Randomness of platelet adhesiveness with respect to their ATP, O2 consumption, and size.
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Adenosine Triphosphate↗
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[Nitrogenase, hydrogenase and nitrate reductase activities, oxygen consumption, and ATP content in nodules formed by strains of Rhizobium leguminosarum 128C53 and 300 in symbiosis with pea plants].
The nitrogenase activity, nitrate reductase activity and oxygen uptake as well as the hydrogen incorporation and ATP content were examined in the root nodules and bacteroids, respectively, formed by Rhizobium leguminosarum strains 128C53 (hydrogenase positive) and 300 (hydrogenase negative) in symbiosis with Pisum sativum plants grown in the presence of 2 mM KNO3. The strain 128C53 showed the greatest values for all parameters analyzed, except for the nitrate reductase activity, which was higher for the strain 300. Similarly, nodule nitrate reductase activity in strain 300 was greater than that in strain 128C53 when plants grew in the absence of combined nitrogen. In general, the highest values were obtained when determinations were made after 7 hours of plant illumination. However, the hydrogenase activity of strain 128C53 and the nitrate reductase activities of both strains increased with the light period, reaching a maximum after 14 hours of illumination. These results suggest that the benefits derived from the superior symbiotic properties and from the presence of hydrogenase activity in strain 128C53 could be counteracted by the higher rates of the nodule nitrate reductase activity in strain 300.
Adenosine Triphosphate↗
[Morphologic characteristics and ATPase activity in permeabilized epididymal bull sperm].
The treatment of bull spermatozoa from epididymal cauda with 5 micrograms digitonin per microliters cells led to the destruction of the plasma membrane which was shown by electron microscopy. Structural changes of mitochondria and of the axoneme were not found. The functional intactness was maintained. The plasma membranes of hypotonically treated spermatozoa were permeable for succinate and the mitochondria showed a diminished functional intactness. For the total ATPase activity of digitonin-treated cells, mainly representing the dynein ATPase, a maximal activity of 20.3 nmol ATP x min-1 x microliters cells-1 (mean +/- S.D.; n = 8) and an apparent half saturation constant of 0.29 mM ATP were determined. The portions of Na(+)-K(+)-ATPase and mitochondrial ATPase in the total ATP-splitting activity were found to be less than 15%. In comparison to the capacity of mitochondrial ATP production, the maximal activity of ATP consuming reactions amounted to about 70%. These results support findings that the ATP turnover of spermatozoa is more limited by the ATP consumption than by the ATP production.
Adenosine Triphosphatases↗
Is it possible to predict any properties of oxidative phosphorylation in a theoretical way?
Two theoretical approaches applied to oxidative phosphorylation, namely Metabolic Control Analysis (MCA) [ 1-7] and Non-Equilibrium Thermodynamics (NET) [8-11], turned out to be very useful tools for quantitative description and understanding of control and regulation of this process. However, they were not able to predict any new properties of the considered system. On the other hand, the previously developed dynamic model of oxidative phosphorylation [12-17], representing a kinetic approach, allowed to formulate several interesting predictions which can be tested experimentally. The most important of these predictions are: (1) Different steps of ATP-production must be directly activated to a similar extent as ATP-consumption during stimulation of ATP turnover by calcium-acting hormones as well as by neural signals during muscle contraction; (2) A universal activator/regulatory mechanism responsible for such a precise balance of activation should be identified; (3) The flux-force relationship for cytochrome oxidase can be inverse during the transition towards hypoxia and anoxia, when oxygen concentration falls below 30 microM; (4) The flux-force relationship can depend on the way in which the thermodynamic force is changed; (5) The pattern of metabolic control is completely different in normoxic and hypoxic conditions; in the latter case cytochrome oxidase has the flux control coefficient close to unity. Thus, the kinetic model of oxidative phosphorylation seems to be a useful scientific tool, offering some novel theoretical predictions, which then can be tested in the experimental way.
