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At least 595 records · Page 33Linked to original sources
PubMed1993

Effects of substrate and inhibition of oxidative metabolism on contraction and myosin phosphorylation in ASM.

Steady-state active stress in smooth muscle is maintained by cross bridges which undergo continuous cycling and myosin phosphorylation, and the two processes both consume ATP. In this study, we investigated whether energy utilization by cross-bridge cycling and myosin phosphorylation is compartmentalized and examined their relative affinities for ATP in airway smooth muscle. We measured active stress, myosin phosphorylation, O2 consumption, and tissue ATP content in bovine tracheal smooth muscle activated by K+ depolarization when glucose was replaced by pyruvate and when oxidative metabolism was inhibited by hypoxia or uncoupled by 2,4-dinitrophenol. The results indicate that ATP produced from both glycolysis and oxidative metabolism is available to both cross-bridge cycling and myosin phosphorylation. However, steady-state myosin phosphorylation was insensitive to the inhibition of oxidative metabolism by hypoxia and mitochondrial uncoupling when steady-state isometric stress and tissue ATP content were significantly reduced. These results suggest that, relative to actomyosin adenosine 5'-triphosphatase, myosin light chain kinase has a higher affinity for ATP in intact airway smooth muscle. However, peak myosin phosphorylation associated with the initial rapid stress development was sensitive to inhibition of oxidative metabolism, probably reflecting a lower content of intracellular calcium store as a result of metabolic inhibition.

2,4-Dinitrophenol↗
PubMed1990

Energetic recovery from hypothermic preservation in the rat liver.

Changes in energy metabolism induced by norepinephrine were observed in liver perfused immediately after dissection and in liver stored in Euro-Collins solution at 0 degrees C for 24 hr. Oxygen consumption, glucose output, ATP content, and tissue pH were measured in isolated perfused rat liver at 37 degrees C. In fresh liver, a two-fold increase in glucose output and oxygen consumption was induced by norepinephrine (1 microM), while changes in ATP content and tissue pH were minimal. In stored liver, the cumulative increments in glucose output and oxygen consumption induced by norepinephrine were 30 and 27% those of fresh liver, respectively. ATP content of the unstimulated liver was 76% that of the fresh liver, then decreased to 50% during stimulation. A transient decrease in tissue pH (0.14 pH unit) was significant compared with that of fresh liver. These results suggest that norepinephrine stimulation is useful for assessing energetic and functional recovery of reperfused liver following hypothermic storage.

Adenosine Triphosphate↗
PubMedDate not supplied

Cellular adenosine triphosphate production and consumption in the descending thin limb of Henle's loop in the rat.

To characterize the properties of cellular adenosine triphosphate (ATP) production and consumption in the descending thin limb of Henle's loop (DTL) in rats, we measured the cellular ATP content by applying the microchemiluminescence method. For ATP production, isolated DTL from the short- and long-loop nephron (SDL and LDL, respectively) was incubated with several substrates such as alanine, glucose, glutamine, beta-hydroxybutyrate (beta-HBA), lactate, and pyruvate; for ATP production from each substrate indicated that glucose and pyruvate were the preferred substrates to maintain cellular ATP in both SDL and LDL. ATP production from glutamine, beta-HBA, and lactate was substantial in LDL. In SDL, glutamine was the preferred substrate, and beta-HBA and lactate were minimal. The utilization of alanine was minimal in both LDL and SDL. The cellular ATP was significantly restored by ouabain at concentrations of 1.5 x 10(-5) and 1.5 x 10(-3) M in LDL, but in SDL only at 1.5 x 10(-3) M. In both segments, the cellular ATP level was significantly decreased by monensin above the concentrations of 1 micrograms/ml in LDL and 5 micrograms/ml in SDL. From these observations, we conclude that there exist clear differences between LDL and SDL in ATP-supplying substrate specificities and ATP-consuming properties.

Adenosine Triphosphate↗
PubMed2005

ATP accelerates respiration of mitochondria from rat lung and suppresses their release of hydrogen peroxide.

