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PubMed1984

Quantification of energy consumption in platelets during thrombin-induced aggregation and secretion. Tight coupling between platelet responses and the increment in energy consumption.

The involvement of metabolic energy in platelet responses was investigated by measuring the energy consumption during aggregation and secretion from dense, alpha- and acid-hydrolase-containing granules. Gel-filtered human platelets were stimulated with different amounts of thrombin (0.05-5.0 units X ml-1). At various stages during aggregation and secretion the energy consumption was measured from the changes in metabolic ATP and ADP following abrupt arrest of ATP resynthesis. Stimulation with 5 units of thrombin X ml-1 increased the energy consumption from 6.2 +/- 0.9 to 17.8 +/- 0.4 mumol of ATPeq. X min-1 X (10(11) platelets)-1 during the first 15 s. It decreased thereafter and returned to values found in resting cells after about 30 s. With 0.05 unit of thrombin X ml-1, the energy consumption accelerated more slowly and took at least 3 min before it normalized. A strong positive correlation was found between the velocities of the three secretion responses and the concurrent energy consumption (a) at different stages of the responses induced by a given dose of thrombin, and (b) at different secretion velocities initiated by different amounts of thrombin. When, at different stages of the responses, the extent of secretion was compared with the amount of energy that had been consumed, a strong linear correlation was found with the increment in energy consumption but not with the total energy consumption. This correlation was independent of the concentration of thrombin and indicated that complete secretion from dense, alpha- and acid-hydrolase-containing granules was paralleled by an increment of 4.0, 6.5 and 6.7 mumol of ATPeq. X (10(11) platelets)-1, respectively. An energy cost of 0.7 mumol of ATPeq. X (10(11) platelets)-1 was calculated for separate dense-granule secretion, whereas the combined alpha- and acid-hydrolase granule secretion required 5.3 mumol of ATPeq. X (10(11) platelets)-1. There was no correlation between energy consumption and optical aggregation. In contrast, the rate of single platelet disappearance, which is a measure for the early formation of small aggregates, correlated closely with the rate of energy consumption. Compared with secretion, however, the energy requirement of single platelet disappearance was minor, since 2mM-EDTA completely prevented this response but decreased the energy consumption only slightly. An increase of 0.5-1.0 mumol of ATPeq. X (10(11) platelets)-1 was seen before single platelet disappearance and the three secretion responses were initiated, indicating an increase in energy consuming processes that preceded these responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylglucosaminidase↗
PubMed1992

Theoretical studies on the control of the oxidative phosphorylation system.

The dynamic model developed in our previous publications [1,2] was used to calculate the flux control coefficients of oxidation, phosphorylation and proton leak fluxes for isolated mitochondria and for three modes of work of intact cells (hepatocytes). The results obtained were compared with experimental data, especially those measured in the frame of the 'top-down approach' of the metabolic control theory. A good agreement for mitochondria and for intact cells was found. The control of the oxygen consumption flux is shared between the ATP utilization (main controlling factor), substrate dehydrogenation, proton leak and, in some conditions, the ATP/ADP carrier. The phosphorylation subsystem seemed to be controlled mainly by itself, while the proton leak was influenced by all three subsystems. It was also shown that the large relative change in the enzyme activity during inhibitor titration of mitochondria or cells could lead to the overestimation of some flux control coefficient values in experimental measurements. An influence of some hormones (glucagon, vasopressin, adrenaline and others) on the mitochondrial respiration was also simulated. Our results suggest that these hormones stimulate the substrate dehydrogenation as well as the phosphorylation system (ATP usage and, possibly, the ATP/ADP carrier).

Adenosine Triphosphate↗
PubMed1993

Effects of plasmid pBR322 on respiratory and ATPase activities in Escherichia coli.