Adenosine Triphosphate↗
Life at acidic pH imposes an increased energetic cost for a eukaryotic acidophile.
Organisms growing in acidic environments, pH<3, would be expected to possess fundamentally different molecular structures and physiological controls in comparison with similar species restricted to neutral pH. We begin to investigate this premise by determining the magnitude of the transmembrane electrochemical H+ gradient in an acidophilic Chlamydomonas sp. (ATCC PRA-125) isolated from the Rio Tinto, a heavy metal laden, acidic river (pH 1.7-2.5). This acidophile grows most rapidly at pH 2 but is capable of growth over a wide pH range (1.5-7.0), while Chlamydomonas reinhardtii is restricted to growth at pH>or=3 with optimal growth between pH 5.5 and 8.5. With the fluorescent H+ indicator, 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF), we show that the acidophilic Chlamydomonas maintains an average cytosolic pH of 6.6 in culture medium at both pH 2 and pH 7 while Chlamydomonas reinhardtii maintains an average cytosolic pH of 7.1 in pH 7 culture medium. The transmembrane electric potential difference of Chlamydomonas sp., measured using intracellular electrodes at both pH 2 and 7, is close to 0 mV, a rare value for plants, animals and protists. The 40,000-fold difference in [H+] could be the result of either active or passive mechanisms. Evidence for active maintenance was detected by monitoring the rate of ATP consumption. At the peak, cells consume about 7% more ATP per second in medium at pH 2 than at pH 7. This increased rate of consumption is sufficient to account for removal of H+ entering the cytosol across a membrane with relatively high permeability to H+ (7x10(-8) cm s-1). Our results indicate that the small increase in the rate of ATP consumption can account for maintenance of the transmembrane H+ gradient without the imposition of cell surface H+ barriers.
Acid-Base Equilibrium↗
AMP deamination delays muscle acidification during heavy exercise and hypoxia.
In silico studies carried out by using a computer model of oxidative phosphorylation and anaerobic glycolysis in skeletal muscle demonstrated that deamination of AMP to IMP during heavy short term exercise and/or hypoxia lessens the acidification of myocytes. The concerted action of adenylate kinase and AMP deaminase, leading to a decrease in the total adenine nucleotide pool, constitutes an additional process consuming ADP and producing ATP. It diminishes the amount of ADP that must be converted to ATP by other processes in order to meet the rate of ADP production by ATPases (because the adenylate kinase + AMP deaminase system produces only 1 ATP per 2 ADPs used, ATP consumption is not matched by ATP production, and the reduction of the total adenine nucleotide pool occurs mostly at the cost of [ATP]). As a result, the rate of ADP consumption by other processes may be lowered. This effect concerns mostly ADP consumption by anaerobic glycolysis that is inhibited by AMP deamination-induced decrease in [ADP] and [AMP], and not oxidative phosphorylation, because during heavy exercise and/or hypoxia [ADP] is significantly greater than the Km value of this process for ADP. The resultant reduction of proton production by anaerobic glycolysis enables us to delay the termination of exercise because of fatigue and/or to diminish cell damage.
AMP Deaminase↗
Effects of endurance physical training on hydroxyl radical generation in rat tissues.
Physical exercise is known to increase oxygen consumption to compensate for enhanced ATP consumption and thus to induce oxidative stress in tissues. Our previous data indicate that training significantly increased the hydroxyl radical level in rat tissues after physical exercise, but reduced the basal level in aged rats. This result suggests the paradoxical effect of physical training, which may be to increase or scavenge reactive oxygen species (ROS) generated by physical exercise. In this paper, the effects of training on the levels of hydroxyl radicals and the anti-oxidative glutathione system, were examined in rats. After 3 weeks' training, rats were sacrificed at rest or after treadmill running, and the levels of hydroxyl radicals trapped with salicylic acid, reduced (GSH); and oxidized glutathione (GSSG) in tissues were quantified by high-performance liquid chromatography-electrochemical detection (HPLC-ECD). Endurance training reduced the basal level of hydroxyl radicals significantly in plasma and soleus muscle. In liver and brain a similar tendency was observed, but the difference was not statistically significant. In liver the basal level of GSH increased significantly after training. Slower training with longer duration reduced the basal levels of hydroxyl radical in plasma more markedly than more intense training. These results suggest that endurance exercise can increase the anti-oxidative capacity in rats.