Lung mitochondria were isolated by differential centrifugation from pentobarbital-anesthetized male rats. One to three millimolar Mg2+-ATP increased the consumption of oxygen of lung mitochondria oxidizing 10 mM succinate > fourfold (P < 0.01) whereas ATP increased the respiration of liver mitochondria by < 35%. ATP also hyperpolarized partially uncoupled lung mitochondria in the presence of the mitochondria-specific antagonist, oligomycin. However, only 20% of the ATPase activity in the lung mitochondria was blocked by oligomycin compared to a blockade of 91% for liver mitochondria. We investigated the effect of reducing the non-mitochondrial ATPase activity in the lung preparation. A purer suspension of lung mitochondria from a Percoll gradient was inhibited 95% by oligomycin. The volume fraction identified as mitochondria by electron microscopy in this suspension (73.6+/- 3.5%) did not differ from that for liver mitochondria (69.1+/- 4.9%). ATP reduced the mean area of the mitochondrial profiles in this Percoll fraction by 15% (P <0.01) and increased its state 3 respiration with succinate as substrate by 1.5-fold (P < 0.01) with no change in the state 4 respiration measured after carboxyatractyloside. Hence, ATP increased the respiratory control ratio (state 3/state 4, P <0.01). In contrast, state 3 respiration with the complex 1-selective substrates, glutamate and malate, did not change with addition of ATP. The acceleration of respiration by ATP was accompanied by decreased production of H2O2. Thus ATP-dependent processes that increase respiration appear to improve lung mitochondrial function while minimizing the release of reactive oxygen species.

Adenosine Diphosphate↗
PubMed2000

Chronic ethanol-induced myocardial protection requires activation of mitochondrial K(ATP) channels.

Moderate alcohol consumption protects against coronary heart disease by unclear mechanisms. We tested whether chronic ethanol preconditioning requires activation of mitochondrial K(ATP)channels. Rats were fed 18% (v/v) ethanol in drinking water for 10 months. Blood alcohol levels at sacrifice were 3 mmol/l (0.015 gram percent). Isolated crystalloid-perfused hearts were subjected to global ischemia and reperfusion on a modified Langendorff apparatus. Prior alcohol exposure doubled the recovery of LVDP during reperfusion (45+/-5%v 20+/-3% of baseline for controls, n=6, P<0.01) and blunted the rise in LVEDP (3.5+/-0.5 v 5.5+/-0.4 times baseline for controls, n=6, P<0.01). Ethanol feeding also reduced creatine kinase release during reperfusion. Inhibition of mitochondrial K(ATP)channels with 5-hydroxydecanoate had no effect on baseline LVDP, LVEDP, or coronary flow but abolished the beneficial effects of alcohol on LV contractile recovery and myocyte necrosis. We conclude that mitochondrial K(ATP)channel activity is required for chronic ethanol-induced protection.

Alcohol Drinking↗
PubMed1987

Implications of myocardial transformation for cardiac energetics.

The influence of isoenzyme pattern of myosin on cardiac energetics was investigated in a modified in situ heart-lung preparation in the rat. Chronic pressure load (spontaneous hypertension, aortic stenosis, Goldblatt hypertension), intermittent feeding, and swim-training elicited redistribution in the concentration of alpha chains of myosin ranging from 18 to 94%. The influence of isoenzyme pattern of myosin on cardiac energetics could be quantitatively assessed by extrapolation of the regression line of oxygen and substrate consumption related to tension time index. Fast myocardium with 100% alpha chains had an ATP and oxygen consumption which exceeded that of slow myocardium with 0% alpha chains by about 60%. This corresponds well to the state of activity of myofibrillar ATPase of fast myocardium which also exceeds that of slow myocardium by about 50%. Furthermore it could be shown that acute increase in the ATPase activity depends on the isoenzyme pattern of myosin. Under the influence of catecholamines the oxygen consumption related to tension time index increased by 30-40% in fast myocardium, whereby in a myocardium with 40% alpha chains no increase in oxygen consumption per unit tension time index was observed, when catecholamines were applied.

Adenosine Triphosphatases↗
PubMedDate not supplied

Early metabolic effects of hypotension on rat kidney.