The effects of antibiotic resistance plasmids on respiratory and ATPase activities were investigated in Escherichia coli. The rates of oxygen consumption coupled to the oxidation of succinate and NADH, ATP hydrolysis, and ATP-Pi exchange were measured in isolated membrane vesicles prepared from HB101 strains that contained derivatives of plasmid pBR322. The rates of oxygen consumption coupled to the oxidation of NADH were independent of the presence or absence of plasmids in the strains from which the vesicles were prepared. In contrast, the mean rates of oxygen consumption coupled to the oxidation of succinate, ATP hydrolysis, and ATP-Pi exchange were 140-292% higher in vesicles made from plasmid-containing strains than from plasmid-free HB101 and independent of the expression of the plasmid-encoded tetracycline/H+ antiporter.

Adenosine Triphosphatases↗
PubMed1998

DeltapH-dependent photosystem II fluorescence quenching induced by saturating, multiturnover pulses in red algae

We have previously shown that in the red alga Rhodella violacea, exposure to continuous low intensities of light 2 (green light) or near-saturating intensities of white light induces a DeltapH-dependent PSII fluorescence quenching. In this article we further characterize this fluorescence quenching by using white, saturating, multiturnover pulses. Even though the pulses are necessary to induce the DeltapH and the quenching, the development of the latter occurred in darkness and required several tens of seconds. In darkness or in the light in the presence of 2, 5-dibromo-3-methyl-6-isopropyl-p-benzoquinone, the dissipation of the quenching was very slow (more than 15 min) due to a low consumption of the DeltapH, which corresponds to an inactive ATP synthase. In contrast, under far-red illumination or in the presence of 3-(3,4-dichlorophenyl)-1,1'-dimethylurea (only in light), the fluorescence quenching relaxed in a few seconds. The presence of N, N'-dicyclohexyl carbodiimide hindered this relaxation. We propose that the quenching relaxation is related to the consumption of DeltapH by ATP synthase, which remains active under conditions favoring pseudolinear and cyclic electron transfer.

Journal Article↗
PubMed1987

Ion regulation of phosphatidylserine and phosphatidylethanolamine outside-inside translocation in human erythrocytes.

In previous publications, we have shown, by using spin-labeled derivatives, that the translocation of phosphatidylserine and phosphatidylethanolamine from the outer to the inner monolayer of human erythrocyte membrane is a protein-mediated phenomenon, which requires hydrolisable Mg2+-ATP. The inhibition by intracellular Ca2+ (0.2 microM) or by extracellularly added vanadate (50 microM) was reported (Seigneuret, M. and Devaux, P.F. (1984) Proc. Natl. Acad. Sci. USA 81, 3751-3755; Zachowski, A., Favre, E., Cribier, S., Hervé, P. and Devaux, P.F. (1986) Biochemistry 25, 2585-2590). The present article gives further insight into the effects of intracellular and extracellular ions on the aminophospholipid translocation in human erythrocytes. By measuring the cell ATP concentration, we now show that the inhibitory effect of intracellular calcium on spin-labeled aminophospholipid translocation is partly due to the ATP depletion, which follows the increased consumption by the calcium pump. However, a direct inhibitory effect of cytosolic Ca2+ on the aminophospholipid translocase can be demonstrated by measuring the initial rate of aminophospholipid translocation in the presence of variable amounts of intracellular calcium, at fixed ATP concentrations. Moreover, the transmembrane equilibrium distribution of phosphatidylserine and phosphatidylethanolamine are affected differently by Ca2+: when cytosolic Ca2+ concentration is increased, alteration of phosphatidylethanolamine distribution begins as soon as the inward translocation is affected by Ca2+ (approx. 50 nM), whereas phosphatidylserine distribution remains unchanged within a large inhibitory range of cytosolic Ca2+ concentrations and decreases above 0.2 microM of free Ca2+ within the cytosol. Decrease of the intracellular Mg2+ concentration below its physiological value (approx. 2 mM) results in the inhibition of aminophospholipid inward transport, whereas increase of Mg2+ concentration does not modify this transport. If Mn2+ is substituted for Mg2+, part of the aminophospholipid translocation is maintained, whereas if Co2+ is substituted for Mg2+, the rapid translocation is completely abolished. Concentrations as high as a millimolar of extracellular Ca2+, Mg2+ or Mn2+ have no effect on the aminophospholipid translocation. The less usual cations Cr3+, Fe2+, Cu2+, Sn2+ and Eu3+ are also uneffective. With extracellular Ni2+ or Co2+, some inhibition can be observed, half inhibition by Ni2+ corresponding to 500 microM. Vanadyl (VO2+), on the other hand, is a potent inhibitor of the aminophospholipid translocation when applied on the extracellular surface, half-inhibition being reached around 30 microM.(ABSTRACT TRUNCATED AT 400 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1999