Animals↗
Increase in external glutamate and NMDA receptor activation contribute to H2O2-induced neuronal apoptosis.
The present study aims to investigate the role of extracellular glutamate and NMDA receptor stimulation in the neuronal death induced by a transient exposure to H2O2 of cultured neurons originating from mouse cerebral cortex. Most of the neuronal loss following a transient exposure to H2O2 of cortical neurons results from an apoptotic process involving a secondary stimulation of NMDA receptors, which occurs after H2O2 washout. Indeed, (a) the neurotoxic effect of H2O2 was strongly reduced by antagonists of NMDA receptors, (b) the neurotoxic effect of H2O2 was enhanced in the absence of Mg2+, (c) the protective effect of MK-801 progressively decayed when it was applied with increasing delay time after H2O2 exposure, and (d), finally, the extracellular concentration of glutamate was increased after H2O2 exposure. The major part of H2O2-induced neurotoxicity is mediated by the formation of hydroxyl radicals, which might be involved in (a) the delayed accumulation of extracellular glutamate and NMDA receptor activation and (b) the poly(ADP-ribose) polymerase activation and the related NAD content decrease. The combination of these two mechanisms could lead to both an increase in ATP consumption and a decrease of ATP synthesis. The resulting large decrease in ATP content might be finally responsible for the neuronal death.
Adenosine Triphosphate↗
ATP concentration gradients in cytosol of liver cells during hypoxia.
The activities of two ATP-requiring systems with different subcellular localizations were studied in cells in which average cellular ATP concentration was varied. The cytosolic ATP-sulfurylase activity varied linearly with the cellular ATP concentration; however, the plasma membrane Na+-K+-ATPase was substantially more sensitive to decreased ATP concentration. Under conditions where the cellular ATP concentration was lowered to 40% of control, Rb+ uptake was nearly zero. The results indicate that ATP-utilizing enzymes located in the plasma membrane in liver cells are exposed to a lower ATP concentration than are enzymes present in the cytosolic fluid surrounding the mitochondria. Analysis of radial diffusion of ATP from mitochondria, assuming that mitochondria are spherical and ATP consumption is zero order in ATP concentration, shows that the average ATP supply radius decreases as mitochondrial ATP production decreases. Hence, during limited ATP supply, enzymes with a greater average distance from mitochondria (e.g., plasma membrane ATPases) experience a more dramatic decrease in ATP concentration than enzymes in close proximity to mitochondria (e.g., cytoplasmic enzymes). Thus microheterogeneity of ATP supply can occur in cells without membranal compartmentation due to nonuniform distribution of ATP-generating and ATP-consuming systems.
Adenosine Triphosphate↗
Sperm-triggered [Ca2+] oscillations and Ca2+ homeostasis in the mouse egg have an absolute requirement for mitochondrial ATP production.