Saturation-transfer phosphorus nuclear magnetic resonance (STNMR) has been applied to the rat kidney in vivo. The rate of renal metabolism determined by this method compares favorably with the renal oxygen consumption, assuming an ATP:oxygen ratio of 2. Hemorrhagic hypotension resulted in a 20% fall in renal blood flow and a significant fall in oxygen consumption. The rate of renal metabolism fell by 50%. This rate of ATP synthesis was below that required to maintain a normal [ATP], but renal [Pi] was not increased. When renal perfusion was reduced by 60%, intrarenal [Pi] rose. When [P1] was elevated, the method os STNMR no longer gave a reliable measure of the rate ATP synthesis, indicating that this new Pi pool was not in rapid chemical exchange with ATP. STNMR represents a useful noninvasive means of monitoring renal metabolic rate, with limitations due to insensitivity and the existence of multiple pools of intrarenal Pi.

Adenosine Diphosphate↗
PubMed1999

[Cellular energy metabolism: physiologic and pathologic aspects].

Cellular homeostasis requires permanent energy production and consumption. Adenosine triphosphate (ATP) is the major energy component for the cell. Its synthesis occurs mainly in mitochondria where the oxidative phosphorylations realise the coupling between oxygen consumption and phosphorylation of adenosine diphosphate. The anaerobic production of ATP plays an important role in the intermediary metabolism. The enzymatic complexes of the mitochondrial respiratory chain are energy transducers acting as proton pumps. In cardiomyocytes, the phosphocreatine circuit allows a substrate channelling between mitochondria and myofibrils. This metabolic compartmentation explains the difficulties of studying energetic metabolism in the beating heart and the lack of correlation between cardiac function and the usual energy parameters. Mitochondria are a potential site of action of anaesthetic agents. Lipophilic local anaesthetics impair cellular energy metabolism and mitochondrial ATP production. Such effects could be associated with toxic effects of these molecules. NMR or near-infrared spectroscopy are non invasive techniques for monitoring energetic metabolism in vivo. Clinical applications are developed for analysing brain, muscle or cardiac function in physiological and pathological conditions.

Adenosine Triphosphate↗
PubMed1989

Selective utilization of L-isomer of lactate in the smooth muscle of the guinea pig taenia caeci.

Utilization of D- and L-lactate in the isolated intestinal smooth muscle of the guinea pig taenia caeci was examined by measuring contractile tension, oxygen consumption, and adenosine triphosphate (ATP) and creatine phosphate (PCr) concentrations. In the absence of glucose in the medium, muscle contraction induced by a high concentration of K+ was inhibited and the rate of oxygen consumption and the concentrations of ATP and PCr were decreased. Addition of glucose, L-lactate, and D,L-lactate, but not D-lactate, led to recovery of muscle contraction, rate of oxygen consumption, and ATP and PCr concentrations when the tissue had been incubated in the high K+, glucose-free solution. These results suggest that the isolated guinea pig taenia caeci selectively utilizes the L-isomer of lactate as a substrate for energy metabolism.

Adenosine Triphosphate↗
PubMed1985

Reaction rates of creatine kinase and ATP synthesis in the isolated rat heart. A 31P NMR magnetization transfer study.

The NMR technique of magnetization transfer can be used to define intracellular reaction kinetics. In order to determine the relationship between ATP synthesis and flux through the creatine kinase reaction in the intact heart, we used this technique to measure flux through the creatine kinase reaction in the isolated, isovolumic rat heart at five levels of cardiac performance and oxygen consumption. The unidirectional reaction rate constants (s-1) calculated from a two-site exchange model for both the forward and reverse creatine kinase reactions increased with cardiac performance and oxygen consumption. As the rate-pressure product varied from 0 to 44.7 X 10(3) mm Hg/min and oxygen consumption rose from 5.9 to 45.8 mumol of O2/g dry weight/min, kforward increased from 0.27 to 1.30 and kreverse increased from 0.31 to 1.14. The relationship between creatine kinase flux and oxygen consumption, and thus ATP synthesis, took the form of the Michaelis-Menten equation. Rates of ATP synthesis estimated from magnetization transfer were similar to values calculated from oxygen consumption. The longitudinal relaxation time of creatine phosphate (2.06 s), the gamma-phosphorus atom of ATP (0.75 s), and inorganic phosphate (0.81 s) did not change with cardiac performance. These results show that myocardial energy transfer via the creatine kinase reaction is closely coupled to energy production.