Structural changes of mitochondria related to apoptosis: swelling and megamitochondria formation.

Recently we have found that the formation of megamitochondria in culture cells of various sources, induced by chemicals capable of generating free radicals, is followed by apoptotic changes of the cell. Detailed analysis on functional and morphological aspects of megamitochondria has enabled us to speculate that the formation of megamitochondria may be a prerequisite for free radical-mediated apoptosis: free radicals modify the mitochondrial membranes resulting in the fusion of adjacent mitochondria (megamitochondria formation). If the intracellular level of free radicals is continuously kept high, the permeability transition pores of the megamitochondria membranes are opened and megamitochondria become swollen. Oxygen consumption and the ability to synthesise ATP by swollen megamitochondria decrease distinctly. At the same time, cytochrome c is released from swollen megamitochondria into the cytoplasm. If lowered rates of the generation of reactive oxygen species from swollen megamitochondria, possibly due to decrease in their oxygen consumption, are effective enough to lower the intracellular level of free radicals, megamitochondria may return to normal. If not, decrease in the membrane potential of megamitochondria membranes causes the release of apoptosis-inducing factor into the cytoplasm. Cytochrome c and apoptosis-inducing factor thus released into the cytoplasm may cause cytoplasmic and nuclear apoptotic changes. Experimental data to support this hypothesis are presented.

Animals↗
PubMed1993

31P and 13C NMR spectroscopic study of wild type and multidrug resistant Ehrlich ascites tumor cells.

Steady-state 31P NMR spectra of wild type EHR2 Ehrlich ascites tumor cells and multidrug resistant EHR2/DNR+ cells, immobilized in agarose threads, and continuously perfused with medium, showed temperature-dependent differences in the levels of intracellular phosphate metabolites. At 37 degrees C, the EHR2/DNR+ cells contained four times more phosphocreatine (PCr) than the EHR2 cells. At 20 degrees C, the EHR2 cells contained 80% more of phosphodiesters (PDE), the levels of PCr being equal. The quantitative metabolite level data are based on T1 relaxation times data and are normalized for the protein content of the cells. Perfusion of the cells with azide, an inhibitor of mitochondrial respiration, had no effect on the ATP level, and caused no changes in glucose consumption and lactate production. Azide perfusion, combined with glucose depletion, caused rapid drop in the ATP content, which was reestablished after renewed perfusion with glucose. Similarly, perfusion with 2,4-dinitrophenol, an uncoupler of the respiration chain, had no effect on the phosphate metabolites. These results demonstrate that aerobic glycolysis is the main route by which glucose is metabolised under the conditions used (glucose concentration in medium 2 g/L). Rates of uptake and phosphorylation of 2-deoxy-D-glucose were measured by following the formation of intracellular [6-13C]2-deoxy-D-glucose-6-phosphate by 13C NMR; at 37 degrees C the observed rates for EHR2 and EHR2/DNR+ cells were equal, about 10 nmol/(min x mg protein), whereas at 20 degrees C the wild type cells produced the 6-phosphate at an approximately twice the rate found for the resistant cells [about 4 and 2 nmol/(min x mg protein), respectively].(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Adenine nucleotide metabolism and contractile dysfunction in heart failure--biochemical aspects, animal experiments, and human studies.