At fertilisation, repetitive increases in the intracellular Ca2+ concentration, [Ca2+]i, drive the completion of meiosis and initiate the development of the quiescent egg into an embryo. Although the requirement for an ATP supply is evident, the relative roles of potential ATP sources remains unclear in the mammalian egg, and the specific role of mitochondria in [Ca2+]i regulation as well as in the sperm-triggered [Ca2+] oscillations is unknown. We have used fluorescence and luminescence imaging to investigate mitochondrial activity in single mouse eggs. Simultaneous imaging of mitochondrial redox state (NADH and flavoprotein autofluorescence) and [Ca2+]i revealed that sperm-triggered [Ca2+] oscillations are transmitted to the mitochondria where they directly stimulate mitochondrial activity. Inhibition of mitochondrial oxidative phosphorylation caused release of Ca2+ from the endoplasmic reticulum because of local ATP depletion. Mitochondrial ATP production is an absolute requirement for maintaining a low resting [Ca2+]i and for sustaining sperm-triggered [Ca2+] oscillations. Luminescence measurements of intracellular [ATP] from single eggs confirmed that mitochondrial oxidative phosphorylation is the major source of ATP synthesis in the dormant unfertilised egg. These observations show that a high local ATP consumption is balanced by mitochondrial ATP production, and that balance is critically poised. Mitochondrial ATP supply and demand are thus closely coupled in mouse eggs. As mitochondrial ATP generation is essential to sustain the [Ca2+] signals that are crucial to initiate development, mitochondrial integrity is clearly fundamental in sustaining fertility in mammalian eggs.
Adenosine Triphosphate↗
Actin-ATP hydrolysis is a major energy drain for neurons.
In cultured chick ciliary neurons, when ATP synthesis is inhibited, ATP depletion is reduced approximately 50% by slowing actin filament turnover with jasplakinolide or latrunculin A. Jasplakinolide inhibits actin disassembly, and latrunculin A prevents actin assembly by sequestering actin monomers. Cytochalasin D, which allows assembly-disassembly, but only at pointed ends, is less effective in conserving ATP. Ouabain, an Na(+)-K(+)-ATPase inhibitor, and jasplakinolide both prevent approximately 50% of the ATP loss. When applied together, they completely prevent ATP loss over a period of 20 min, suggesting that filament stabilization reduces ATP consumption by decreasing actin-ATP hydrolysis directly rather than indirectly by modulating the activity of Na(+)-K(+)-ATPase, a major energy consumer.
Actin Cytoskeleton↗
Uptake of calcium by pancreatic islet cell microsomes: inhibition by a monoclonal antibody to heart sarcoplasmic reticulum.
The uptake of Ca2+ by microsomes is thought to participate in the control of cytosolic Ca2+ activity in the insulin-producing pancreatic B-cell. In order to study such a phenomenon methods were developed to isolate microsomes from rat parotid cells, pancreatic islets and tumoral islet cells of the RINm5F line. In the latter case, a subcellular microsomal fraction was prepared in which the ratio of microsomal/mitochondrial enzyme markers, as well as that of ruthenium red-resistant/sensitive 45Ca2+ uptake was 20 times higher than in the corresponding mitochondrial subcellular fraction. The ATP-dependent net uptake of 45Ca2+ by RINm5F cell microsomes was inhibited at low temperature and by either vanadate or a monoclonal antibody to dog heart sarcoplasmic reticulum. Although the uptake of Ca2+ by microsomes may account for only a minor fraction of ATP consumption, its synarchistic regulation by ATP and Ca2+, at close-to-physiological concentrations, appeared well suited to play a major regulatory role in the control of cytosolic Ca2+ activity in intact islet cells.
Animals↗
Adenosine triphosphate consumption by bacterial arginyl-transfer ribonucleic acid synthetases.
ATP consumption by arginyl-tRNA synthetases from Escherichia coli and Bacillus stearothermophilus has been investigated by the firefly luciferin--luciferase assay. Arginyl-tRNA synthetase from E. coli utilizes ATP only for aminocylation of tRNA with a 1:1 stoicheiometry. In contrast, we have shown an adenosine triphosphatase activity of arginyl-tRNA synthetase from B. stearothermophilus in the absence of tRNAArg. Dowex chromatography revealed the formation of ADP by the thermophile enzyme; under aminoacylation conditions, AMP was also formed in amounts stoicheiometric with arginyl-tRNA formation.
Adenosine Triphosphate↗
Protective effects of riluzole on dopamine neurons: involvement of oxidative stress and cellular energy metabolism.