Adenosine Triphosphate↗
PubMed1996

Inhibition of N-acetylaspartate production: implications for 1H MRS studies in vivo.

The effect of specific irreversible inhibitors of complexes I, III, IV and V of the mitochondrial respiratory chain, (rotenone, myxothiazol, cyanide and oligomycin, respectively) on mitochondrial N-acetylaspartate production, and its relationship to oxidative phosphorylation (ATP production and oxygen consumption) were investigated in isolated rat brain mitochondria. Mitochondrial N-acetylaspartate production, ATP production and oxygen consumption were all significantly decreased in the presence of each of the inhibitors used compared with control incubations, and correlated positively with each other. It is postulated that decreased N-acetylaspartate levels seen in disease states by 1H NMR spectroscopy in vivo may reflect primarily an impaired mitochondrial energy production rather than neuronal cell loss.

Analysis of Variance↗
PubMed1990

A 31P-NMR study of bovine adrenocortical mitochondrial metabolic activities.

High-field 31P-NMR spectroscopy has been used to study the metabolic activities of coupled bovine adrenocortical mitochondria in vitro. These differentiated organelles use oxygen as a substrate to support both oxidative phosphorylation and specific steroid hydroxylation reactions. The NMR technique allowed the resolution of two inorganic phosphate signals, attributed to the matrix and external medium phosphate pools, at low and high field, respectively. These signals were used to calculate the respective Pi concentrations and to obtain the pH of the two corresponding compartments. In addition, the NMR spectra displayed resonance signals corresponding to ADP added to the medium and to ATP synthesized during oxidative phosphorylation. NMR analysis of the mitochondrial perchloric acid extracts identified the major phosphate-containing metabolites, namely NADP+, NAD+, phosphocholine, phosphoethanolamine, sn-glycero-(3)phosphocholine, AMP, ADP, ATP and Pi. Upon addition of ADP and malate to the oxygenated suspension, the kinetics of mitochondrial external Pi consumption and of ATP synthesis, along with the intra- and extraorganelle pH variations could be monitored over time periods of approximately 30 min, in the absence and presence of different steroid hydroxylation substrates. A major observation was that oxidative phosphorylation, which takes place in the absence of steroid, was markedly inhibited as soon as steroid hydroxylation was operating. These observations show the potential of 31P-NMR spectroscopy in the study of metabolic activities of isolated intact mitochondrial organelles. Such an approach appears promising for further determination of the underlying mechanisms in the balance between vital oxidative phosphorylation and differentiated steroid hydroxylation which are under hormonal control in adrenocortical mitochondria as well as in other steroidogenic cell systems.

Adenosine Triphosphate↗
PubMed1996

Phospholipase A2: a potentially important determinant of adenosine triphosphate levels during hypoxic-reoxygenation tubular injury.

During the course of O2 deprivation-induced proximal tubular injury, profound alterations in ATP homeostasis exist. This study sought to characterize direct cellular determinants of these abnormalities further. Mouse proximal tubular segments (PTS) were isolated and their adenine nucleotide profiles were determined during hypoxic-reoxygenation injury. The extent of oxidant stress, Ca2+ overload, cytoskeletal disruption, and phospholipase activity were experimentally manipulated by H2O2, Ca2+ ionophore, cytochalasin D, or PLA2 addition, respectively. Hypoxia induced the expected deterioration in adenylate profiles, and a persistent defect in ATP homeostasis was observed during reoxygenation (decreased ATP/ADP ratios and absolute ATP content). H2O2, Ca2+ ionophore, and cytochalasin D had no significant impact on adenylate profiles. However, doses of PLA2 that had no overt effect on normal tubules caused 50 to 75% reductions in both hypoxic and reoxygenation ATP/ADP ratios and absolute ATP content. This effect was completely reproduced by the addition of arachidonic acid (C20:4). No other test fatty acid (C16:0, C18:1, C18:3) reproduced this result. Despite its profound negative impact on hypoxic/reoxygenation ATP concentrations, PLA2 and C20:4 each decreased lethal cell injury (lactate dehydrogenase release), as previously reported. The reductions in ATP and lethal cell injury were not mechanistically linked, because C18:1 and C18:3 reproduced the protective action of C20:4 without altering adenine nucleotide profiles. Ouabain, mannitol, or plasma membrane fatty acid "scavenger" therapy (albumin) did not improve the posthypoxic/PLA2-induced depressions in ATP. The addition of C20:4 caused a modest decrease in posthypoxic tubule oxygen consumption, compared to controls. It was concluded that: (1) PLA2 can be a major determinant of ATP concentrations during both hypoxic and reoxygenation tubular injury; (2) this action is mediated via C20:4 release; (3) a primary defect in mitochondrial ATP production, rather than increased ATP consumption, is likely to be responsible for this action.