In myocardial hypertrophy and heart failure a series of adaptational changes occur some multiplying contractile units, others slowing shortening velocity and increasing economy of contraction. The demonstration of energy-saving mechanisms in heart failure has prompted further investigations of energy providing and utilizing metabolic pathways. The use of myocardial ATP as a substrate occurs mainly at the myosin-ATPase and at the Ca-ATPase of the sarcoplasmic reticulum. As the Michaelis constant of both enzymes for ATP is in the micromolar (microM) range, whereas cellular ATP content is about 5000 microM, these enzymes are not controlled by the availability of ATP as a substrate. In experimental heart failure in large animals, normal or reduced creatine phosphate levels (in most cases together with normal adenine nucleotides) have been described. Reduced creatine phosphate is found in models with increased oxygen consumption, and creatine phosphate may buffer the ATP pool in these models. In human heart failure due to dilated cardiomyopathy, where resting oxygen consumption per unit mass and lactate extraction are normal in most patients, normal adenine nucleotides, creatine phosphate, and mitochondrial function have been described in the initial studies. These results have been challenged by one study showing decreased ATP levels in dilated cardiomyopathy, correlating with the decrease in ejection fraction. However, only ATP has been measured in this study, whereas total adenine nucleotides may be a more suitable parameter. Recently published results have again demonstrated normal ATP and total adenine nucleotides in human heart failure. In the same patients, significantly decreased myocardial norepinephrine was measured, indicating that metabolic changes had occurred in these hearts, but were independent of adenine nucleotides.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1984

Comparison of catecholamine effects on canine myocardial metabolism and regional blood flow during and after cardiopulmonary bypass.

The acute metabolic and hemodynamic effects of dopamine, dobutamine (both at 10 micrograms . kg-1 . min), and isoproterenol (at 0.05 or 0.1 micrograms . kg-1. min) were determined in dogs following 20 minutes of normothermic global myocardial ischemia. The catecholamines were started 10 minutes before cardiopulmonary bypass (CPB) was discontinued and were continued for 1 hour after bypass. Regional myocardial and systemic blood flow distribution was measured by means of the radioactive microsphere technique. On bypass all catecholamines sharply increased heart rate, myocardial oxygen consumption, and left ventricular blood flow (p less than 0.01). Because the hearts were unloaded, these data suggest that velocity of contraction is an important component of myocardial oxygen consumption. Although these drugs did not lower myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) levels, the significant rise in oxygen consumption suggested that inotropic treatment on bypass may not be beneficial. Furthermore, renal blood flow was diminished in dobutamine-treated dogs (p less than 0.01) and tended to decrease with isoproterenol infusion. No change was seen with dopamine infusion. After bypass, dobutamine treatment increased cardiac output (p less than 0.01) and stroke volume (p = 0.017) with no change in heart rate, myocardial oxygen consumption, high-energy phosphate levels, and total or transmural distribution of left ventricular blood flow. Dopamine infusion did not change cardiac output but did increase oxygen consumption (p less than 0.01). Isoproterenol showed a slight inotropic effect, but frequent ventricular arrhythmias were present during weaning from bypass. In all treatment groups, blood flow in the other systemic beds (cerebral, gastrointestinal, and renal) was similar to that in control dogs. These data suggest that dobutamine is the most efficient of the drugs tested for support of the heart following global myocardial ischemia but, when given during bypass, it appears to decrease renal blood flow.

Adenosine Triphosphate↗
PubMed1995

Perinatal maturation of rat kidney mitochondria.

