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PubMed1993

Catecholamines: important factors in the increase of oxidative phosphorylation coupling in rat-liver mitochondria during the early phase of burn injury.

Thirty minutes after Sprague-Dawley rats had been injected subcutaneously with epinephrine or norepinephrine, the respiratory control ratio (RCR), the rate of O2 consumption in state 3 and the rate of ATP formation in liver mitochondria succinate respiratory chain were increased. The rate of O2 consumption in state 4 was increased or only slightly increased. When the rats were injected with the adrenergic blocking agents, timolol or phenoxybenzamine, 1 h before the burn, the activities of the succinate respiratory chain was partly inhibited 30 min postburn. Compared with our previous results, it can be suggested that catecholamines may play an important role in the increase of oxidative phosphorylation coupling in the early phase of burn injury.

Animals↗
PubMed1993

Mitochondrial oxidative phosphorylation in saponin-skinned human muscle fibers is stimulated by caffeine.

The addition of 15 mM caffeine to saponin-skinned human muscle fibers from M. vastus lateralis caused in the presence of 2 mM ATP an approx. 2-fold stimulation of respiration with glutamate+malate. This effect can be abolished by either the addition of the Ca2+ chelator EGTA, the inhibitor of Ca2+ transport Ruthenium red and the inhibitor of the myosin ATPase vanadate. The caffeine concentration dependency of respiration of fibers coincided with the caffeine-caused stimulation of myosin ATPase activity. The activation of oxidative phosphorylation in saponin-skinned human muscle fibers by caffeine can be explained by a stimulation of myosin ATPase caused by Ca2+ release from sarcoplasmic reticulum.

Caffeine↗
PubMed1976

Effect of insulin on mitochondrial oxidative phosphorylation and energy charge of the perfused guinea pig liver.

The effect of insulin was investigated in the isolated guinea pig liver perfused with Krebs-Ringer bicarbonate buffer containing red blood cells and albumin. In the mitochondria isolated from livers perfused with 10 units of insulin per hour, the phosphorylative activity with glutamate as a substrate increased to about 160 per cent of control 60 minutes after the beginning of perfusion (p less than 0.01). Such an enhanced phosphorylative activity was accompanied by increases in the respiratory control ratio, state 3 respiration, and P/O ratio. On the other hand, in the liver perfused with insulin, the levels of the energy charge and adenine nucleotide quotient increased to a significant degree as compared to the liver without insulin (p less than 0.01 and p less than 0.05, respectively). It is suggested that insulin plays an important role as a portal factor in regulating mitochondrial oxidative phosphorylation and the levels of the phosphorylated adenine nucleotides.

Adenosine Diphosphate↗
PubMed1979

Response of oxidative phosphorylation in liver of protein-energy malnourished rats.

State 3, state 4 respiratory rates, respiratory control ratio (RCR = state 3/state 4), ADP/O ratio and swelling in salt medium were determined in liver mitochondria from three groups of rats: group 1--controls; group 2--energy-restricted, and group 3--protein-deficient. Experiments were carried out between 3 and 5 weeks and between 7 and 9 weeks after initiation of the experimental diets. State 3 respiration of mitochondria from group 2 rats was reduced after 3-5 weeks on the experimental diet as compared to group 1 rats. However, state 4 respiration, RCR and ADP/O ratio were not different in groups 2 and 3 as compared to those in controls. Between 7 and 9 weeks it was found that state 3 respiration with both the substrates was higher in groups 2 and 3 as compared to group 1. State 4 respiration was increased in group 2 but was unaltered in group 3, compared to controls. Mitochondrial preparations from group 2 rats showed faster rates of swelling in KC1 medium, compared to group 1, at both periods. On the other hand, the rates of swelling were slower as compared to controls in the case of mitochondria isolated from group 3 rats. Results of these experiments indicate that the terminal effect of severe restriction of calories and protein on mitochondrial oxidative phosphorylation is similar.

Animals↗
PubMed1997

Expression of oxidative phosphorylation genes in muscle cell cultures from patients with mitochondrial myopathies.

