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PubMed1984

Thyroid hormone action on intermediary metabolism. Part I: respiration, thermogenesis and carbohydrate metabolism.

The effect of thyroid hormones on mitochondrial respiration are summarized: T3 directly stimulates mitochondrial respiration and the synthesis of adenosine 5'-triphosphate (ATP). Cytosolic ATP availability is increased by a thyroid hormone-induced increase in adenine nucleotide translocation across the mitochondrial membrane; the steady state ATP concentration and the cytosolic ATP/adenosine 5'-diphosphate (ADP) ratio is even decreased in hyperthyroid tissues because of the simultaneous stimulation of the synthesis and consumption of ATP. With regard to the thyroid hormone-induced energy wasting processes, heart work, intra- and interorgan futile cycling and Na+/K+-ATPase are involved to varying degrees. As a consequence of the thyroid hormone-induced hydrolysis of ATP, thermogenesis is increased in hyper- and decreased in hypothyroidism. Despite an increased rate of glucose utilization, clinical and experimental hyperthyroidism is often characterized by an abnormal oral glucose tolerance test. This finding is due to the thyroid hormone-induced increase in intestinal glucose absorption as well as the still enhanced endogenous glucose production in the liver. Hypothyroid patients show a reduced glucose tolerance test because of a decrease in intestinal glucose absorption and a sometimes reduced glucose turnover. The thyroid hormone-induced alterations in glucose metabolism are most probably not due to alterations in serum insulin levels and/or to a peripheral insulin resistance at the receptor level.

Adenosine Triphosphate↗
PubMed2005

5-HT uptake blockade prevents the increasing effect of K(ATP) channel blockers on electrically evoked [3H]-5-HT release in rat and mouse neocortical slices.

To explore if prolonged--as opposed to acute--5-HT uptake blockade can lead to changes in the function of ATP-dependent potassium (K(ATP)) channels, we investigated in rat and mouse neocortical slices the effects of K(ATP) channel blockers on electrically evoked [3H]-serotonin ([3H]-5-HT) release after short- and long-term exposure to 5-HT uptake blockers. Glibenclamide (1 microM), a K(ATP) channel blocker, enhanced the electrically evoked [3H]-5-HT release by 66 and by 77%, respectively, in rat and in mouse neocortex slices. This effect was confirmed in the rat by tolbutamide (1 microM), another K(ATP) channel antagonist. After short-term blockade (45 min) of 5-HT uptake, glibenclamide still increased the release of [3H]-5-HT in the rat. Glibenclamide, however, failed to enhance [3H]-5-HT release after long-term uptake blockade (210 min). In the mouse, however, both short- and long-term inhibition of 5-HT reuptake by citalopram (1 microM) prevented the facilitatory effect of glibenclamide. The Na(+)/K(+)-ATPase inhibitor ouabain (3.2 microM) abolished the glibenclamide-induced increase in [3H]-5-HT release in both rat and mouse, suggesting that an operative Na(+)/K(+)-ATPase is a prerequisite for activation of K(ATP) channels. The terminal 5-HT(1B) autoreceptor-mediated feedback control was involved in the glibenclamide-induced increase in [(3)H]-5-HT release only in mouse neocortical tissue, as evident from the use of the 5-HT(1B) autoreceptor ligands metitepin (1 microM) and cyanopindolol (1 microM). These results suggest that in the rat long-term uptake blockade leads to an impaired activity of the Na(+)/K(+)-ATPase, which increases intracellular ATP and consequently closes K(ATP) channels. In the mouse, however, short-term uptake blockade seems to already reduce the activity of the Na(+)/K(+)-ATPase and thereby the consumption of ATP. Blockade of 5-HT transporters thus may close K(ATP) channels through increased intracellular ATP. The following slight depolarisation seems to facilitate 5-HT release. These results may contribute to a better understanding of the mechanisms involved in the clinical time latency of antidepressant efficacy of monoamine uptake blockers.

Animals↗
PubMed2006

Mitochondrial DNA depletion and thymidine phosphate pool dynamics in a cellular model of mitochondrial neurogastrointestinal encephalomyopathy.