In the rat kidney, NaK-ATPase activity increased between days 19 and 20 of gestation (+50%) and between 1 and 24 h after birth (+20%), requiring an increased energy supply. In order to determine whether mitochondrial changes were involved, renal mitochondrial development was investigated from day 19 of gestation to 1 day after birth. Slot-blot analyses of mitochondrial-DNA/nuclear-DNA ratio and determination of citrate synthase activity showed a doubling in the mitochondrial pool between days 19 and 20 of gestation. In isolated mitochondria, oxygen consumption remained unchanged between days 19 and 20 of gestation, and then it was enhanced between days 20 and 21 of gestation (+70%) and between 1 and 24 h after birth (+50%). We also focused on one of the respiratory-chain complexes, ATP synthase, and measured its activity and content during the perinatal period. We demonstrated increases in both activity and content of ATP synthase between days 20 and 21 of gestation and between 1 and 24 h after birth, thus suggesting that changes in ATP synthase activity are ascribed to an increase in the mitochondrial density of ATP synthase complexes. Moreover, the mitochondrial ATP/ADP ratio only increased between 1 and 24 h (+90%), indicating a critical step in the renal respiratory-chain maturation at that time. We therefore conclude that the postnatal enhancement of renal mitochondrial oxidative capacity might depend on protein synthesis de novo and on changes in the adenine nucleotide concentrations.

Adenine Nucleotides↗
PubMed1991

Simulated weightlessness and bone metabolism: impairment of glucose consumption in bone tissue.

The effect of simulated weightlessness on bone glucose consumption was investigated in skeletal unloading for up to 4 days. Skeletal unloading was designed using the model of hind-limb hang in rats. Femoral-diaphyseal fragments obtained from rats bred with skeletal unloading were cultured for 24 h at 37 degrees C in 5% CO2/95% air in Dulbecco's Modified Eagle Medium (high glucose, 4.5 g/dl). The consumption of medium glucose by bone tissues was significantly decreased by skeletal unloading for 2 and 4 days, while the production of lactic acid from bone tissues was not significantly altered. In addition, adenosine triphosphate (ATP) content in the cultured bone was significantly decreased by skeletal unloading. The presence of calcitonin (synthetic [Asu1,7] eel, 3 and 30 nM) fairly restored bone glucose consumption impaired by skeletal unloading. However, the effect of insulin (1 and 10 nM) on bone glucose consumption and ATP content was not seen in the bone tissues with skeletal unloading. These results suggest that the sensitivity of bone response for insulin action is reteriorated by skeletal unloading.

Adenosine Triphosphate↗
PubMed1995

Stimulation of motility and respiration of intact fowl spermatozoa by calyculin A, a specific inhibitor of protein phosphatase-1 and -2A, via a Ca2+-dependent mechanism.

Intact fowl spermatozoa became almost immotile at 40 degrees C. In contrast, the presence of 10-1000 nmol calyculin A l-1, a specific inhibitor of protein phosphatase-1 (PP1) and -2A (PP2A), permitted activation of sperm motility in a dose-dependent manner. Calyculin A also stimulated the rate of oxygen consumption by spermatozoa, and induced a concomitant decrease in ATP concentrations, suggesting a coupling of ATP hydrolysis to the rate of oxidative phosphorylation. However, the motility and oxygen consumption of spermatozoa loaded with an intracellular Ca2+ chelator, 1,2-bis (2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, tetraacetoxymethyl ester (BAPTA/AM), were not stimulated by calyculin A alone, but only after the subsequent addition of 2 mmol CaCl2 l-1. These results suggest that inhibition of the activities of endogenous PP1 and PP2A may stimulate the motility and metabolic activity of fowl spermatozoa at 40 degrees C via a mechanism that requires intracellular free Ca2+.

Animals↗
PubMed1994

The importance of the creatine kinase reaction: the concept of metabolic capacitance.

The creatine kinase reaction is traditionally viewed as providing an energy reserve in muscle. However, the physiological importance of this reaction (and the analogous invertebrate reaction catalyzed by arginine kinase) is better understood when viewed as providing metabolic capacitance. This capacitance allows reduction of peak rates of ATP synthesis in cells that alternate between periods of high and low energy consumption. Furthermore, the capacitance allows repayment of energy "debt" that is incurred during periods of high energy demand to occur during periods of low rates of energy consumption. The creatine kinase reaction provides facilitated diffusion of ATP and ADP, which leads to spatial buffering in addition to temporal buffering. Data are presented which suggest that the existence of the creatine kinase reaction allows muscle cells to maintain reduced mitochondrial volume, support larger diameter fibers, and express faster isoforms of myosin. These data lead to speculation that there may be a coupling in the expression of metabolic and contractile proteins.

