The effect of bile salts on oxygen consumption, oxidative phosphorylation and ATP-ase activity of mucosal homogenates from rat jejunum and ileum.
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Adenosine Triphosphatases↗
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Use of phosphorous-31 nuclear magnetic resonance spectroscopy to determine safe timing of chemotherapy after hepatic resection.
Liver resection induces accelerated growth of residual hepatic micrometastases. Adjuvant chemotherapy may improve outcome if administered early after resection but may prove lethal if initiated prior to completion of DNA synthesis in regenerating liver. This study investigates phosphorus-31 nuclear magnetic resonance ((31)P-NMR) as a noninvasive tool for measuring energy changes reflective of hepatic DNA synthesis and for predicting safe timing of chemotherapy after 70% hepatectomy. To evaluate metabolic changes in regenerating liver, quantitative three-dimensional (31)P-NMR was performed, using the technique of chemical shift imaging at various time points after 70% hepatectomy in adult male Fischer rats. Animals receiving a course of 2'-deoxy-5-fluorouridine (FUDR; 100 mg/kg, i.p. four times per day x 5), initiated at the time of operation, were also evaluated to observe the effects of chemotherapy on liver regeneration. Forty-eight hours after resection, hepatic nucleoside triphosphate (NTP), which reflects ATP content, fell 37% (P < 0.03) in animals undergoing hepatectomy alone. By contrast, animals receiving FUDR after hepatectomy demonstrated a mitigated NTP response, with a drop of only 17% (P = not significant), suggesting that interruption of DNA synthesis leads to a reduced consumption of ATP. Direct measures of DNA synthesis and nuclear proliferation were correlated with NMR findings. [(3)H]Thymidine incorporation and Ki67 immunohistochemistry were performed on liver samples from rats undergoing 70% hepatectomy with and without FUDR. Both [(3)H]thymidine incorporation and Ki67 expression were inhibited significantly at 48 h in animals receiving hepatectomy and FUDR, compared with those not treated with FUDR. To determine whether NMR changes could be used to identify safe timing of chemotherapy after hepatectomy, rats were treated with a 5-day course of FUDR initiated either prior to or after NMR changes normalized. Animals treated with FUDR at the point of NTP normalization (72 h) showed significantly improved survival over those that began treatment at operation (75 % versus 17 %; P = 0.0005, log rank test). FUDR inhibits hepatic DNA synthesis and influences mortality if administered too early after hepatectomy. Chemical shift imaging is a noninvasive tool that can identify metabolic changes coinciding with DNA synthesis and nuclear proliferation after hepatectomy. (31)P-NMR may be useful for determining safe timing of chemotherapy after liver resection.
Animals↗
Effects of chromium(VI) and chromium(III) on energy charge and oxygen consumption in rat thymocytes.
The cytotoxic effects of chromium compounds in two oxidation states have been studied in rat thymocytes. endogenous nucleotide levels and oxygen consumption were examined as relevant parameters of the physiological state of the cell. Incubation of rat thymocytes with Cr(VI) produced a marked unbalance of endogenous purine nucleotide pool and a parallel decrease in oxygen consumption. A close correlation between the reduction of oxygen consumption and ATP level in rat thymocytes treated with increasing concentrations of Cr(VI) has been found. In rat thymocytes permeabilized with digitonin and in isolated rat liver mitochondria both Cr(VI) and Cr(III) showed, at different range of concentrations, a marked inhibition of maximal oxygen consumption rate (uncoupled respiration). The effects observed were depending on chromium oxidation state and on different mitochondrial sites of substrate oxidation.
Adenosine Diphosphate↗
Impact of altered substrate utilization on cardiac function in isolated hearts from Zucker diabetic fatty rats.