Mitochondrial (mt) neurogastrointestinal encephalomyopathy (MNGIE) is an autosomal recessive disease associated with depletion, deletions, and point mutations of mtDNA. Patients lack a functional thymidine phosphorylase and their plasma contains high concentrations of thymidine and deoxyuridine; elevation of the corresponding triphosphates probably impairs normal mtDNA replication and repair. To study metabolic events leading to MNGIE we used as model systems skin and lung fibroblasts cultured in the presence of thymidine and/or deoxyuridine at concentrations close to those in the plasma of the patients, a more than 100-fold excess relative to controls. The two deoxynucleosides increased the mt and cytosolic dTTP pools of skin fibroblasts almost 2-fold in cycling cells and 8-fold in quiescent cells. During up to a two-month incubation of quiescent fibroblasts with thymidine (but not with deoxyuridine), mtDNA decreased to approximately 50% without showing deletions or point mutations. When we removed thymidine, but maintained the quiescent state, mtDNA recovered rapidly. With thymidine in the medium, the dTTP pool of quiescent cells turned over rapidly at a rate depending on the concentration of thymidine, due to increased degradation and resynthesis of dTMP in a substrate (=futile) cycle between thymidine kinase and 5'-deoxyribonucleotidase. The cycle limited the expansion of the dTTP pool at the expense of ATP hydrolysis. We propose that the substrate cycle represents a regulatory mechanism to protect cells from harmful increases of dTTP. Thus MNGIE patients may increase their consumption of ATP to counteract an unlimited expansion of the dTTP pool caused by circulating thymidine.

Adenosine Triphosphate↗
PubMed1987

Threshold requirements for oxygen in the release of acetylcholine from, and in the maintenance of the energy state in, rat brain synaptosomes.

An oxystat was designed to enable maintenance of very low, predetermined oxygen tensions (below 1 microM) in incubated suspensions of synaptosomes. The oxygen thresholds for the energy state (ATP and creatine phosphate levels), for lactate production, and for acetylcholine release were compared. The approximate thresholds (microM O2) in veratridine-stimulated preparations were: oxygen consumption, 10; ATP, 10; creatine phosphate, 15; lactate release, 20; and acetylcholine release, 25. The results for release of total acetylcholine and of the acetylcholine newly synthesized from [14C]glucose were indistinguishable. The results from this study are discussed in relation to hypoxia and to reported in vivo observations.

Acetylcholine↗
PubMed2004

Transgenic expression of Bcl-2 modulates energy metabolism, prevents cytosolic acidification during ischemia, and reduces ischemia/reperfusion injury.

The antiapoptotic protein Bcl-2 is targeted to the mitochondria, but it is uncertain whether Bcl-2 affects only myocyte survival after ischemia, or whether it also affects metabolic functions of mitochondria during ischemia. Hearts from mice overexpressing human Bcl-2 and from their wild-type littermates (WT) were subjected to 24 minutes of global ischemia followed by reperfusion. During ischemia, the decrease in pH(i) and the initial rate of decline in ATP were significantly reduced in Bcl-2 hearts compared with WT hearts (P<0.05). The reduced acidification during ischemia was dependent on the activity of mitochondrial F1F0-ATPase. In the presence of oligomycin (Oligo), an F1F0-ATPase inhibitor, the decrease in pH(i) was attenuated in WT hearts, but in Bcl-2 hearts, Oligo had no additional effect on pH(i) during ischemia. Likewise, addition of Oligo to WT hearts slowed the rate of decline in ATP during ischemia to a level similar to that observed in Bcl-2 hearts, but addition of Oligo had no significant effect on the rate of decline in ATP in Bcl-2 hearts during ischemia. These data are consistent with Bcl-2-mediated inhibition of consumption of glycolytic ATP. Furthermore, mitochondria from Bcl-2 hearts have a reduced rate of consumption of ATP on uncoupler addition. This could be accomplished by limiting ATP entry into the mitochondria through the voltage-dependent anion channel, and/or the adenine nucleotide transporter, or by direct inhibition of the F1F0-ATPase. Immunoprecipitation showed greater interaction between Bcl-2 and voltage-dependent anion channel during ischemia. These data indicate that Bcl-2 modulation of metabolism contributes to cardioprotection.