Animals↗
PubMed1990

Fatty acid lessens halothane's inhibition of energy metabolism in isolated hepatocytes.

This study has examined whether adverse halothane effects on liver-cell energy metabolism are influenced by the availability of alternate substrates for energy-generating reactions. Halogenated volatile anesthetics affect both energy supply and energy demand in tissues, and cellular energy deficits have been implicated in anesthetic hepatotoxicity. Using hepatocytes isolated from fed rats either pretreated with phenobarbital or not treated (+PB or -PB cells, respectively), we studied the cellular energetic effects of providing fatty acid (oleic acid) along with glucose as substrate(s) for energy metabolism, while exposing the cells to 0%-2% halothane. In -PB cells incubated with glucose alone, there were halothane dose-related decreases in the oxygen (O2) consumption rate (VO2) and in the balance between adenosine triphosphate (ATP) supply and demand (ATP/ADP ratio), but no effect on lactate metabolism (lactate consumption or production) over the 10-min incubation period. Adding oleate along with glucose (a) raised VO2 but lowered ATP/ADP in the absence of halothane; (b) eliminated the decreases in VO2 and ATP/ADP seen when halothane was introduced; and (c) increased lactate consumption in both the presence and absence of halothane. In +PB cells, VO2 was higher, ATP/ADP lower, and lactate consumption also lower than in -PB cells under comparable conditions. Halothane or oleate effects, or both, on energy metabolism were thus qualitatively similar in +PB and -PB cells, except that in +PB cells incubated without oleate, lactate formation developed as halothane was increased from 0% to 2%, reflecting activation of glycolysis due to insufficient mitochondrial ATP production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

Exogenous ATP and carbohydrate metabolism in the rat liver.

The present study analyzed the actions of exogenous ATP on liver carbohydrate metabolism by using both isolated perfused rat livers and hepatocytes as model systems. The metabolic parameters measured in the perfused livers were glucose production, lactate production, oxygen consumption, and K+ movement. All parameters were monitored continuously during the perfusions in order to assess transient effects. ATP increased both glucose and lactate production in the isolated rat liver when perfused with either constant pressure or constant flow. ATP increased oxygen consumption in the perfused liver at a low concentration (10 microM) but was inhibitory at high concentrations (40 and 160 microM). ATP also increased K+ efflux in the isolated perfused liver. ATP did not alter basal glucose production in isolated hepatocytes; however, it did inhibit glucagon-stimulated glucose output by hepatocytes. ATP inhibited lactate production in the isolated hepatocytes. Extracellular ATP has the potential to modify basal as well as hormonal modulation of hepatic carbohydrate metabolism during shock.

Adenine Nucleotides↗
PubMed2004

Effects of the carbamates fenoxycarb, propamocarb and propoxur on energy supply, glucose utilization and SH-groups in neurons.

Carbamates belonged to an older insecticide group, with propoxur being representative of this group. However, today carbamates with hormonal effects on insects, like fenoxycarb, or with fungicide properties, like propamocarb, are also used. The goal was a comparison of three structurally and functional different carbamates with a possibly common toxicological mechanism. Primary neuronal cell cultures of the rat are a well established model to identify neurotoxic compounds like n-hexane or acrylamide. In this cell culture model endpoints such as viability, energy supply, glucose consumption, glutathione (GSH) levels and cytoskeleton elements were determined. Added to cultured rat cortical neurons for 1 week, fenoxycarb, propamocarb and propoxur considerably decreased ATP levels, mitochondrial membrane potential and glucose consumption. Besides this, fenoxycarb and propamocarb had an impact on neurofilaments. After recovery for 1 week, propoxur also showed effects on neurofilaments, whereas with the other carbamates no tendency for a recovery was seen. These effects were prevented completely by pyruvate for propoxur and propamocarb, and partly so for fenoxycarb. In contrast to the main experimental design, GSH was determined after 1-h treatment with the test substances. Surprisingly, the compounds had only slight or no effect on the GSH level within this time. Further mechanistic studies indicated that carbamates primarily interacted with SH-groups, most likely by interfering with glycolysis and the construction of fibrillary proteins like neurofilaments. The prevention by pyruvate and acetylcysteine pointed to these biochemical endpoints.