The goal of this study was to determine whether changes in cardiac metabolism in Type 2 diabetes are associated with contractile dysfunction or impaired response to ischemia. Hearts from Zucker diabetic fatty (ZDF) and lean control rats were isolated and perfused with glucose, lactate, pyruvate, and palmitate. The rates of glucose, lactate, pyruvate, and palmitate oxidation rates and glycolysis were determined during baseline perfusion and low-flow ischemia (LFI; 0.3 ml/min for 30 min) and after LFI and reperfusion. Under all conditions, ATP synthesis from palmitate was increased and synthesis from lactate was decreased in the ZDF group, whereas the contribution from glucose was unchanged. During baseline perfusion, the rate of glycolysis was lower in the ZDF group; however, during LFI and reperfusion, there were no differences between groups. Despite these metabolic shifts, there were no differences in oxygen consumption or ATP production rates between the groups under any perfusion conditions. Cardiac function was slightly depressed before LFI in the ZDF group, but during reperfusion, function was improved relative to the control group despite the increased dependence on fatty acids for energy production. These data suggest that in this model of diabetes, the shift from carbohydrates to fatty acids for oxidative energy production did not increase myocardial oxygen consumption and was not associated with impaired response to ischemia and reperfusion.
Animals↗
Effect of ammonia on survival and adenylate energy charge in the shrimp Palaemonetes varians.
Shrimps Palaemonetes varians were submitted to lethal and sublethal concentrations of ammonia in order to measure lethality, ATP and adenylate nucleotide levels, and adenylate energy charge (AEC) index. LC50 was of about 3 mg/liter of ammonia. Adenylate measurements were performed over a period of 14 days and for two different concentrations. A population submitted to 0.5 mg/liter of ammonia exhibited high survival and a marked consumption of ATP, whereas high mortality and disordered ATP metabolism are the characteristics of the population submitted to 3 mg/liter of ammonia. An homeostatic model was applied in order to explain the significance of the AEC signal. Here, AEC is proposed as a measure of the limits of active response of an organism to environmental stress.
Adenosine Diphosphate↗
Mitochondrial nitric oxide inhibits ATP synthesis. Effect of free calcium in rat heart.
Nitric oxide is a small potentially toxic molecule and a diatomic free radical. We report the interaction of L-arginine, oxygen and calcium with the synthesis of nitric oxide in heart mitochondria. Nitric oxide synthesis is increased in broken rat heart mitochondria compared with intact and permeabilized mitochondria. Intact mitochondria subjected to hypoxia-reoxygenation conditions accumulated nitric oxide that inhibits oxygen consumption and ATP synthesis. ATPase activity is not affected during this augment of nitric oxide. Physiological free calcium concentrations protected mitochondria from the damage caused by the accumulation of nitric oxide. Higher concentrations of the divalent cation increase the damage exerted by nitric oxide.
Adenosine Triphosphate↗
Effects of inotropic stimulation on energy metabolism and systolic function of ischemic right ventricle.
This study determined whether dobutamine enhances regional systolic function in the ischemic right ventricle (RV) at the cost of adverse effects on regional energy metabolism. Seventeen alpha-chloralose-anesthetized, open-chest pigs were studied under four conditions: 1) control; 2) dobutamine infusion (mean dose 9 micrograms.kg-1.min-1); 3) RV ischemia (45 +/- 5% reduction in RV free wall blood flow for 100 min); and 4) continued ischemia with dobutamine. Regional RV free wall high-energy phosphate metabolites were measured by 31P nuclear magnetic resonance (NMR) spectroscopy or by high-speed drill biopsies of the RV free wall. Regional RV free wall substrate and O2 consumption were measured using coronary venous blood sampling. Global RV systolic function was assessed by the maximal first derivative of RV pressure (dP/dtmax), and regional RV free wall systolic function was assessed by systolic segment shortening in the ischemic zone. Right coronary artery constriction caused markedly depressed regional RV systolic function, net lactate production, and coronary venous acidosis. Surprisingly, high-energy phosphates were unchanged compared with control. Addition of dobutamine caused a further decline in coronary venous pH and continued lactate production but did not reduce high-energy phosphates. While dobutamine markedly enhanced global RV systolic function (RV dP/dtmax 201 +/- 19% of control), systolic shortening in the ischemic RV free wall remained severely depressed (47 +/- 18% of control) despite dobutamine. The mechanism of high-energy phosphate preservation is likely due to diminished consumption of ATP in the hypocontractile ischemic region.
Animals↗
Influence of D-glucose upon the respiratory and secretory response of insulin-producing tumor cells to 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid.