Adenosine Triphosphate↗
PubMed2004

Mitochondrial biogenesis by NO yields functionally active mitochondria in mammals.

We recently found that long-term exposure to nitric oxide (NO) triggers mitochondrial biogenesis in mammalian cells and tissues by activation of guanylate cyclase and generation of cGMP. Here, we report that the NO/cGMP-dependent mitochondrial biogenesis is associated with enhanced coupled respiration and content of ATP in U937, L6, and PC12 cells. The observed increase in ATP content depended entirely on oxidative phosphorylation, because ATP formation by glycolysis was unchanged. Brain, kidney, liver, heart, and gastrocnemius muscle from endothelial NO synthase null mutant mice displayed markedly reduced mitochondrial content associated with significantly lower oxygen consumption and ATP content. In these tissues, ultrastructural analyses revealed significantly smaller mitochondria. Furthermore, a significant reduction in the number of mitochondria was observed in the subsarcolemmal region of the gastrocnemius muscle. We conclude that NO/cGMP stimulates mitochondrial biogenesis, both in vitro and in vivo, and that this stimulation is associated with increased mitochondrial function, resulting in enhanced formation of ATP.

Adenosine Triphosphate↗
PubMed2000

[The metabolic characteristics of the adaptation of athletes to cyclic types of sports to the point of physical loading].

The article considers problems of peculiarities of energetic adaptation of athletics of cyclic sports activity for significant sports loadings by POL indices, antioxidant system. ATP before and after veloergometric test by PWC 170. Adaptation of high class sportsmen for acute and chronic stress was taking place at the expense of more economic consumption of ATP at rest. Optimal indices of energy supply and metabolic adaptation were found at sportsmen with high level of physical state, while a slight disbalance was found at the sportsmen with average level of physical state.

Adaptation, Physiological↗
PubMed2005

Regulation of oxidative phosphorylation in intact mammalian heart in vivo.

A dynamic computer model of oxidative phosphorylation in intact heart was developed by modifying the model of oxidative phosphorylation in intact skeletal muscle published previously. Next, this model was used for theoretical studies on the regulation of oxidative phosphorylation in intact heart in vivo during transition between different work intensities. It is shown that neither a direct activation of ATP usage alone nor a direct activation of both ATP usage and substrate dehydrogenation, including the calcium-activated tricarboxylate acid cycle dehydrogenases, can account for the constancy of [ADP], [PCr], [P(i)] and [NADH] during a significant increase in oxygen consumption and ATP turnover encountered in intact heart in vivo. Only a direct activation of all oxidative phosphorylation complexes in parallel with a stimulation of ATP usage and substrate dehydrogenation enabled to reproduce the experimental data concerning the constancy of metabolite concentrations. The molecular background of the differences between heart and skeletal muscle in the kinetic behaviour of the oxidative phosphorylation system is also discussed.

Adenosine Triphosphate↗
PubMed2002

Molecular devices of chloroplast F(1)-ATP synthase for the regulation.

In chloroplasts, synthesis of ATP is energetically coupled with the utilization of a proton gradient formed by photosynthetic electron transport. The involved enzyme, the chloroplast ATP synthase, can potentially hydrolyze ATP when the magnitude of the transmembrane electrochemical potential difference of protons (Delta(micro)H(+)) is small, e.g. at low light intensity or in the dark. To prevent this wasteful consumption of ATP, the activity of chloroplast ATP synthase is regulated as the occasion may demand. As regulation systems Delta(micro)H(+) activation, thiol modulation, tight binding of ADP and the role of the intrinsic inhibitory subunit epsilon is well documented. In this article, we discuss recent progress in understanding of the regulation system of the chloroplast ATP synthase at the molecular level.

Adenosine Triphosphate↗
PubMed1989

ATP-dependent proteolysis of mitochondria of reticulocytes.

