is linked to redox proton pump properties, i.e., to the degree of intrinsic uncoupling induced by uncoupler addition. (3) The effect of almitrine, a new kind of ATPase/ATPsynthase inhibitor, was studied in mammalian mitochondria. (i) Almitrine inhibits oligomycin-sensitive ATPase - it decreases the ATPase/O value without any change in delta mu H+; (ii) almitrine increased the mechanistic H+/ATP stoichiometry of ATPase/ATPsynthase; (iii) almitrine-induced changes in H+/ATPase stoichiometry depend on the flux magnitude through ATPase. These results are discussed in terms of the following interdependent parameters; flux value, force, pump efficiency and control coefficient.

Adenosine Triphosphatases↗
PubMed1967

Biochemical genetics of oxidative phosphorylation.

The usefulness of mutants in the unraveling of complex, highly organized, membrane-bound processes such as oxidative phosphorylation is illustrated by a study of a single recessive gene mutation in yeast, designated op(1), which has abolished the efficiency in vivo and in vitro of oxidative phosphorylation without impairing the electron transfer.

Adenosine Triphosphatases↗
PubMed1997

Metabolic control analysis and threshold effect in oxidative phosphorylation: implications for mitochondrial pathologies.

We have shown that the Metabolic Control Analysis (MCA) can explain the threshold effect observed in the expression of mitochondrial diseases. As a matter of fact, the effect of a specific inhibitor on the flux of O2 consumption mimics a defect in a step of oxidative phosphorylation. The observed threshold is correlated to the value of the control coefficient of the inhibited step. For this reason, we have studied the repartition of the control coefficients of different steps in oxidative phosphorylation on various tissues (liver, kidney, brain, skeletal muscle and heart). We discuss the results in terms of metabolic control theory and provide a possible explanation for the heterogeneous phenotype of those pathologies. We present the double threshold hypothesis of both a threshold in the energy demand of a tissue and in the energy supply by oxidative phosphorylation.

Animals↗