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At least 829 records · Page 46Linked to original sources
PubMed1980

Effect of clozapine on the oxygen, glucose uptake and oxidative phosphorylation of rat brain in vitro.

Clozapine, a neuroleptic drug isostere of the phenothiazines, at a dose of 10(-3) M decreased the oxygen consumption of rat brain slices and homogenates. However, this effect was not potentiated when brain slices were incubated with 100 mM potassium or in a calcium-free medium, the uncoupling of brain mitochondrial oxidative phosphorylation by 10(-3) M clozapine can also be rulled out.

Animals↗
PubMed1993

The Regulation of Pyruvate Dehydrogenase Activity in Pea Leaf Mitochondria (The Effect of Respiration and Oxidative Phosphorylation).

The regulation of the pea (Pisum sativum) leaf mitochondrial pyruvate dehydrogenase complex by respiratory rate and oxidative phosphorylation has been investigated by measuring the respiratory activity, the redox poise of the quinone pool (Q-pool), and mitochondrial pyruvate dehydrogenase (mtPDC) activity under various metabolic conditions. It was found that, under state 4 conditions, mtPDC activity was unaffected by either the addition of succinate, 2-oxoglutarate, or glycine or the overall respiratory rate and redox poise of the Q-pool but was partially inhibited by NADH due to product inhibition. In the presence of ADP significant inactivation of PDC, which was sensitive to oligomycin, was observed with all substrates, apart from pyruvate, suggesting that inactivation was due to ATP formation. Inactivation of PDC by ADP addition was observed even in the presence of carboxyatractyloside, an inhibitor of the ATP/ADP translocator, suggesting that other mechanisms to facilitate the entry of adenylates, in addition to the adenylate carrier, must exist in plant mitochondria.

Journal Article↗
PubMed1975

Energy-dependent accumulation of iron by isolated rat liver mitochondria. V. Effect of factors controlling respiration and oxidative phosphorylation.

1. Depending on the metabolic state, the addition of iron(III)-sucrose induces an inhibition or a stimulation of the respiration rate when added to isolated rat liver mitochondria. 2. Under conditions identical to those used in the accumulation studies (Romslo, I. and Flatmark T. (1973) Biochim. Biophys. Acta 305, 29-40), the ferric complex induces a decrease in the oxygen uptake concomitant to an oxidation of cytochromes c (+c1) and a(+a3). These results suggest that ferric iron is reduced to ferrous iron by the respiratory chain prior to or simultaneously with its energy-dependent accumulation. 3. On the other hand, the addition of iron(III)-sucrose induces a stimulation of respiration in State 4 and State 3 provided Mg-2+ is present in the suspending medium. In contrast to Ca-2+, iron stimulates State 4 respiration in a cyclic process only within narrow concentration limits; at concentrations of iron above 100 mu M the respiration remains in the activated state until anaerobiosis. The stimulation of State 4 respiration is more pronounced with succinate than with NAD-linked substrates, a difference which partly may be attributed to a stimulation of the succinate dehydrogenase complex. 4. The stimulation of respiration by iron is approx. 3 times higher in State 3 than in State 4 and this difference can be attributed to a stimulation of the adenine mucleotide exchange reaction in State 3 with a concomitant increase in the rate of oxidative phosphorylation, although the P/O ration is slightly diminished.

Adenine Nucleotides↗
PubMed1995

Human diseases with defects in oxidative phosphorylation. 2. F1F0 ATP-synthase defects in Alzheimer disease revealed by blue native polyacrylamide gel electrophoresis.

F1F0 ATP-synthase (complex V) deficiencies in Alzheimer's disease are reported. Tissue specimens from the hippocampus of brains from patients with Alzheimer's disease were screened by blue native electrophoresis for alterations of the proteins of oxidative phosphorylation. Ubiquinol:cytochrome-c reductase (complex III) and cytochrome-c oxidase (complex IV) were found to be present at almost normal concentrations, however, complex V was substantially reduced in most cases studied. The specific reduction of complex V and the absence of electrophoretically detectable degradation products do not exclude a secondary defect of complex V, but should stimulate the search for genetic defects related to protein subunits of complex V.