Since its discovery in 1956 the physiological function of the ATP-dependent proteolysis in reticulocytes has become an area of intensive interest. The evidence that mitochondria are the main substrate of the process during maturation of reticulocytes is summarized. The large consumption of ATP related to the degradation of mitochondria is discussed in context with possible mechanisms for ATP requirement. A novel ATP-dependent peptide release from reticulocyte mitochondria, which may be the first step in the degradation of the organelles, is demonstrated. Ubiquitin and tRNA are involved in the degradation process. Their roles, however, are not yet clear. The whole degradation cascade consisting of lipoxygenase, mitochondria susceptibility factor and ATP-dependent proteolysis, may function as a defense system against uncontrolled degradation of mitochondria in reticulocytes.

Amino Acids↗
PubMed1995

Metabolic responses of rabbit corpus cavernosum tissue to various forms of stimulation.

The present study was designed to investigate the effect of various forms of stimulation on the levels of high energy phosphates (ATP + CP) in the rabbit corpora cavernosa. Prestimulation with the alpha agonist phenylephrine (200 microM) for five minutes caused a significant decrease in both ATP and Creatine phosphate (CP) when compared with control tissue. Field stimulation (64 Hz) of the precontracted tissue induced an immediate decrease in tension by approximately 50%. The level of ATP + CP after field stimulated-relaxation was not significantly different from that from the initial prestimulation. Field stimulation (FS) from basal tone (2 g) caused a contraction and a significant decrease in both ATP and CP. Phentolamine (10 microM) (alpha-adrenergic antagonist) induced a significant decrease in the 2 g basal tension and a significant increase in the intracellular concentrations of both ATP and CP from that of control levels. In summary, the contractile response to both neuronal and pharmacologic stimulation was similar to that of other smooth muscle, producing a decrease in high energy phosphates. Field stimulated relaxation did not change the level of high energy phosphates from that of prestimulated levels. Finally, our data indicates that in the presence of the alpha blocker phentolamine (10 microM), high energy phosphate levels (ATP + CP) increase significantly. This indicates that in the corpus cavernosum, there is significant basal tone that is linked to significant tonic alpha receptor stimulation and is maintained by a net consumption of ATP.

Adenosine Triphosphate↗
PubMed2007

Influence of slaughtering method on some aspects of quality of gilthead seabream and smoked rainbow trout.

The effects of several slaughter methods on the quality of fresh and smoked trout and fresh gilthead seabream were evaluated during storage at 2 degrees C. Electrically stunned trout had slower ATP depletion of raw muscle and lower lipid oxidation in smoked product during storage. Gilthead seabream immersed in an ice slurry (IS group) after the harvest showed a more regular ATP depletion than in fish exposed to CO2. Nevertheless, in the case of the IS group, self-initiated behaviour, response to handling and breathing all ceased only after 15-20 min, whereas carbon dioxide-stunned fish appeared dead after 5 min. However, gilthead seabream group having slower ATP depletion also showed lower lipid oxidation of muscle during storage. In both species this could be due to the rapid conversion of xanthine dehydrogenase to xanthine oxidase induced by the rapid consumption of ATP. Xanthine oxidase, in the presence of redox iron and reintroduced oxygen, can produce hydrogen peroxide and, consequently, hydroxyl radicals.

Adenosine Triphosphate↗
PubMed1981

Effect of a 'sickling pulse' on calcium and potassium transport in sickle cell trait red cells.

1. To trace the early development of the extensive functional membrane abnormalities found in sickle cell anaemia red cells which result from polymerization of haemoglobin S, we followed the effects on Ca and K transport of an in vitro sickling pulse in sickle cell trait (SA) red cells, whose membranes are initially normal.2. Sickling induced a progressively larger uptake of Ca in fed, starved and ATP-depleted SA cells, always substantially higher than that in normal (AA) red cells under comparable conditions. The fraction of ionized Ca within the SA cells, estimated from the equilibrium distribution of (45)Ca induced by the ionophore A23187 was about 0.4 of the total Ca content and similar in SA and AA cells.3. With ATP-depleted SA cells, Ca uptake (representing Ca permeability) was maximal during sickling and was only partially reduced towards normal after desickling. Net Ca uptake during sickling of fed or starved SA cells reverted to net Ca loss upon reoxygenation, irrespective of the Ca gradient, indicating full restoration of the low Ca permeability of the control conditions.4. Following desickling of both fed and starved SA cells, the rates of uphill extrusion of Ca gained during sickling were much smaller than those expected with normal Ca pumps operating at similar internal Ca concentrations.5. After 2 hr sickling ATP levels in starved SA cells were reduced by 50% regardless of the presence or absence of Ca in the medium; therefore sickling-induced Ca uptake was associated with no measurable consumption of ATP due to Ca-pump activity.6. With ATP-depleted SA cells, a Ca uptake of 2-3 mumole/l. cells elicited a maximal response of the K permeability system resulting in full equilibration of the K pools in the cell suspensions. Sickling of fed and starved SA cells produced a small increase in K permeability which was entirely independent of the presence or absence of Ca.7. Sickled forms persisted after reoxygenation only with ATP-depleted SA cells and were more frequent after sickling in the presence of Ca (about 20%) than in a Ca-free medium (about 4%).8. These findings show that initial sickling produces an increased Ca permeability whose extent and reversibility depends on the metabolic state of the cells, and a partial Ca-pump failure, which appears to be irreversible. We confirm a small sickling-related, reversible increase in K permeability but a Ca-dependent increase in K permeability does not occur unless the cells are fully depleted of ATP. The implications for sequential development of related abnormalities in SS cells are discussed.