The expression of several mitochondrial and nuclear genes involved in ATP production was examined in cells cultured from muscle biopsies of patients harboring mitochondrial pathologies. The transcript patterns in muscle cells from the patients affected by carnitine palmitoyl transferase II or 2-ketoglutarate dehydrogenase deficiencies were almost similar to control patterns. In the opposite, patterns were strikingly abnormal in all the other cell cultures from patients with defects in enzymatic complexes involved in oxidative phosphorylation: mitochondrial complex II and III deficiencies, two MELAS syndromes (myopathy, encephalopathy, lactic acidosis and stroke like episodes), a case of Kearns-Sayre syndrome and a case of chronic progressive external ophthalmoplegia. In cultured muscle cells from patients with mtDNA mutations, the percentage of mutated mtDNA was low as compared with those determined in the corresponding skeletal muscle biopsy. Moreover, the complex II defect resulting of a nuclear mutation was not expressed in the cell cultures. Thus, an undetermined transcriptional event, transmitted from muscle biopsies to cultured muscle cells, should be involved to account for such abnormal transcript patterns.

Adolescent↗
PubMed1995

Regulation of oxidative phosphorylation: the flexible respiratory network of Paracoccus denitrificans.

Paracoccus denitrificans is a facultative anaerobic bacterium that has the capacity to adjust its metabolic infrastructure, quantitatively and/or qualitatively, to the prevailing growth condition. In this bacterium the relative activity of distinct catabolic pathways is subject to a hierarchical control. In the presence of oxygen the aerobic respiration, the most efficient way of electron transfer-linked phosphorylation, has priority. At high oxygen tensions P. denitrificans synthesizes an oxidase with a relatively low affinity for oxygen, whereas under oxygen limitation a high-affinity oxidase appears specifically induced. During anaerobiosis, the pathways with lower free energy-transducing efficiency are induced. In the presence of nitrate, the expression of a number of dehydrogenases ensures the continuation of oxidative phosphorylation via denitrification. After identification of the structural components that are involved in both the aerobic and the anaerobic respiratory networks of P. denitrificans, the intriguing next challenge is to get insight in its regulation. Two transcription regulators have recently been demonstrated to be involved in the expression of a number of aerobic and/or anaerobic respiratory complexes in P. denitrificans. Understanding of the regulation machinery is beginning to emerge and promises much excitement in discovery.

Aerobiosis↗
PubMedDate not supplied

HGF/SF activates glycolysis and oxidative phosphorylation in DA3 murine mammary cancer cells.

Hepatocyte growth factor/scatter factor (HGF/SF) is a paracrine growth factor which increases cellular motility and has also been implicated in tumor development and progression and in angiogenesis. Little is known about the metabolic alteration induced in cells following Met-HGF/SF signal transduction. The hypothesis that HGF/SF alters the energy metabolism of cancer cells was investigated in perfused DA3 murine mammary cancer cells by nuclear magnetic resonance (NMR) spectroscopy, oxygen and glucose consumption assays and confocal laser scanning microscopy (CLSM). 31P NMR demonstrated that HGF/SF induced remarkable alterations in phospholipid metabolites, and enhanced the rate of glucose phosphorylation (P < .05). 13C NMR measurements, using [13C1]-glucose-enriched medium, showed that HGS/SF reduced the steady state levels of glucose and elevated those of lactate (P < .05). In addition, HGF/SF treatment increased oxygen consumption from 0.58+/-0.02 to 0.71+/-0.03 micromol/hour per milligram protein (P < .05). However, it decreased CO2 levels, and attenuated pH decrease. The mechanisms of these unexpected effects were delineated by CLSM, using NAD(P)H fluorescence measurements, which showed that HGF/SF increased the oxidation of the mitochondrial NAD system. We propose that concomitant with induction of ruffling, HGF/SF enhances both the glycolytic and oxidative phosphorylation pathways of energy production.

Adenocarcinoma↗
PubMed2005

A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle.

Obesity and type 2 diabetes have been associated with a high-fat diet (HFD) and reduced mitochondrial mass and function. We hypothesized a HFD may affect expression of genes involved in mitochondrial function and biogenesis. To test this hypothesis, we fed 10 insulin-sensitive males an isoenergetic HFD for 3 days with muscle biopsies before and after intervention. Oligonucleotide microarray analysis revealed 297 genes were differentially regulated by the HFD (Bonferonni adjusted P < 0.001). Six genes involved in oxidative phosphorylation (OXPHOS) decreased. Four were members of mitochondrial complex I: NDUFB3, NDUFB5, NDUFS1, and NDUFV1; one was SDHB in complex II and a mitochondrial carrier protein SLC25A12. Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC1) alpha and PGC1beta mRNA were decreased by -20%, P < 0.01, and -25%, P < 0.01, respectively. In a separate experiment, we fed C57Bl/6J mice a HFD for 3 weeks and found that the same OXPHOS and PGC1 mRNAs were downregulated by approximately 90%, cytochrome C and PGC1alpha protein by approximately 40%. Combined, these results suggest a mechanism whereby HFD downregulates genes necessary for OXPHOS and mitochondrial biogenesis. These changes mimic those observed in diabetes and insulin resistance and, if sustained, may result in mitochondrial dysfunction in the prediabetic/insulin-resistant state.