Adenine Nucleotides↗
PubMed1987

Effect of humic substances on mitochondrial respiration and oxidative phosphorylation.

Fulvic and humic acids extracted from a podzol were shown to stimulate respiration in rat liver mitochondria, when present at concentrations of between 40 and 360 mg L-1. Low molecular weight fractions induced a more significant increase in respiration than high molecular weight material. Humic substances, at concentrations of between 40 and 400 mg L-1, normally also increased the efficiency of the process of oxidative phosphorylation in vitro, particularly after contact periods with the mitochondria of over 1 hour.

Animals↗
PubMed1998

Comparison of oxidative phosphorylation in the anastomosis of the small and large bowel. An experimental study in the rabbit.

Dehiscence of anastomosis in the large bowel (LB) is more frequent compared with that in the small bowel (SB). The pathophysiological mechanisms underlying the phenomenon are well known. The goal of this study is to demonstrate the different oxidative phosphorylation roles in the response of the anastomosed SB and LB. In 45 male rabbits under general anaesthesia, the ileum and colon were transected always on the same side and an end-to-end anastomosis was constructed using single-layer inverting interrupted 5-0 Ethilon sutures. Tracts containing bowel anastomoses were collected at 3, 12 and 24 h and 3, 7 and 21 days after the operation and compared with non-anastomosed bowel. Respiratory rates with different substrates, enzymatic activities, respiratory complex structures and cytochrome contents were measured in smooth muscle purified mitochondria. Mitochondrial respiration showed significant differences in the LB versus anastomosed SB: respiratory rates were markedly reduced in the LB (residual activity: 25 vs. 95% of the SB). Detailed analysis of other mitochondrial parameters confirmed a better tolerance of the ileum to anastomosis. From these preliminary studies we can consider two different aerobic thresholds for either the large or the small rabbit intestine, the latter being oxygen dependent. This can explain the mitochondrial sufferance of anastomosis in the LB whose prevalent aerobic metabolism can be more easily affected by different noxae if compared with the tendency to glycolytic metabolism of the small intestine.

Anastomosis, Surgical↗
PubMed1976

[Participation of thyroid hormones in realization of the action of diphtheria toxin on oxidative phosphorylation in rabbit liver mitochondria].

Experiments were conducted on rats with an experimental hypo- and hyperthyroidism. In hypothyroidism there was no disturbance of the capacity to phosphorylation conjugated with respiration in the mitochondria from the liver in intravenous injection of diphtheria toxin, but in hyperthyroidism sensitivity of mitochondria of the liver to the uncoupling action of diphtheria toxin was much increased. It is supposed that of great significance for the uncoupling action of diphtheria toxin on the oxidative phosphorylation was the incretory function of the thyroid gland.

Animals↗
PubMedDate not supplied

[Mechanism of oxidative phosphorylation. III. Relationship between the composition of the mitochondrial incubation medium and functional parameters].

Functional properties of rat brain mitochondria were different in Krebs-Ringer solution as compared to these in the media with mannit. Mitochondria in the presence of cytochrme c increased endogenous respiration essentially after the introduction of mannit into the polarographic cell. It is concluded that mannit metabolised by mitochondria as other non-cell compounds, must not be in the media of incubation of mitochondria, while studying the oxidative phosphorylation mechanism.

Adenosine Diphosphate↗
PubMed2000

Characterisation of oxidative phosphorylation in skeletal muscle mitochondria subpopulations in pig: a study using top-down elasticity analysis.

In skeletal muscle, two mitochondrial populations are present which, on the basis of their localisation, are termed intermyofibrillar and subsarcolemmal mitochondria (IMF and SS, respectively). These two populations have different biochemical characteristics and show different responses to physiological stimuli. In this paper, we characterise the oxidative phosphorylation of SS and IMF using 'top-down' elasticity analysis. We excluded the possibility that their different characteristics can be attributed to a different degree of breakage of the two types of mitochondria due to the different isolation procedures used in their preparation. The higher respiration rate and higher respiratory control ratio shown by IMF compared with those shown by SS are principally due to the higher activities of the reactions involved in substrate oxidation as confirmed by the measurement of cytochrome oxidase activity. There is no difference in the leak of protons across the inner mitochondrial membrane between IMF and SS; a faster rate of ATP synthesis and turnover is driven by the lower membrane potential in SS compared with in IMF.