Adenosine Triphosphate↗
PubMed1994

Brain ATP depletion induced by acute ammonia intoxication in rats is mediated by activation of the NMDA receptor and Na+,K(+)-ATPase.

Injection of large doses of ammonia into rats leads to depletion of brain ATP. However, the molecular mechanism leading to ATP depletion is not clear. The aim of the present work was to assess whether ammonium-induced depletion of ATP is mediated by activation of the NMDA receptor. It is shown that injection of MK-801, an antagonist of the NMDA receptor, prevented ammonia-induced ATP depletion but did not prevent changes in glutamine, glutamate, glycogen, glucose, and ketone bodies. Ammonia injection increased Na+,K(+)-ATPase activity by 76%. This increase was also prevented by previous injection of MK-801. The molecular mechanism leading to activation of the ATPase was further studied. Na+,K(+)-ATPase activity in samples from ammonia-injected rats was normalized by "in vitro" incubation with phorbol 12-myristate 13-acetate, an activator of protein kinase C. The results obtained suggest that ammonia-induced ATP depletion is mediated by activation of the NMDA receptor, which results in decreased protein kinase C-mediated phosphorylation of Na+,K(+)-ATPase and, therefore, increased activity of the ATPase and increased consumption of ATP.

Acetates↗
PubMedDate not supplied

Adenosine triphosphate (ATP) in human spermatozoa.

The seminal adenosine triphosphate (ATP) content was determined by bioluminescence after treatment with trichloroacetic acid (TCA) in 81 semen samples 1.5 h after ejaculation obtained from men attending our fertility clinic, and selected to contain either 20% or less spermatozoa with good progressive motility (n = 22), or 60% or more spermatozoa with good progressive motility (n = 59) (Study I), and in 18 semen samples from fertile men 30 min and 3.5 h after ejaculation (Study II). The latter samples were divided into 2 equally large groups according to sperm motility. In Study I the mean sperm ATP concentration was significantly higher in the semen samples with bad motility (0.63 nmol per living spermatozoa x 10(-6)) than in semen samples with good motility (0.39 nmol per living spermatozoa x 10(-6); P less than 0.01). In Study II the ATP concentration per living spermatozoa was also lower in the group with the best motility in comparison with the spermatozoa with lower motility (P less than 0.01), both 30 min and 3.5 h after ejaculation. During the 3-5 h incubation the sperm ATP concentration decreased by 21% (P less than 0.01) in the former group of samples but remained unchanged in the latter group. The results indicate that, in semen samples with highly motile spermatozoa, the consumption of ATP is higher than in semen samples with impaired sperm motility. It is therefore essential that the time between ejaculation and ATP measurement is as short as possible to obtain comparable results. Repeated ATP measurements in combination with an analysis of the number of living spermatozoa, may provide further information on the fertilizing capacity of spermatozoa.

Adenosine Triphosphate↗
PubMedDate not supplied

[Quantitative model of human erythrocyte glycolysis. I. Relationship between the stationary rate of glycolysis and the ATP concentration].