Adenosine Diphosphate↗
PubMed2000

High phosphorylation efficiency and depression of uncoupled respiration in mitochondria under hypoxia.

Mitochondria are confronted with low oxygen levels in the microenvironment within tissues; yet, isolated mitochondria are routinely studied under air-saturated conditions that are effectively hyperoxic, increase oxidative stress, and may impair mitochondrial function. Under hypoxia, on the other hand, respiration and ATP supply are restricted. Under these conditions of oxygen limitation, any compromise in the coupling of oxidative phosphorylation to oxygen consumption could accentuate ATP depletion, leading to metabolic failure. To address this issue, we have developed the approach of oxygen-injection microcalorimetry and ADP-injection respirometry for evaluating mitochondrial function at limiting oxygen supply. Whereas phosphorylation efficiency drops during ADP limitation at high oxygen levels, we show here that oxidative phosphorylation is more efficient at low oxygen than at air saturation, as indicated by higher ratios of ADP flux to total oxygen flux at identical submaximal rates of ATP synthesis. At low oxygen, the proton leak and uncoupled respiration are depressed, thus reducing maintenance energy expenditure. This indicates the importance of low intracellular oxygen levels in avoiding oxidative stress and protecting bioenergetic efficiency.

Adenosine Triphosphate↗
PubMed1997

Alveolar type II cell cNOS activity and ATP levels are increased by lung surfactant or DPPC vesicles.

In a previous study, we reported that nitric oxide (.NO) affects surfactant synthesis and ATP levels in alveolar type II cells and suggested that there is constitutive nitric oxide synthase (cNOS) activity in the cells. In the present study, we performed experiments to confirm further the presence of cNOS and to determine the effects of lung surfactant on type II cell .NO and ATP levels. The supernatant from freshly isolated cells contains .NO (0.26 +/- 0.08 nmol/10(6) cells). During incubation, the cells produce additional .NO at a rate of approximately 0.3 nmol.10(5) cells-1.h-1. .NO formation is inhibited by 28-46% by three inhibitors of cNOS and inducible NOS (iNOS), NG-monomethyl-L-arginine (L-NMMA), L-N5-(1-iminoethyl)ornithine hydrochloride, and NG-nitro-L-arginine methyl ester, but a specific inhibitor of iNOS, aminoguanidine, has no effect. The production of .NO is reduced in Ca(2+)-free medium, is stimulated by the Ca2+ ionophore A-23187, and is independent of extracellular L-arginine. One known type of cNOS, endothelial NOS (eNOS), can be detected in the cells by using Western blot analysis. Incubation of the cells with lung surfactant leads to a relatively rapid (approximately 15 min), concentration-dependent increase in .NO formation that reaches levels as high as 238 +/- 14% of control. The surfactant effects appear to be caused by its major component, dipalmitoyl phosphatidylcholine (DPPC). Exposure of type II cells to DPPC results in maximal increases in .NO formation, ATP content, and O2 consumption, which are 268 +/- 32, 234 +/- 24, and 131 +/- 6% of control, respectively. The DPPC-induced increases in .NO, ATP, and O2 consumption are inhibited by L-NMMA. These results confirm the presence of type II cell cNOS and suggest that it may have a role in the cellular processing of lung surfactant.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1983

Energy metabolism and ATP turnover time during the cell cycle in roentgen irradiated Ehrlich ascites tumour cells.