Adenosine Triphosphate↗
PubMed1979

[Effect of aflatoxin B 1 on respiration and oxidative phosphorylation in the rabbit. I. Studies of the hepatic mitochondria].

The effect of various concentrations of aflatoxin B1 (AB1) is studied "in vitro" on rabbit liver mitochondria. AB1 inhibits at concentrations from 1 to 2-4 x 10(-4) M, the respiratory rate from 20% a maximum 41-35% by glutamate and succinate as substrates, but it does not uncouple oxidative phosphorylation nor does it inhibit site III (ascorbate + TMPD). The inhibited site appears to be between cytochromes b and c (c1). AB1 seems to be easily transported across the mitochondrial membrane. The maximum degree of inhibition and the promoting AB1 concentration are too high to explain the liver cell necrosis in rabbit induced by AB1 "in vivo".

Aflatoxins↗
PubMed2002

BCL-2 improves oxidative phosphorylation and modulates adenine nucleotide translocation in mitochondria of cells harboring mutant mtDNA.

Members of the BCL-2-related antiapoptotic family of proteins have been shown previously to regulate ATP/ADP exchange across the mitochondrial membranes and to prevent the loss of coupled mitochondrial respiration during apoptosis. We have found that BCL-2/BCL-x(L) can also improve mitochondrial oxidative phosphorylation in cells harboring pathogenic mutations in mitochondrial tRNA genes. The effect of BCL-2 overexpression in mutated cells was independent from apoptosis and was presumably associated with a modulation of adenine nucleotide exchange between mitochondria and cytosol. These results suggest that BCL-2 can regulate respiratory functions in response to mitochondrial distress by regulating the levels of adenine nucleotides.

Adenine Nucleotides↗
PubMedDate not supplied

Uncoupling of mitochondrial oxidative phosphorylation alters lipid peroxidation-derived free radical production but not recovery of postischemic rat hearts and post-hypoxic endothelial cells.

The contribution of mitochondrial free radical production towards the initiation of lipid peroxidation (LPO) and functional injury in the post-ischemic heart is unclear. Using the isolated rat heart model, the effects of the uncoupler of mitochondrial oxidative phosphorylation dinitrophenol (DNP, 50 microM final) on post-ischemic lipid peroxidation-derived free radical production and functional recovery were assessed. Hearts were subjected to 30 min total global ischemia followed by 15 min of reperfusion in the presence of DNP. As expected, DNP enhanced oxygen consumption before (11.3 +/- 0.9 mumol/min, p < 0.001) and during reperfusion (at 10 min: 7.9 +/- 0.7 mu umol/min), compared to the heart with control treatment (8.2 +/- 0.5 and 6.7 +/- 0.3, respectively). This effect was only associated with a higher incidence of ventricular tachycardia during reperfusion (80 vs. 50% for control treatment, p < 0.05). Electron spin resonance spectroscopy (ESR) and spin trapping with alpha-phenyl-tert-butylnitrone PBN-radical adducts (untreated: 6.4 +/- 1.0 nM, at 10 min) decreased in the presence of DNP (1.7 +/- 0.4 nM, p < 0.01). The radical concentration inversely correlated with myocardial oxygen consumption. Total liberation of free radical adducts during the initial 10 min of reperfusion was reduced by DNP (0.59 +/- 0.09 nmol, p < 0.01) compared to the respective control treatment (1.26 +/- 0.16 nmol). Similar effects, prevention of PBN adduct formation and unchanged viability in the presence of DNP, were obtained with endothelial cells during post-hypoxic reoxygenation. Since inhibition of mitochondrial phosphorylation can inhibit the formation of LPO-derived free radicals after an ischemic/hypoxic interval, mitochondria may represent an important source of free radicals capable of initiating lipid peroxidative injury during reperfusion/reoxygenation.

2,4-Dinitrophenol↗