Adult↗
PubMedDate not supplied

[Dinitroorthocresol dissociation of oxidative phosphorylation in the rat liver perfused in situ].

Perfusion of the rat liver in situ for 150 min provides for maintaining optimal values of acid-base balance for the following indexes: surplus of bases, content of standard bicarbonate, buffer bases pH, pO2, pCO2, HbO2, the level of bile secretion, content of lactate, pyruvate, ATP, ADP, that evidences for a high functional activity in the tissue. Introduction of dinitro-ortho-cresol (DNC) into the perfusion liquid causes development of acidosis. DNC results in dissociation of oxidative phosphorylation: the content of ATP and intensity of inorganic phosphorus utilization decrease, oxygen uptake intensifies. A compensatory increase in the glycolysis intensity directed to maintaining the level of macroergs under these conditions is is pronounced in the intensified uptake of glucose, in a rise in the content of lactate in perfusate and an increase in the pyruvate kinase activity in the liver. The redox state of NAD-pairs (ratio of [NAD+] : [NADN] calculated from the content of redox metabolites and the equilibrium constant for the lactate dehydrogenase system shifts toward an increase in the reducing properties of hepatocytes cytoplasm. The phosphate potential value calculated from the ratio [ATP] : [ADP] - [Pinor] lowers under conditions of the experiment.

Acid-Base Equilibrium↗
PubMed2005

From oxidative phosphorylation to transcription--a postdoctoral adventure.

The period as a postdoctoral fellow is crucial for the establishment of one's scientific research career. I illustrate here its importance based on my own experience. Although luck played a part, moving to the right place at the right time and having generous leaders who allowed me freedom to express unconventional views were most valuable in my venture into two scientific territories that were previously unfamiliar to me. My first encounter with an unknown field led to me challenging the well-established dogma of uncoupling of oxidative phosphorylation as the explanation for hormone action; the second, led to the demonstration of the multiplicity of eukaryotic RNA polymerase. I hope that the events described here will provide some encouragement to young scientists embarking on a research career and also be of interest to others.

Biochemistry↗
PubMed1983

Preservation of oxidative phosphorylation by lidocaine in ischemic and reperfused myocardium.

The effect of lidocaine (2 mg/kg bolus, 0.04 mg/kg per min infusion) on ischemic and reperfused myocardial respiration was assessed in 32 dogs, using indices of mitochondrial respiration (ADP:O ratio, state 3 and state 4 respiration, and respiratory control index). Heart rate, left ventricular (LV) pressure, LV dp/dt, cardiac index, epicardial ST segment, and regional myocardial blood flow, using 9 +/- 1 micron radiospheres, were measured after 40 min of constriction of the anterior descending coronary artery (N = 16) and after 20 min of reperfusion (N = 16). Results showed that lidocaine increased state 3 respiration and respiratory control in reperfused myocardium (P less than 0.05) with both glutamate and succinate-rotenone as substrate. It is concluded that lidocaine improves postischemic mitochondrial oxidative phosphorylation independent of altered hemodynamics or change in myocardial blood flow.

Animals↗
PubMed1985

Histological, ultrastructural and mitochondrial oxidative phosphorylation studies in liver of rats chronically treated with oral valproic acid.

The effects of oral administration of valproic acid (VPA) have been studied on the liver of female adult Wistar rats, at doses of 60 and 120 mg/kg/day during 4 and 18 weeks (periods I and II). Other groups received the same doses of VPA with phenobarbital (PB). The animals developed periportal steatosis, more intense at the end of period II and in groups non-induced by PB, and also some degree of mitochondrial swelling. An uncoupling of the oxidative phosphorylation was also evident with both doses in the non-induced groups, and only with the high dose of VPA in the induced group. An in vitro study on isolated liver mitochondria showed uncoupling only with very high concentration of VPA (10 mM). We comment on these findings and propose a chronic model of experimental hepatotoxicity of oral VPA in the rat.

Administration, Oral↗
PubMed1988

Metabolism of round spermatids: gossypol induces uncoupling of respiratory chain and oxidative phosphorylation.