In insulin-producing cells of the RINm5F line, the nonmetabolized analogue of L-leucine, 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid decreases O2 consumption, lowers ATP content, and inhibits insulin release despite stimulation of both NH4 production and 14CO2 output from cells prelabeled with L-[U-14C]glutamine. The metabolic and secretory effects of 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid are opposed to those of D-glucose, which increases respiration, ATP content, and insulin release, while lowering NH4+ production and 14CO2 output from the prelabeled cells. D-Glucose also antagonizes the inhibitory action of 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid upon both respiration and secretion. These findings suggest that, in tumor as in normal islet cells, the regulation of insulin release by exogenous nutrients depends on the availability of endogenous ATP.
Adenoma, Islet Cell↗
Ions and energy metabolism in duck salt-gland: possible role of furosemide-sensitive co-transport of sodium and chloride.
1. The effects of methacholine on net ionic movements and energy metabolism of the avian salt-gland have been studied, using slices of glands taken from salt-adapted Pekin ducks. The slices were equilibrated with media and drugs for 120 min at 1 degrees C before the experimental incubation at 38 degrees C.2. During incubation at 38 degrees C the slices accumulated K(+) and lost Na(+) and Cl(-). In the presence of methacholine, they retained more Na(+) and Cl(-) and accumulated less K(+), the maximal effects being given by 0.5-1.0 mM-methacholine. Similar results were obtained whether the medium contained 10 mM-Tris (used in most experiments) or 25 mM-HCO(3) (-) as the major buffer.3. The higher final levels of cell Na(+) and Cl(-) induced by methacholine were not seen when furosemide (1 mM) was also present. Methacholine did not induce a higher level of cell Na(+) when medium Cl(-) was replaced by I(-), NO(3) (-) or SO(4) (2-), and did not induce a higher Cl(-) content when medium Na(+) was replaced by choline or Li(+). The fall of K(+) accumulation caused by methacholine was also prevented by furosemide or by replacing Cl(-) in the medium with other anions. The anion-transport inhibitors, SCN(-) (up to 10 mM) and 4,4'-diisothiocyano-2,2'-disulphonic acid stilbene (DIDS) (up to 2 mM) did not prevent the effects of methacholine.4. Methacholine stimulated respiration and lowered the slice ATP contents, and these effects were both prevented by ouabain or furosemide. Ouabain, but not furosemide, also reduced the basal (i.e. in the absence of methacholine) rate of respiration and raised the ATP level. SCN(-) and DIDS had no effect on basal or stimulated respiration or on ATP contents.5. The respiratory stimulation and fall of ATP induced by methacholine were totally prevented if medium Na(+) was replaced by choline. Replacement of Na(+) by Li(+) caused some stimulation of basal respiration; it also permitted some loss of ATP in the presence of methacholine, but the loss was smaller than that seen in the normal Na(+) medium.6. The respiratory stimulation and fall of ATP induced by methacholine were prevented if medium Cl(-) was replaced by SO(4) (2-). The effects of methacholine were partially blocked when NO(3) (-) replaced Cl(-).7. The results are consistent with the stimulation by methacholine of a furosemide-sensitive, coupled entry of Na(+) and Cl(-) into the cells, associated with a loss of K(+). This would result in a stimulation of Na(+) extrusion by the ouabain-sensitive transport system for Na(+) and K(+) with increased consumption of ATP.
Adenosine Triphosphate↗
Increased sensitivity to oxidative injury in chinese hamster ovary cells stably transfected with rat liver S-adenosylmethionine synthetase cDNA.
Chinese hamster ovary cells were stably transfected with rat liver S-adenosylmethionine synthetase cDNA. As a result, S-adenosylmethionine synthetase activity increased 2.3-fold, an effect that was accompanied by increased S-adenosylmethionine, a depletion of ATP and NAD levels, elevation of the S-adenosylmethionine/S-adenosylhomocysteine ratio (the methylation ratio), increased DNA methylation and polyamine levels (spermidine and spermine), and normal GSH levels. By contrast, the transfected cells showed normal growth curves and morphology. Exposure to an oxidative stress by the addition of H2O2 resulted in a greater consumption of ATP and NAD in the transfected cells than in the wild-type cells. In turn, cell killing by H2O2 was greater in the transfected cells than in the wild-type cells. This killing of Chinese hamster ovary cells by H2O2 involved the activation of poly(ADP-ribose) polymerase with the resultant loss of NAD and ATP. 3-Aminobenzamide, an inhibitor of poly(ADP-ribose) polymerse, but not the antioxidant N,N'-diphenylphenylenediamine, prevented the killing of Chinese hamster ovary cells by H2O2 and maintained the contents of NAD and ATP. The results of this study indicate that a moderate activation of the synthesis of S-adenosylmethionine leads to ATP and NAD depletion and to a greater sensitivity to cell killing by oxidative stress.
