Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ATP consumption”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed2000

A metabolic control analysis of kinetic controls in ATP free energy metabolism in contracting skeletal muscle.

A system analysis of ATP free energy metabolism in skeletal muscle was made using the principles of metabolic control theory. We developed a network model of ATP free energy metabolism in muscle consisting of actomyosin ATPase, sarcoplasmic reticulum (SR) Ca(2+)-ATPase, and mitochondria. These components were sufficient to capture the major aspects of the regulation of the cytosolic ATP-to-ADP concentration ratio (ATP/ADP) in muscle contraction and had inherent homeostatic properties regulating this free energy potential. As input for the analysis, we used ATP metabolic flux and the cytosolic ATP/ADP at steady state at six contraction frequencies between 0 and 2 Hz measured in human forearm flexor muscle by (31)P-NMR spectroscopy. We used the mathematical formalism of metabolic control theory to analyze the distribution of fractional kinetic control of ATPase flux and the ATP/ADP in the network at steady state among the components over this experimental range and an extrapolated range of stimulation frequencies (up to 10 Hz). The control analysis showed that the contractile actomyosin ATPase has dominant kinetic control of ATP flux in forearm flexor muscle over the 0- to 1.6-Hz range of contraction frequencies that resulted in steady states, as determined by (31)P-NMR. However, flux control begins to shift toward mitochondria at >1 Hz. This inversion of flux control from ATP demand to ATP supply control hierarchy progressed as the contraction frequency increased past 2 Hz and was nearly complete at 10 Hz. The functional significance of this result is that, at steady state, ATP free energy consumption cannot outstrip the ATP free energy supply. Therefore, this reduced, three-component muscle ATPase system is inherently homeostatic.

Adenosine Diphosphate↗
PubMed1995

Acidemia and brain pH during prolonged cardiopulmonary resuscitation in dogs.

BACKGROUND AND PURPOSE: Cardiopulmonary resuscitation (CPR) generating low perfusion pressures and beginning immediately after cardiac arrest maintains cerebral ATP but not cerebral pH or arterial pH. We tested the hypothesis that preventing severe arterial acidemia prevents cerebral acidosis, whereas augmenting arterial acidemia augments cerebral acidosis. METHODS: In dogs anesthetized with pentobarbital and fentanyl, cerebral pH and ATP were measured with 31P MR spectroscopy and blood flow was measured with radiolabeled microspheres. A pneumatically controlled vest was placed around the thorax, and chest compressions were begun immediately after electrically induced cardiac arrest. Cerebral perfusion pressure was maintained with epinephrine at 30 mm Hg for 90 minutes. The arterial acidemia observed during CPR was untreated in a control group, corrected to a pH of 7.3 with the use of sodium bicarbonate, or maintained below pH 6.5 with intravenous lactic acid after 14 minutes of CPR. RESULTS: At 10 minutes of CPR, cerebral ATP (99 +/- 1.5%, control), blood flow (35 +/- 3 mL/min per 100 g), O2 consumption (4.0 +/- 0.2 mL/min per 100 g), and cerebral pH (7.05 +/- .03) were unchanged from prearrest values (mean +/- SEM). After 10 minutes of CPR in the control group, cerebral pH progressively fell (6.43 +/- 0.10 at 90 minutes) in parallel with cerebral venous pH. In the bicarbonate group cerebral pH was maintained higher (6.91 +/- 0.08). Cerebral blood flow, O2 consumption, and ATP were sustained near prearrest values in both groups. In the lactate group, however, the rate of decrease of cerebral pH was augmented (6.47 +/- 0.06 by 30 minutes), and cerebral blood flow and metabolism were significantly reduced. CONCLUSIONS: Cerebral pH decreased in parallel with blood pH when resuscitation was started immediately upon arrest even when cerebral O2 consumption and blood flow were near normal. Although cerebral metabolism was near normal during the first hour of CPR, systemic bicarbonate administration ameliorated the cerebral acidosis. This finding indicates that the blood-brain pH gradient is important at the subnormal cerebral perfusion pressures seen in CPR.

Acidosis↗
PubMedDate not supplied

Enhanced cellular respiration in cells exposed to doxorubicin.