A mathematical model is presented of the Embden--Meyerhof pathway in the human red blood cell. The rate of the system stationary flux is determined by the first part of the chain including three enzymatic reactions. The function has been calculated which describes the dependence of the stationary rate of glucose consumption and ATP production on the concentration of ATP. The curve has a bell shape with the physiological normal point situated in the descending segment. The descending segment is a result of the inhibition of the phosphofructokinase by ATP and the strong inhibition of the hexokinase by glucose-6-phosphate.

Adenosine Triphosphate↗
PubMed1992

Verapamil corrects abnormal metabolism of pancreatic islets and insulin secretion in phosphate depletion.

Phosphate depletion (PD) causes impaired insulin secretion and metabolic derangements in pancreatic islets. We studied PD, pair-weighed (PW), and PD and PW rats treated with verapamil (PD-V and PW-V) to examine the mechanisms of these derangements. Cytosolic calcium ([Ca2+]i) in PD islets was higher than that in PW, PD-V, and PW-V islets, and the values in the latter three groups were not different. Both basal and stimulated ATP in PD islets were lower than those in PW, PW-V, or PD-V islets. The maximum velocity (Vmax) of Ca(2+)-ATPase and the Km and Vmax of Na+,K(+)-ATPase were reduced in PD islets. In both PD-V and PW-V, the Vmax of Ca(2+)-ATPase was higher than that in PD, but lower than that in PW. Both initial and second phases of insulin secretion by PD islets were lower than those by PW and PW-V islets. In PD-V rats, insulin secretion was greater than that in PD rats, but only the second phase was significantly higher. The data are consistent with either of the following possibilities: 1) PD causes a change in the permeability of islets, allowing increased entry of Ca2+ into them and a fall in ATP of islets; the latter would impair the activity of both ATPases, leading to reduced Ca2+ extrusion from islets and, hence, an elevation in their [Ca2+]i; or 2) the primary defect in PD is a reduction in the activities of ATPases of islets due to the fall in ATP secondary to phosphorus deficiency. The decreased Ca2+ extrusion that ensues, even in the face of normal Ca2+ entry, will result in high [Ca2+]i. In either of these scenarios the rise in [Ca2+]i would inhibit mitochondrial oxygen consumption and ATP production, further lowering the ATP content of the islets. The higher [Ca2+]i and low ATP of PD underlie the impaired insulin secretion. Verapamil, by blocking normal or augmented Ca2+ entry into the islets, mitigates or prevents the derangements in islet function and metabolism.

Adenosine Triphosphate↗
PubMedDate not supplied

Importance of glycolysis for the energetics of anoxia-tolerant and anoxia-intolerant teleost hepatocytes.

The importance of glycolysis, as an ATP-producing and substrate-providing pathway, was studied in anoxia-tolerant (goldfish) and anoxia-intolerant (trout) hepatocytes. Inhibition of glycolysis with iodoacetic acid (IAA) left aerobic ATP production largely unaffected in hepatocytes from both species but caused a significant decrease of ATP contents in the goldfish cells. Ouabain-sensitive oxygen consumption (osVo2), an estimate of mitochondrial ATP production coupled to ATP consumption by the Na(+) pump, was significantly reduced in IAA-treated goldfish hepatocytes, whereas it was unaltered in trout hepatocytes. Partial reduction of mitochondrial respiration, achieved by titration with cyanide (CN), strongly stimulated glycolytic flux but did not affect ATP contents of hepatocytes from both species. Under these conditions, osVo2 became undetectable. Rb(+)-uptake rates, providing a direct estimate of Na(+)-pump activity, were in good agreement with estimates derived from osVo2 in IAA-treated cells, showing a decrease in goldfish and no change in trout. However, they indicated persistent Na(+)-pump activity despite the lack of osVo2 in CN-treated cells. Overall, these data indicate that in goldfish hepatocytes Na(+)-pump activity is more dependent on glycolytic ATP production as compared to trout hepatocytes. Protein synthesis of goldfish hepatocytes was inhibited in IAA- and CN-treated cells, possibly reflecting the hierarchical organization of energy metabolism. In trout hepatocytes, protein synthesis could be sustained at control levels, given that energetic substrate provision was not limited.

Acclimatization↗