Adenosine Triphosphate↗
Reperfusion injury in skeletal muscle: controlled limb reperfusion reduces local and systemic complications after prolonged ischaemia.
Previous studies in isolated limbs using crystalloid perfusion solutions have shown that control of the initial reperfusion reduces postischaemic complications. However, no experimental study has been undertaken to evaluate the concept of controlled limb reperfusion experimentally in an in vivo blood-perfused model and to assess the local as well as systemic effects of normal blood reperfusion and controlled limb reperfusion. Of 20 pigs undergoing preparation of the infrarenal aorta and iliac arteries, six were observed for 7.5 h and served as controls; 14 others underwent 6 h of complete infrarenal occlusion. Thereafter, embolectomy was simulated in eight pigs by removing the aortic clamp and establishing normal blood reperfusion at systemic pressure. In six other pigs, the composition of the reperfusate and the conditions of reperfusion were controlled during the first 30 min, followed by normal blood reperfusion. Some 6 h of infrarenal aortic occlusion leads to a severe decrease in high-energy phosphates and muscle temperature, together with a slight increase in creatine kinase and potassium in the systemic circulation. Normal blood reperfusion resulted in severe reperfusion injury: massive oedema developed, the tissue showed a marked decrease in oxygen consumption, glucose consumption, tissue ATP, total adenine nucleotides, muscle pH and total calcium in the femoral vein. Furthermore, a massive increase was seen in plasma creatine kinase concentration and potassium, together with the development of muscle rigidity. In sharp contrast, initial treatment of the ischaemic skeletal muscle by controlled limb reperfusion resulted in normal water content, oxygen consumption, glucose consumption, flow and muscle rigidity. Furthermore, controlled limb reperfusion resulted in higher total adenine nucleotides content, less tissue acidosis, markedly reduced creatine kinase release, and potassium release as compared with that of normal blood reperfusion. This study shows that 6 h of acute infrarenal aortic occlusion will result in severe reperfusion injury (postischaemic syndrome) if normal blood at systemic pressure is given in the initial reperfusion phase. In contrast, initial treatment of the ischaemic skeletal muscle by controlled limb reperfusion reduces the metabolic, functional and biochemical alterations.
Acute Disease↗
Nitrite oxidation of myoglobin in perfused myocardium: implications for energy coupling in respiration.
Nitrite oxidation of oxymyoglobin in perfused rat myocardium under nonlimiting oxygen produces a detectable 1H nuclear magnetic resonance metmyoglobin (metMb) signal at -3.9 ppm. When the myocardium is perfused with < 10 mM nitrite, the 1H nuclear magnetic resonance MbO2 gamma CH3 Val E11 signal does not change intensity and the metMb reporter signal at -3.9 ppm is undetectable. However the rate pressure product decreases by 26% from the control level. Phosphocreatine, myocardial oxygen consumption, Pi, ATP, and pH remain constant. With > 10 mM infused nitrite, myoglobin (Mb) oxidation becomes apparent. As the MbO2 gamma CH3 Val E11 signal intensity decreases, the metMb signal intensity at -3.9 ppm increases. At the same time the 31P high-energy phosphate signals, rate pressure product, and lactate formation exhibit significant alterations. Myocardial oxygen consumption, however, remains constant. The data indicate that Mb oxidation does not limit myocardial respiration but does reduce energy production. Pulse-recovery experiments further demonstrate that a transient perfusion with 2 mM infused nitrite depresses the contractile function, which does not recover during reperfusion with oxygenated, nitrite-free buffer. The findings support the view that either Mb mediates energy coupling or nitrite directly uncouples energy production in myocardium. They also reveal a glimpse of the intracellular reductase activity that maintains the Mb in the Fe (II) state.
Animals↗
HIV infection is associated with increased NTPDase activity that correlates with CD39-positive lymphocytes.