Doxorubicin executes topoisomerase II mediated apoptosis, a process known to result in mitochondrial dysfunction, such as the leakage of cytochrome c and the opening of mitochondrial permeability transition pores (PTP). To further define the effects of doxorubicin on cell metabolism, we measured cellular respiration, cellular ATP, DNA fragmentation, and cytochrome c leakage in Jurkat (supersensitive), human leukemia-60 (HL-60, sensitive), and HL-60/MX2 (resistant) cells following exposure to 1.0 microM doxorubicin for 30 min. The measurements were made after 24 h of exposure to the drug. In Jurkat and HL-60 cells, doxorubicin treatment increased cellular mitochondrial oxygen consumption and ATP content by 2-3-fold. The increment in oxygen consumption was blocked by the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone (zVAD-fmk) and by the PTP inhibitor cyclosporin A. In HL-60/MX2 cells, which are resistant because of a reduced topoisomerase II activity, doxorubicin treatment was without effect on either respiration or ATP content, suggesting that topoisomerase II was essential for induction of apoptosis and stimulation of respiration and ATP content. The conclusion that both of the latter processes were products of oxidations in the mitochondrial respiratory chain was supported by the further observation that rotenone and sodium cyanide inhibited oxygen consumption and substantially lowered ATP content in the treated and untreated cells. Thus, oxidative phosphorylation is enhanced in cells briefly incubated with doxorubicin for as long as 24 h post drug exposure despite apoptosis-associated mitochondrial insults caused by the drug.

Adenosine Triphosphate↗
PubMed1986

Magnetic resonance spectroscopy for the determination of renal metabolic rate in vivo.

The method of magnetic resonance spectroscopy has been validated and applied to the determination of renal metabolic rate in vivo. Using an indwelling detector coil, 31P NMR spectra from one kidney of anesthetized rats were quantified. The concentration of ATP was the same as that determined enzymatically, but both ADP and Pi were substantially lower. Only 25% of renal Pi and virtually none of the ADP were detected by NMR. The remainder is assumed to be bound to proteins. These concentrations of metabolites contributed to a significantly increased phosphorylation potential, which in turn should increase the free energy of hydrolysis of ATP. Saturation transfer, a non-destructive magnetic technique for the measurement of chemical exchange, was readily able to detect synthesis of ATP from ADP and inorganic phosphate. The rate of ATP synthesis determined was comparable to that determined in parallel studies of renal oxygen consumption. An ATP:O ratio of approximately 2 was found, indicating that fatty acid is the preferred fuel of respiration of the rat kidney in vivo.

Adenosine Diphosphate↗
PubMed1993

Effect of ethanol on energy status and intracellular calcium of Sertoli cells: a study using immobilized perfused cells.

The effects of ethanol on ATP, O2 consumption, and cytosolic ionized Ca2+ (Ca2+i) were studied in Sertoli cells isolated from the testes of 18- to 21-day-old rats. The cells were immobilized in agarose gel threads and perfused with Dulbecco's Modified Eagle's Medium. Intracellular ATP was determined by 31P nuclear magnetic resonance spectroscopy and enzymatic assay, Cai2+ was measured with the photoprotein aequorin, cell viability was assessed by trypan blue exclusion, and O2 consumption was monitored with a Clark electrode. Ethanol was used with or without pretreatment with the alcohol dehydrogenase inhibitor 4-methylpyrazole (MP). Perfusing the cells for 90 min with 500 mM ethanol produced a 50% reduction in the 31P nuclear magnetic resonance beta ATP signal, and pretreatment with 15 mM MP enhanced this decline of the beta ATP peak to 75%. Enzymatic measurements of ATP revealed that exposure to 500 mM ethanol reduced the ATP levels from 52 +/- 5 to 38 +/- 3 nmol/10(6) cells with MP pretreatment and to 28 +/- 4 nmol/10(6) cells without MP pretreatment (n = 5). Basal O2 consumption was 5.2 +/- 0.5 nmol/min.10(6) cells (n = 5), and it was reduced by ethanol or ethanol plus MP to 4 +/- 0.4 and 3.1 +/- 0.2, respectively (n = 5). The basal concentration of Cai2+ in Sertoli cells was 98 +/- 0.7 nM (n = 32). During perfusion with 500 mM ethanol, Cai2+ increased to 208 +/- 98 nM (n = 5) and was not modified further by the presence of MP. Perfusing the cells for 90 min with 500 mM ethanol with or without MP caused a decrease in cell viability from 93 +/- 2 to 76 +/- 3 and 67 +/- 3, respectively (n = 8). Exposure to 5 mM acetaldehyde produced only a minimal reduction in ATP, with no observable effect at lower concentrations, suggesting that the significant reductions in ATP, O2 consumption, and cell viability evoked by ethanol were not caused by acetaldehyde. These data suggest that ethanol is toxic to Sertoli cells, and its toxicity is not a result of ethanol metabolism.