The cell-cycle related energy metabolism after roentgen irradiation of in vivo growing Ehrlich ascites tumour cells was investigated in cell fractions obtained by elutriator centrifuging. The oxygen consumption and the lactate and pyruvate production, measured in vitro after 4.5, 5 and 9 Gy up to 24 h, were undisturbed, while the decrease in the in vivo ATP content was dose-independent in all parts of the cell cycle. On the basis of these data the ATP turnover time was found to be decreased. The decrease in the ATP content is considered to be less likely to be due to membrane leakage or increased ATP consumption than to reduced ATP production. Since in vitro incubation normalizes the ATP content, it is suggested that environmental factors in the ascites liquid after irradiation cause a decrease in the ATP production. Low ATP contents of the cells do not appear to influence the irradiation-induced changes in the cell flow through the cell cycle.

Adenosine Triphosphate↗
PubMed1980

Changes in contractile function and endogenous fuel supply in rat heart upon perfusion with substrate-free medium.

Isolated rat hearts were perfused with aerobic substrate-free medium for different intervals during which changes in functional and metabolic events were examined. The contractile force was maintained for 30 min but thereafter declined toward zero over a period of 90 min. Before the onset of contractile failure, glycogen decreased by 60% of the control value, various intermediates of glycolytic flux, hexosephosphates, and triosephosphates, except dihydroxyacetone phosphate, reached their lowest level, and hydration of the myocardium became maximal. Furthermore, the phosphate potential, creatine phosphate (CrP), ATP, and oxygen consumption decreased by 60%, 45%, 10%, and 18%, respectively, before the onset of contractile failure. A progressive decrease in citrate, isocitrate, alpha-ketoglutarate, and malate was observed during a 2-hr perfusion period, but a slight increase in the levels of oxaloacetate and acetyl-CoA was apparent at 30 and 60 min, respectively. The early phase of contractile failure (30-60 min) was associated with an increase in the free fatty acid (FFA) and AMP levels, whereas the late phase (90-120 min) was characterized by an increase in resting tension and a decrease in oxygen consumption. The complete failure of the heart to generate contractile force at 120 min of perfusion occurred when about 40% of the glycogen and ATP contents and about 25% of the creatine phosphate and triglyceride contents were still present. Therefore, contractile failure of the hearts perfused with substrate-free medium may be caused by an insufficiency of the mechanisms responsible for the mobilization of endogenous glycogen and triglycerides as well as for the generation and utilization of ATP.

Acetyl Coenzyme A↗
PubMed1999

Presence of two enzymes, different from the F1F0-ATPase, hydrolyzing nucleotides in human term placental mitochondria.

The hydrolysis of ATP, ADP or GTP was characterized in mitochondria and submitochondrial particles since a tightly-bound ATPase associated with the inner mitochondrial membrane from the human placenta has been described. Submitochondrial particles, which are basically inner membranes, were used to define the location of this enzyme. Mitochondria treated with trypsin and specific inhibitors were also used. The oxygen consumption stimulated by ATP or ADP was 100% inhibited in intact mitochondria by low concentrations of oligomycin (0.5 microgram/mg) or venturicidine (0.1 microgram/mg), while the hydrolysis of ATP or ADP was insensitive to higher concentrations of these inhibitors but it was inhibited by vanadate. Oligomycin or venturicidine showed a different inhibition pattern in intact mitochondria in relation to the hydrolysis of ATP, ADP or GTP. When submitochondrial particles were isolated from mitochondria incubated with oligomycin or venturicidine, no further inhibition of the nucleotide hydrolysis was observed, contrasting with the partial inhibition observed in the control. By incubating the placental mitochondria with trypsin, a large fraction of the hydrolysis of nucleotides was eliminated. In submitochondrial particles obtained from mitochondria treated with trypsin or trypsin plus oligomycin, the hydrolysis of ATP was 100% sensitive to oligomycin at low concentrations, resembling the oxygen consumption; however, this preparation still showed some ADP hydrolysis. Native gel electrophoresis showed two bands hydrolyzing ADP, suggesting at least two enzymes involved in the hydrolysis of nucleotides, besides the F1F0-ATPase. It is concluded that human placental mitochondria possesses ADPase and ATP-diphosphohydrolase activities (247).

Adenosine Triphosphate↗