Acetylcysteine↗
PubMed1979

The relationship between initial creatine phosphate breakdown and recovery oxygen consumption for a single isometric tetanus of the frog sartorius muscle at 20 degrees C.

A previous paper (Mahler, M. 1978 J. Gen. Physiol. 71:559--580) describes the time-course of the suprabasal rate of oxygen consumption (delta QO2) in the sartorius muscle of R. pipiens after isometric tetani of 0.1--1.0 s at 20 degrees C. To test whether these were the responses to impulse changes in the rate of ATP hydrolysis, we compared the total suprabasal oxygen consumption during recovery (delta[O2]) with the amount of ATP hydrolyzed during a contraction, measured indirectly as the decrease in creatine phosphate (delta[CP]O). If suprabasal ATP hydrolysis during recovery is negligible in comparison with that during contraction, delta[CP]0/delta[O2] should approximate the P:O2 ratio for oxidative metabolism, which has an expected value of 6.1--6.5. We found: formula; see text. We conclude that in this muscle at 20 degrees C: (a) after a tetanus of 0.2--1.0 s, delta QO2(t) can be considered the response to an impulse increase in the rate of ATP hydrolysis; (b) the reversal during recovery of unidentified exothermic reactions occurring during the contraction (Woledge, R. C. 1971. Prog. Biophys. Mol. Biol. 22:39--74) can be coupled to an ATP hydrolysis that is at most a small fraction of delta[CP]0; (c) the pooled mean for delta[CP]0/delta[O2], 6.58 +/- 0.55, sets an experimental lower bound for the P:O2 ratio in vivo.

Adenosine Triphosphate↗
PubMed1991

Temperature effects on ischemic and hypoxic renal proximal tubular injury.

UNLABELLED: Body temperature (T) profoundly alters the severity of ischemic acute renal failure. Therefore, the present study evaluated T effects on: (a) in vitro proximal tubular cell killing during hypoxia/reoxygenation to assess when it exacerbates injury; (b) renal ATP losses and metabolic rate (O2 consumption) during hemorrhagic shock (55-60 mm Hg); and (c) membrane deacylation (assessed by free fatty acid, FFA, release) to determine if T modifies this pathway of ischemic renal damage. Hypoxic cell kill (45 minutes) was 20 +/- 1% 47 +/- 4%, and 61 +/- 2% at 32 degrees C, 37 degrees C, and 40 degrees C respectively (by lactate dehydrogenase release; p less than 0.001). During reoxygenation (15 minutes), minimal lactate dehydrogenase was released, irrespective of T. ATP decrements during shock were profoundly T dependent (% loss of ATP; 15%, 30%, 58% at 32.5 degrees C, 37 degrees C, and 39.5 degrees C, respectively; p less than 0.001), reflecting T-dependent increments in renal metabolic rate, not decreased O2 delivery (arterial O2 content; renal blood flow). ATP losses during shock correlated with the extent of S3 proximal tubular morphologic damage. O2 deprivation dramatically increased FFA levels both in vivo and in vitro but the increments were only slightly T dependent. In vitro, % lactate dehydrogenase release and FFA levels did not significantly correlate and bovine serum albumin, a FFA binder, conferred no protection. CONCLUSIONS: (a) T dramatically accentuates hypoxic, not reoxygenation, injury; (b) changes in membrane deacylation do not appear to underlie this effect; and (c) T has a profound impact on renal ATP losses during shock, thereby affecting the severity of ischemic renal damage.

Adenine Nucleotides↗