Adenosine Triphosphate↗
PubMed1997

Types and sources of fuels for platelets in a medium containing minimal added fuels and a low carryover plasma.

The storage of platelets in synthetic media can result in plasma savings and reduced transfusion reactions. Accordingly, a wide range of storage formulations have been developed with the aim of replacing at least a proportion of the plasma in the storage medium. However, the concentrations and types of fuels in the carryover plasma, and the utilization of these fuels by platelets in storage, has not been investigated. We have developed a system which can measure total ATP turnover, and the contribution to total ATP turnover by the oxidation of various fuels and by lactate production, in a bag of partially purified platelets in a buffered saline with minimal carryover citrate phosphate double dextrose (CP2D) plasma. Carryover plasma was about 1% and the final platelet suspension contained, on average, 0.62 mM glucose, 9.6 mg/l free fatty acids, 32 mg/l triglycerides and 0.23 mM total amino acids. The oxidation of carbohydrate (glucose, glycogen and lactate) accounted for 60% of total ATP turnover. The platelets also produced lactate (<6% of total ATP turnover) and consumed free fatty acids and amino acids/proteins (15.2% of total ATP turnover). Therefore we have identified the fuels that account for about 80% of oxygen consumption and ATP turnover by platelets in a medium with low carryover plasma. The implications of these data for storage strategies are discussed.

Adenosine Triphosphate↗
PubMed1987

Higher ATP level and reduced glucose consumption of red cells stored in PVC bags compared to glass bottles.

Whole blood stored for 21 days at +4 degrees C in glass bottles showed a decrease in plasma glucose content of 6.6 mM/l, while blood stored in polyvinylchloride bags had a decrease of only 5.3 mM/l. At the same time, red cell ATP was reduced to 69% in bottles compared to 80% in bags (statistically proved differences). The higher red cell ATP level may explain the increased stability of red cells stored in DEHP-plasticized blood bags. The reduction in glucose consumption suggested that the decrease of red cell ATP and plasma glucose content may be a result of some unidentified inhibitory effects of DEHP on biochemical processes.

Adenosine Triphosphate↗
PubMedDate not supplied

[Glycolytic metabolites and adenosine triphosphoric acid in the herpes-infected eye].

In the tissues of the herpes-infected eye of a rabbit the content of adenosine triphosphoric acid (ATP), glucose and pyroracemic acid decreases and the level of lactic acid rises, i.e. anaerobic glycolysis prevails over the aerobic decomposition of glucose. A sharp decrease in the amount of ATP in the cornea and the iris in herpetic keratitis is due to the increased consumption of ATP for the synthesis of DNA and polypeptides of herpes simplex virus, as well as to disturbances in the oxidation transformations of glucose linked with the increased proportion of anaerobic glycolysis.

Adenosine Triphosphate↗
PubMed1989

Phenylarsine oxide inhibition of endocytosis: effects on asialofetuin internalization.

The aim of this work was to establish to what extent the concentrations over which phenylarsine oxide (PAO) inhibits oxygen consumption and decreases cellular ATP content overlap with those used to inhibit protein internalization. The effects of PAO (1-100 microM) on 125I-labeled asialofetuin internalization, oxygen consumption, ATP content, and lactate dehydrogenase (LDH) latency of isolated rat hepatocytes were determined. Ten micromoles/liter PAO blocked 125I-asialofetuin internalization but had no effect on ATP content up to 20 min, only a slight inhibition (18%) on oxygen consumption, and no effect on LDH latency. Higher concentrations of PAO had increasingly deleterious effects on the parameters. These results show that higher concentrations of PAO severely affect the energy stores as well as integrity of the hepatocyte. We concluded that 1) use of PAO requires careful evaluation of its effects in each experimental preparation and 2) it should be possible to establish time and concentration parameters for use of PAO as an inhibitor of endocytosis while minimizing the influence of its other cellular actions.