The effect of gossypol on energy metabolism of round spermatids of rats was examined. When spermatids were treated with various concentrations of gossypol for 30 min at 32 degrees C, a biphasic response (stimulation at low concentrations and inhibition at high concentrations) was seen in pyruvate and CO2 production from lactate. At the early period of incubation, gossypol at even high concentrations stimulated CO2 production to an extent similar to that stimulated by 2,4-dinitrophenol (DNP). At longer periods of incubation, however, the rates of CO2 production from lactate dropped to those seen in the rotenone-treated cells. The rates of oxygen consumption were not increased further by DNP when cells were pretreated with gossypol. The adenosine triphosphate (ATP) content in spermatids was reduced markedly, although lactate oxidation to CO2 and mitochondrial respiration were stimulated by gossypol. These results suggest that gossypol probably exerts its effect on spermatids by uncoupling respiratory chain and oxidative phosphorylation.

2,4-Dinitrophenol↗
PubMedDate not supplied

[The mitochondria of poikilothermic vertebrates: oxidative phosphorylation and adenine nucleotides].

The respiration and phosphorylation velocities in lamprey liver mitochondria are high and with some Krebs cycle substrates they even exceed those of mammals. These parameters in frog liver mitochondria during winter period are 2-3 times lower as compared to rat mitochondria. The adenine nucleotide contents in liver mitochondria of lampreys, fish and frogs are 2-8 times lower than in mitochondria of adult mammals; they are comparable to these parameters in liver mitochondria of rats at the earliest stages of postnatal ontogenesis. Participation of intramitochondrial adenine nucleotides in regulation of oxidative phosphorylation of poikilothermic vertebrates in vivo is discussed.

Adenine Nucleotides↗
PubMed1996

Gene expression of ND4, a subunit of complex I of oxidative phosphorylation in mitochondria, is decreased in temporal cortex of brains of Alzheimer's disease patients.

Gene expression of mitochondrial DNA-encoded ND4 in brains of Alzheimer's disease (AD) patients and age-matched controls was measured using Northern blot. The level of ND4 message in temporal cortex of control subjects was higher than in motor cortex, whereas the level of ND4 gene expression in temporal cortex of AD brains was decreased compared with that in temporal cortex of controls. A control probe showed no difference in expression between the two areas of AD and control brains. These and previous data suggest that neurons vulnerable to AD express higher levels of enzymes of oxidative phosphorylation than do spared neurons, and that this difference may promote selective neuronal vulnerability of AD.

Alzheimer Disease↗
PubMed1989

A study on Na+ -coupled oxidative phosphorylation: ATP formation supported by artificially imposed delta pNa and delta pK in Vibrio alginolyticus cells.

Addition of Na+ to the K+-loaded Vibrio alginolyticus cells, creating a 250-fold Na+ gradient, is shown to induce a transient increase in the intracellular ATP concentration, which is abolished by the Na+/H+ antiporter, monensin. The delta pNa-supported ATP synthesis requires an additional driving force supplied by endogenous respiration or, alternatively, by a K+ gradient (high [K+] inside). In the former case, ATP formation is resistant to the protonophorous uncoupler. Dicyclohexylcarbodiimide and diethylstilbestrol, but not vanadate, completely inhibit Na+ pulse-induced ATP formation. The data agree with the assumption that Na+ -ATP-synthase is involved in oxidative phosphorylation in V alginolyticus. Interrelation of H+ and Na+ cycles in bacteria is discussed.

Adenosine Triphosphate↗
PubMed1991

The effect of thyroid state and cold exposure on rat liver oxidative phosphorylation.

In this paper we have examined the effect of cold exposure on hepatic mitochondrial state 3 respiration and ATP synthesis, using succinate as the substrate, in euthyroid, hypothyroid and hyperthyroid rats. The results show that cold exposure does not elicit any variation in the above parameters in euthyroid and hyperthyroid rats, whereas when hypothyroid rats are exposed to cold, a significant increase (about +45%) occurs in state 3 respiration and ATP synthesis. We have also measured succinic dehydrogenase specific activity and uncoupled respiration during cold exposure in various thyroid states. The finding that cold exposure elicits no variation in the above parameters indicates that there is some control on ATP synthase and/or adenine nucleotide translocator. The above findings, as a whole, suggest that cold exposure acts on oxidative phosphorylation only if triiodothyronine is lacking, by controlling ATP synthase and/or adenine nucleotide translocator.

Adenosine Triphosphate↗