Riluzole is neuroprotective in patients with amyotrophic lateral sclerosis and may also protect dopamine (DA) neurons in Parkinson's disease. We examined the neuroprotective potential of riluzole on DA neurons using primary rat mesencephalic cultures and human dopaminergic neuroblastoma SH-SY5Y cells. Riluzole (up to 10 microM:) alone affected neither the survival of DA neurons in primary cultures nor the growth of SH-SY5Y cells after up to 72 h. Riluzole (1-10 microM:) dose-dependently reduced DA cell loss caused by exposure to MPP(+) in both types of cultures. These protective effects were accompanied by a dose-dependent decrease of intracellular ATP depletion caused by MPP(+) (30-300 microM:) in SH-SY5Y cells without affecting intracellular net NADH content, suggesting a reduction of cellular ATP consumption rather than normalization of mitochondrial ATP production. Riluzole (1-10 microM:) also attenuated oxidative injury in both cell types induced by exposure to L-DOPA and 6-hydroxydopamine, respectively. Consistent with its antioxidative effects, riluzole reduced lipid peroxidation induced by Fe(3+) and L-DOPA in primary mesencephalic cultures. Riluzole (10 microM) did not alter high-affinity uptake of either DA or MPP(+). However, in the same cell systems, riluzole induced neuronal and glial cell death with concentrations higher than those needed for maximal protective effects (> or =100 microM:). These data demonstrate that riluzole has protective effects on DA neurons in vitro against neuronal injuries induced by (a) impairment of cellular energy metabolism and/or (b) oxidative stress. These results provide further impetus to explore the neuroprotective potential of riluzole in Parkinson's disease.
1-Methyl-4-phenylpyridinium↗
Heat shock protein 70 and ATP as partners in cell homeostasis (Review).
Heat shock proteins (HSP) are molecular chaperones, involved in many cellular functions such as protein folding, transport, maturation and degradation. Since they control the quality of newly synthesized proteins, HSP take part in cellular homeostasis. The Hsp70 family in particular exerts these functions in an adenosine triphosphate (ATP)-dependent manner. ATP is the main energy source used by cells to assume fundamental functions (respiration, proliferation, differentiation, apoptosis). Therefore, ATP levels have to be adapted to the requirements of the cells and ATP generation must constantly compensate ATP consumption. Nevertheless, under particular stress conditions, ATP levels decrease, threatening cell homeostasis and integrity. Cells have developed adaptive and protective mechanisms, among which Hsp70 synthesis and overexpression. In this review, we focus on the mechanisms which regulate Hsp70 expression under ATP depletion, using ischaemia as a paradigmatic model for ATP depletion in vivo, and analyze the molecular targets for Hsp70-mediated protection against ATP depletion. We also consider how these Hsp70-mediated protective effects could be applied in the therapeutical approaches of human diseases associated with cellular ATP depletion.
Adenosine Triphosphate↗
GRP78 induction by calcium ionophore potentiates photodynamic therapy using the mitochondrial targeting dye victoria blue BO.
The cationic photosensitizing triaryl methane dye Victoria Blue BO (VBBO) localizes in mitochondria and causes oxidative damage to this organelle during photodynamic therapy (PDT). Oxidative stresses from other photosensitizers induce a variety of stress proteins. The endoplasmic reticulum (ER)-based, calcium-binding stress protein GRP78 is a putative protective factor for photosensitizers such as Photofrin that damage multiple intracellular sites and for several cytotoxic agents. In the current study VBBO-PDT was found to induce glucose-regulated protein (GRP)78. However, in contrast to other drugs, rather than being protected, human squamous carcinoma cells (FaDu) induced to express GRP78 by calcium ionophore A23187 became more sensitive to PDT. A line of Chinese hamster ovary cells (C-1) constitutively overexpressing GRP78 also were more sensitive. Cytotoxicity of the A23187 treatment and VBBO was synergistic, with more than 11-fold potentiation with light irradiation, but was only additive in the dark. The increased cell killing was not due to differences in VBBO uptake or to changes in the intracellular localization of VBBO caused by calcium ionophore or GRP78. Thus, GRP78 appears to enhance rather than protect against VBBO-induced mitochondrial photodamage and contributes to cell death. This novel finding possibly may stem from the effects of GRP78, ER Ca2+ stores and ATP consumption on the Ca2+ and ATP-dependent mitochondrial permeability transition that may be evoked by PDT damage to the mitochondrial respiratory chain. The work suggests interventions that may potentiate PDT with mitochondrial targeting sensitizers and potential enhancements in efficacy when GRP78 is upregulated biologically or pharmacologically.