Adenosine Triphosphate↗
PubMed1982

Mitochondrial function in the presence of myoglobin.

The effect of myoglobin on oxygen consumption and ATP production by isolated rat skeletal muscle mitochondria was studied under steady-state conditions of oxygen supply. A method is presented for the determination of steady-state oxygen consumption in the presence of oxygen-binding proteins. Oxygen consumed in suspensions of mitochondria was replenished continuously by transfer from a flowing gas phase. Liquid-phase oxygen pressure was measured with an oxygen electrode; the gas-phase oxygen concentration was held constant at a series of fixed values. Oxygen consumption was determined from the characteristic response time of the system and the difference in the steady-state gas- and liquid-phase oxygen concentrations. ATP production was determined from the generation of glucose 6-phosphate in the presence of hexokinase. During steady-state mitochondrial oxygen consumption, the oxygen pressure in the liquid phase is enhanced when myoglobin is present. Functional myoglobin present in the solution had no effect on the relation of mitochondrial respiration and ATP production to liquid-phase oxygen pressure. Myoglobin functions in this system to enhance the flux of oxygen into the myoglobin-containing phase. Myoglobin may function in a similar fashion in muscle by increasing oxygen flux into myocytes.

Adenosine Triphosphate↗
PubMed2002

Ouabain suppresses glucose-induced mitochondrial ATP production and insulin release by generating reactive oxygen species in pancreatic islets.

We examined the effects of reduced Na(+)/K(+)-ATPase activity on mitochondrial ATP production and insulin release from rat islets. Ouabain, an inhibitor of Na(+)/K(+)-ATPase, augmented 16.7 mmol/l glucose-induced insulin release in the early period but suppressed it after a delay of 20-30 min. Unexpectedly, the ATP content in an islet decreases in the presence of 16.7 mmol/l glucose when Na(+)/K(+)-ATPase activity is diminished by ouabain, despite the reduced consumption of ATP by the enzyme. Ouabain also suppressed the increment of ATP content produced by glucose even in Ca(2+)-depleted or Na(+)-depleted conditions. That mitochondrial membrane hyperpolarization and O(2) consumption in islets exposed to 16.7 mmol/l glucose were suppressed by ouabain indicates that the glycoside inhibits mitochondrial respiration but does not produce uncoupling. Ouabain induced mitochondrial reactive oxygen species (ROS) production that was blocked by myxothiazol, an inhibitor of site III of the mitochondrial respiratory chain. An antioxidant, alpha-tocopherol, also blocked ouabain-induced ROS production as well as the suppressive effect of ouabain on ATP production and insulin release. However, ouabain did not directly affect the mitochondrial ATP production originating from succinate and ADP. These results indicate that ouabain suppresses mitochondrial ATP production by generating ROS via transduction, independently of the intracellular cationic alternation that may account in part for the suppressive effect on insulin secretion.

Adenosine Triphosphate↗
PubMed1990

Consequences of acute ischemia for the electrical and mechanical function of the ventricular myocardium. A brief review.

Reduction or interruption of the blood supply to the myocardium leads to marked disturbances of electrical and mechanical function within a few seconds. Electrical dysfunction is characterized by an initial depolarization of the resting membrane, and a decrease of the amplitude, the upstroke velocity and the duration of the action potential. Both depolarization and depression of the action potential are closely associated with intracellular metabolic acidosis. After this initial phase, electrical cell-to-cell uncoupling develops, probably as a consequence of increased cytosolic free [Ca++]. Mechanical dysfunction is characterized by a dissociation of the initial decrease of active force development from the subsequent ischemic contracture. Active force development in acute ischemia is inhibited by the accumulation of ischemic metabolic products (H+, inorganic phosphate (Pi), Mg++) but not by a marked decrease of [ATP]. The subsequent ischemic contracture is probably initiated by release of Ca++ from intracellular stores. This release causes rapid consumption of ATP and the development of rigor within 1-2 minutes.

Acute Disease↗
PubMed2003

Cryopreservation of rat precision-cut liver slices is associated with major metabolic stress and ionic perturbations.