Infection with the human immunodeficiency virus (HIV) results in alterations in immune cells such as an increase or decrease of cytokine secretion and immunodeficiency. HIV causes a state of chronic cellular activation that can induce apoptosis in lymphocyte T-helpers, making the patient susceptive to opportunistic infections. The biochemical mechanisms involved in this immune response to HIV have been researched. Here, we have shown for the first time that ATP and ADP hydrolysis are essential for the immune response to HIV. Our results clearly indicate an increase of NTPDase-1 (EC 3.6.1.5) activity in lymphocytes of HIV-positive patients, confirmed by an enhanced CD39 expression on its surface. These results suggest that NTPDase-1 may be important to keep an adequate balance between the generation and consumption of ATP and to preserve cellular integrity and immune response to the HIV infection.
Adult↗
Relationships between adenylate cyclase and Na+, K(+)-ATPase in rat pancreatic islets.
We tested the hypothesis that the adenylate cyclase system and Na+, K(+)-ATPase are reciprocally related in rat pancreatic islets. We studied the effect of theophylline, caffeine, and dibutyryl cyclic AMP on Na+, K(+)-ATPase activity in a membrane preparation from collagenase-isolated rat islets. Theophylline, caffeine, or dibutyryl cyclic AMP, in concentrations of 1 mM, all inhibited Na+, K(+)-ATPase activity (44,62, and 43%, respectively). Kinetic analysis indicated that theophylline and dibutyryl cAMP inhibit Na+, K(+)-ATPase by different mechanisms; theophylline decreased Vmax and decreased apparent Km (ATP), whereas dibutyryl cAMP decreased Vmax and increased apparent Km (ATP). Similar inhibition of Na+, K(+)-ATPase by theophylline or dibutyryl cAMP was noted in a particulate fraction from rat kidney and in a purified porcine brain Na+, K(+)-ATPase preparation. The adenylate cyclase system and Na+, K(+)-ATPase may act reciprocally in pancreatic islets and in other tissues. In the beta cell this relationship may be essential in coordinating consumption of ATP in the stimulated, as opposed to the rest, state.
Adenylyl Cyclases↗
Influence of in vitro lactic acidosis and hypercapnia on respiratory activity of isolated rat brain mitochondria.
Respiratory activity and the ADP/O ratio of isolated rat brain mitochondria were measured following incubation with varying concentrations of lactic acid in reaction media buffered either with bicarbonate and CO2 or with phosphate alone, at a pH of 7.1. Increasing lactic acid levels caused a progressive decrease in substrate-, phosphate-, and ADP-stimulated (State 3) respiration and ADP/O ratios. Fifteen millimolar lactic acid, pH 6.4, caused approximately 50% inhibition of State 3 respiration (with malate + glutamate as substrate). At lower pH values (5.3-6.1), addition of ADP caused little or no increase in O2 consumption; i.e., ATP formation ceased. Addition of lactic acid at constant pH moderately affected respiratory control ratios but did not change State 3 respiration or ADP/O ratios. Thus, the effect of lactic acid was related to the pH change. Increasing CO2 concentrations in the reaction medium had similar effects on mitochondrial respiration, indicating that changes in extramitochondrial pH rather than in transmembrane H+ gradients determined the respiratory alterations. Following a 5-min incubation of mitochondria with lactic acid, pH 6.1, there was an incomplete recovery of State 3 respiration and respiratory control ratios. It is concluded that mitochondrial respiration is inhibited by a decrease in pH which, if excessive, may lead to a permanent suppression of ATP production. These results may, at least partly, explain the deleterious effects of enhanced lactic acidosis in brain ischemia.
Acidosis↗
Effect of D-600 on ischemic and reperfused rabbit myocardium: relation with timing and modality of administration.