Animals↗
Control of oxidative phosphorylation, gluconeogenesis, ureagenesis and ATP turnover in isolated perfused rat liver analyzed by top-down metabolic control analysis.
We have analyzed the control exerted by the pathways of oxidative phosphorylation, gluconeogenesis, ureagenesis, and maintenance ATP consumption over each other's rates in isolated, perfused rat liver using top-down metabolic control analysis. The livers from fasted rats were perfused with 3-hydroxybutyrate as respiratory substrate, lactate as substrate for gluconeogenesis, and ammonium as substrate for urea synthesis, in conditions where these pathways were only linked by their common intermediates: ATP, ADP, and Pi. The rates of oxygen consumption, glucose and urea synthesis were measured continuously. The pathways were perturbed either by adding specific inhibitors or by adding new pathways that consumed ATP, and the relative changes in pathway rates were used to calculate the flux control coefficients of each pathway over all pathway rates. When the liver was in a relatively inactive metabolic state, where ATP was only being used by the maintenance ATP-consuming pathways, then essentially all the control over ATP production and consumption was located in the maintenance ATP consumers with ATP production having no control. Whereas, when the liver was in a highly active state using extra ATP for both glucose and urea synthesis, then ATP production (from oxidative phosphorylation) had strong control over its own rate and the rates of glucose and urea synthesis, but gluconeogenesis and ureagenesis still had strong control over their own rates and negative control over each others rates, i.e. they competed for the limited ATP supply. The rate of the maintenance ATP consumers is remarkably insensitive to changes in ATP production and consumption, but exerts considerable control over all other pathways. These results indicate that the general assumption that the rates of ATP production and consumption are controlled exclusively by ATP consumers is false under conditions where a significant amount of ATP is used for biosynthetic processes, such as glucose and urea synthesis, and indicate that the latter processes may be partly controlled by regulators of ATP production and by other ATP-consuming pathways.
3-Hydroxybutyric Acid↗
Sensitive kinetic bioluminescent assay of glycerol release from human fat cells.
A sensitive and accurate assay of lipolysis has been developed, measuring the rate of glycerol release from fat cells with a bioluminescent assay. The rate of glycerol-dependent ATP-consumption in a system consisting of glycerokinase, ATP, luciferin, and luciferase was determined kinetically as a decrease of the ATP-induced luminescence and used for calculation of the concentration of glycerol. Under the conditions employed, it was possible to measure the concentration of glycerol down to a level of about 0.5 micron mol/l. Under the same conditions, the detection limit of the usual fluorometric method was about 15 micron mol/l. The coefficient of variation obtained with the bioluminescent assay was 11% at a level of 1.0 micron mol of glycerol, 2-6% at a level of about 5 micron mol/l, and 1-3% at a level of about 20 micron mol/l. Satisfactory results were obtained in different recovery experiments. Using human fat cells, it was possible to determine the rate of glycerol release with a cell concentration in the medium of only 5,000-10,000 cells/ml. It is concluded that the bioluminescent assay of glycerol release should be preferred when there is a demand for sensitivity, e.g., when the rate of lipolysis is low and when only a small amount of biopsy material is available.
Adipose Tissue↗