BACKGROUND/AIMS: Cryopreserved precision-cut liver slices (PCLS) in culture exhibit a rapid decline in ATP level and anabolic processes by unknown mechanisms. The aim of this study is to elucidate the key events explaining the alterations occurring in cryopreserved PCLS. METHODS: Glucose metabolism, mitochondrial activities, ionic homeostasis and caspase-3 activity were assessed in fresh or cryopreserved (rapid freezing-thawing conditions) rat PCLS within the first hour of incubation in Williams' medium E at 37 degrees C. RESULTS: Despite a similar glycolytic activity under both conditions, only fresh PCLS were able to gradually recover their ATP and potassium content. Glycogen content dropped more rapidly in cryopreserved than in control PCLS. Only cryopreserved PCLS exhibited a decline in O2 consumption and a lower ATP/ADP ratio from 30 min of incubation with a loss of coupling of oxygen consumption to ATP synthesis and mitochondrial calcium transport after 1 hour of incubation. Caspase-3 activation was already present in cryopreserved PCLS after a few minutes of incubation. CONCLUSIONS: The lack of restoration of potassium/sodium exchange might be a primary event in the metabolic alterations occurring in cryopreserved PCLS after thawing, that contributes to further mitochondrial alterations, caspase activation and compromises ATP-dependent anabolic pathways.

Animals↗
PubMedDate not supplied

Platelet adenine nucleotide levels during room-temperature storage of platelet concentrates.

Platelet adenine nucleotide levels were measured in freshly prepared platelet concentrates and daily during storage at room temperature. Marked depletions in platelet adenosine triphosphate (ATP) and adenosine diphosphate (ADP) levels were associated with decrease in both plasma glucose levels and poststorage pH. In those concentrates with only moderate glucose consumption, platelet ATP and ADP levels were well preserved and the plasma pH remained above 6.0. The rate of glucose utilization and poststorage pH were greatly influenced by the concentration of contaminating leukocytes. These studies indicate that the rate of exogenous glucose consumption is an important factor affecting platelet adenine nucleotide levels during room temperature storage of platelet concentrates.

Adenosine Diphosphate↗
PubMed2003

Differential effects of K(ATP) channel blockers on [(3)H]-noradrenaline overflow after short- and long-term exposure to (+)-oxaprotiline or desipramine.

To test whether prolonged uptake blockade can lead to changes in the function of ATP-dependent potassium (K(ATP)) channels we investigated in rat neocortex slices the effects of K(ATP) channel blockers on electrically evoked [(3)H]-noradrenaline ([(3)H]-NA) overflow after short- (45 min) and long-term (210 min) exposure to the NA uptake blockers (+)-oxaprotiline or desipramine (1 microM each). The K(ATP) channel blocker glibenclamide (1 micro M) increased the evoked [(3)H]-NA overflow by 42% after short-term uptake inhibition. This effect was confirmed by tolbutamide and glipizide, two other K(ATP) channel antagonists. The evoked [(3)H]-NA overflow was enhanced by 73% following short-term uptake blockade (15 min) and by 110% following long-term blockade (180 min). After long-term blockade (210 min), however, glibenclamide failed to further enhance the overflow of [(3)H]-NA. The alpha(2)-autoreceptor-mediated feedback control was not involved in the glibenclamide-induced increase in [(3)H]-NA overflow after short-term uptake blockade or in the increase in [(3)H]-NA overflow due to long-term uptake blockade per se. The Na(+)/K(+)-ATPase inhibitor ouabain diminished the glibenclamide-induced enhancement of [(3)H]-NA overflow after short-term uptake blockade, suggesting that an operative Na(+)/K(+)-ATPase is the prerequisite of activation of K(ATP) channels. These results suggest that short-term uptake blockade activates the Na(+)/K(+)-ATPase, thereby reducing intracellular ATP which allows transient opening of K(ATP) channels. Activation of the Na(+)/K(+)-ATPase may increase the Na(+) gradient, probably over the membrane of noradrenergic nerve terminals. The resulting hyperpolarisation leads to inhibition of the evoked overflow which can be reversed, i.e. enhanced, by K(ATP) channel blockers. In contrast, longer lasting uptake blockade seems to reduce the activity of the Na(+)/K(+)-ATPase and hence the consumption of ATP. As a consequence, reduced Na(+) and K(+) gradients may facilitate transmitter release. Closure of K(ATP) channels by accumulating ATP may further promote membrane depolarisation and transmitter release. The unexpected effect of longer exposure to uptake blockers could be somehow related to the clinical time latency of the antidepressant efficacy of monoamine uptake blockers.