In this study we have investigated the possibility that D-600, a phenylalkylamine calcium antagonist, protects the isolated rabbit heart against ischemia and reperfusion-induced damage. D-600 was either subcutaneously injected (2mg/kg, twice daily for 5 to 6 days) in the rabbit before isolation of the heart, or delivered to the isolated hearts in the perfusate (10(-7) M), either at the onset of ischemia and during reperfusion, or only during post-ischemic reperfusion. Ischemia (90 min) was induced by reducing coronary flow from 25 to 1 ml/min, followed by 30 min of reperfusion. Myocardial damage was determined in terms of mechanical function, release of creatine phosphokinase (CPK) and noradrenaline, mitochondrial function, calcium homeostasis, and endogenous stores of ATP and creatine phosphate (CP). Administration of D-600 to the rabbits or to the isolated hearts at the time of ischemia exerted protection. There are four groups of evidence in support of this conclusion: 1) the rise in diastolic pressure during ischemia was diminished with greater recovery of developed pressure during reperfusion; 2) CPK and noradrenaline release during reperfusion were reduced; 3) the oxygen consumption and ATP generating capacities of mitochondria were better maintained; and 4) associated with this preservation of mitochondrial function was the maintenance of near normal calcium homeostasis and of endogenous ATP and CP stores. The two different modalities of administration did not produce substantially different results. When administered to the isolated hearts after the ischemic period, D-600 failed to improve mechanical recovery and release of endogenous substances. However, it reduced mitochondrial calcium overload and improved ATP production. The mechanism of the protective effect of D-600 seems to be multiple: energy-sparing effect, reduction of the toxicity mediated by endogenous catecholamines, and direct inhibition of mitochondrial calcium transport.
Adenosine Triphosphate↗
Dynamic changes in the organophosphate profile upon treatment of the crystalline lens with dexamethasone.
Dynamic changes in organophosphate metabolites during incubations of the intact crystalline lens in a medium containing 2 X 10(-3) M dexamethasone were studied using phosphorus-31 nuclear magnetic resonance intact-tissue spectroscopy. ATP, ADP, inorganic orthophosphate, alpha-glycerophosphate, nicotinamide adenine dinucleotides, uridine diphosphorylglucose and diphosphorylgalactose, glycerol 3-phosphorylethanolamine and -phosphorylcholine, and an unidentified phosphorus-containing molecule at 6 ppm were quantitated. Time-dependent changes in lens metabolism involving these compounds were examined during a 24-hr incubation period with dexamethasone. The first event in the decline of the tissue after steroid incubation was the consumption of ATP, which was linear with time until the ATP was reduced to 10% of its initial value. The sugar phosphates, inorganic orthophosphate, and the nucleoside diphosphorylsugars increased linearly with time, whereas the dinucleotides decreased. The ADP concentration was unaffected by the steroid treatment, as was that of the other organophosphates in the intact tissue profile. The steroid-induced alterations in lens phosphate metabolite levels follow a distinctive pattern that differs substantially from that observed in response to experimental hypoglycistic or hyperglycistic conditions. These findings suggest that pharmacologic steroid doses may directly alter lens metabolism through a complex mechanism involving, at least in part, a steroid-mediated antagonism of lens glucose uptake and/or utilization.
Adenosine Diphosphate↗
Dynamic changes in the organophosphate profile of the experimental galactose-induced cataract.
Dynamic changes in lens organophosphate metabolites during 24 hr incubation in 30 mM galactose media were measured with phosphorus-31 nuclear magnetic resonance spectroscopy. The following phosphates were quantitated from the intact crystalline lens: adenosine triphosphate (ATP), adenosine diphosphate (ADP), inorganic orthophosphate, alpha-glycerophosphate, phosphorylated hexoses and trioses, nicotinamide adenine dinucleotide, uridine diphosphoglucose and uridine diphosphogalactose, glycerol-3-phosphorylethanolamine and 3-phosphorylcholine, and an unidentified phosphorus-containing molecule. The temporal sequences of metabolic events that define the dynamic rates of accumulation or depletion of lens organophosphates reveal that the first event in the decline of the tissue upon galactose incubation is a net consumption of ATP, which occurs as a sigmoidal function with time and which is typified by a characteristic half-life of 18 hr. Alpha-glycerophosphate accumulated at an increasing rate with time, whereas ADP, inorganic orthophosphate, and the other organophosphates were essentially unchanged. Cataract formation in the subcapsular and superficial cortical regions was visible after 16 hr incubation in the experimental buffer. These findings support the hypothesis that alterations in the organophosphate levels of the lens are contributing factors to the initial formation of the experimental galactose cataract.
Adenosine Diphosphate↗