Adenosine Triphosphate↗
PubMedDate not supplied

[ATPase activity and processes of calcium transport in membranes of sarcoplasmic reticulum of skeletal muscles with E-avitaminotic dystrophy].

Peculiarities of functioning of the sarcoplasmic reticulum muscles membranes with E-avitaminotic distrophy were studied. It was determined that the level of ATP-dependent consumption of Ca2+, value of the Mg2+, Ca2+-ATPase activity and an amount of the intermediate phosphorylated product forming in the reaction of ATP hydrolysis decrease. The rate of this product formation in the sarcoplasmic reticulum of the distrophic muscles is inhibited as compared to normalcy. Elimination of Ca2+ into calcium-free medium from the vesicular membranes of the reticulum preliminarily loaded with Ca2+ occurs more rapidly under dystrophy than in normalcy. The data obtained evidence for a disturbance of mechanism of Ca2+ active transport and for an increase in the membrane permeability for Ca2+ in the membranes of the dystrophic muscles sarcoplasmic reticulum. A problem is considered on a dependence of the skeletal muscles observed in the reticulum under dystrophy of the functional changes on the membrane structure, in particular on their lipid composition.

Adenosine Triphosphatases↗
PubMed2003

Regulation of oxidative phosphorylation in different muscles and various experimental conditions.

It has been shown previously that direct stimulation of oxidative-phosphorylation complexes in parallel with the stimulation of ATP usage is able to explain the stability of intermediate metabolite (ATP/ADP, phosphocreatine/creatine, NADH/NAD+, protonmotive force) concentrations accompanied by a large increase in oxygen consumption and ATP turnover during transition from rest to intensive exercise in skeletal muscle. It has been also postulated that intensification of parallel activation in the ATP supply-demand system is one of the mechanisms of training-induced adaptation of oxidative phosphorylation in skeletal muscle. In the present paper, it is demonstrated, using the computer model of oxidative phosphorylation in intact skeletal muscle developed previously, that the direct activation of oxidative phosphorylation during muscle contraction can account for the following kinetic properties of oxidative phosphorylation in skeletal muscle encountered in different experimental studies: (i) increase in the respiration rate per mg of mitochondrial protein at a given ADP concentration as a result of muscle training and decrease in this parameter in hypothyroidism; (ii) asymmetry (different half-transition time, t(1/2)) in phosphocreatine concentration time course between on-transient (rest-->work transition) and off-transient (recovery after exercise); (iii) overshoot in phosphocreatine concentration during recovery after exercise; (iv) variability in the kinetic properties of oxidative phosphorylation in different kinds of muscle under different experimental conditions. No other postulated mechanism is able to explain all these phenomena at the same time and therefore the present paper strongly supports the idea of the parallel activation of ATP usage and different oxidative-phosphorylation complexes during muscle contraction.

Adenosine Diphosphate↗
PubMed2004

Mitochondrial dysfunction measured in vivo.

AIMS: Mitochondria are responsible for meeting the majority of the energetic demand of most tissues. They also play a major role in regulating cell survival. These dual roles of mitochondria place them at the centre of many pathologies leading to tissue degeneration and disruption of energy balance. The prominent role of mitochondria in ageing and disease has led to a tremendous growth in mitochondrial research at the cellular and molecular level. We describe below a new non-invasive approach to measure mitochondrial function that will bridge the gap between our understanding of mitochondrial function in vitro and that in the intact organism. METHODS AND RESULTS: This approach uses optical and magnetic resonance spectroscopy to measure in vivo O2 consumption and ATP synthesis rates, respectively, from skeletal muscle. These values lead to a quantitative assessment of the mitochondrial ATP/O2 or P/O. The P/O represents the efficiency of coupling between phosphorylation and oxygen consumption in the mitochondria, which is a measure of mitochondrial dysfunction. CONCLUSIONS: This work represents a significant advance in research on the role of mitochondria in degenerative disease and ageing because it allows a quantitative measure of mitochondrial pathology in vivo. The non-invasive nature of this approach also enables repeated measures of mitochondrial function on the same individual, thereby making this a potentially useful diagnostic technique. The results from this work have led to insights into the coupling of ATP synthesis to oxidation and the regulation of oxidative phosphorylation by intracellular PO2.

Adenosine Triphosphate↗