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At least 991 records · Page 55Linked to original sources
PubMed1998

Relationship between intracellular phosphate, proton motive force, and rate of nongrowth energy dissipation (energy spilling) in Streptococcus bovis JB1.

When the rate of glucose addition to nongrowing Streptococcus bovis cell suspensions was increased, the fermentation was homolactic, fructose-1,6-diphosphate (FDP) increased, intracellular inorganic phosphate (P(i)) declined, and the energy-spilling rate increased. ATP and ADP were not significantly affected by glucose consumption rate, but the decrease in P(i) was sufficient to cause an increase in the free energy of ATP hydrolysis (delta G'p). The increase in delta G'p was correlated with an increase in proton motive force (delta p). S. bovis continuous cultures (dilution rate of 0.65 h-1) that were provided with ammonia as the sole nitrogen source also had high rates of lactate production and energy spilling. When Trypticase was added as a source of amino acids, lactate production decreased; a greater fraction of the glucose was converted to acetate, formate, and ethanol; and the energy-spilling rate decreased. Trypticase also caused a decrease in FDP, an increase in P(i), and a decrease in delta p. The change in delta p could be explained by P(i)-dependent changes in the delta G'p. When P(i) declined, delta G'p and delta p increased. The ratio of delta G'p to delta p (millivolt per millivolt) was always high (> 4) at low rates of energy spilling but declined when the energy-spilling rate increased. Based on these results, it appears that delta p and the energy-spilling rate are responsive to fluctuations in the intracellular P(i) concentration.

Adenosine Triphosphate↗
PubMed2003

Substrate channelling in a creatine kinase system of rat skeletal muscle under various pH conditions.

The aim of this study was to evaluate myofibrillar creatine kinase (CK) activity and to quantify the substrate channelling of ATP between CK and myosin ATPase under different pH conditions within the integrity of myofibrils. A pure myofibrillar fraction was prepared using differential centrifugation. The homogeneity of the preparation and the purity of the fraction were confirmed microscopically and by enzymatic assays for contaminant enzyme activities. The specific activity of myofibrillar CK reached 584 +/- 33 nmol PCr min(-1) mg(-1) at pH 6.75. Two methods were used to detect CK activity: (1) measurement of direct ATP production, and (2) measurement of PCr consumption. This method of evaluation has been tested in experiments with isolated creatine kinase. No discrepancy in CK activity between the methods was observed in the pH range tested (6.0-7.5). However, the same procedures resulted in a significant discrepancy between the amounts of reacted PCr and produced ATP within the pure myofibrillar fraction. This discrepancy represents the portion of ATP produced by the CK reaction, which is preferentially channelled to the myosin ATPase before diffusing into the bulk solution. The maximum evaluated difference reached 42.3 % at pH 6.95. The substrate channelling between myofibrillar-bound CK and myosin ATPase was evaluated under various pH levels within the physiological range and it reached a maximum value in a slightly acidic environment. These results suggest that ATP/ADP flux control by the CK system is more important at lower pH, corresponding to the physiological state of muscle fatigue.

Adenosine Triphosphate↗
PubMed2005

[Effect of alcohol on brain mitochondria development of mouse embryos].

OBJECTIVE: To probe the effect of alcohol consumption on brain mitochondria development of mouse embryos. METHODS: Pregnant mice were given alcohol intragastrically from pregnant day (PD) 6 - 5. On PD 18, embryos were dissected out and the brain mitochondria were extracted. Then mitochondria membrane potential, activities of mitochondria respiratory chain complex I, IV and ATPase, and ATP content were measured in vitro. RESULTS: The ratio of fetal brain/body weight decreased as the maternal alcohol dosage increasing. An increased proportion of immature mitochondria, from 18 percent to 34 percent, was detected by flow cytometry. Reduced activities of respiratory chain complexes I and IV were found in 3.0 g/kg/day (91.7% and 87.9% respectively) and 6.0 g/kg/day alcohol exposure groups (72.4% and 69.7% respectively). Only 6.0 g/kg/day ethanol exposure group showed significantly reduced activity (80.3% of control) of ATPase. ATP contents in the fetal brain mitochondria of 3.0 g/kg/day and 6.0 g/kg/day maternal alcohol exposure groups were significantly less than that of control, implying an impaired mechanism of ATP synthesis and/ or uptake. CONCLUSION: Alcohol consumption during pregnancy can affect embryo brain mitochondria development, which may be related to the neural tube defects induced by alcohol.

Animals↗
PubMed2003

Acetylcholine affects rat liver metabolism via type 3 muscarinic receptors in hepatocytes.

Although the role of acetylcholine (Ach) in hepatic glucose metabolism is well elucidated, it is still unclear if it influences gluconeogenesis, glycogenolysis and high-energy phosphate metabolism, and if it does what the mechanisms of this influence are. Therefore, using isolated perfused rat liver as a model, we have studied the effect of Ach on oxygen consumption, synthesis of glucose from lactate and pyruvate, glycogen formation, mitochondrial oxidative phosphorylation and ATP-synthesis. We have established that effects of Ach on oxygen consumption depend on its concentration. When used at a concentration of 10(-7) M, Ach exerts maximum stimulatory effect, while its infusion at 10(-6) M causes a decrease of oxygen consumption by the liver. Moreover, when used at a concentration of 10(-6) M or 10(-7) M, Ach increases rates of glucose production from the gluconeogenic substrates lactate and pyruvate, leading to enhanced glycogen content in perfused liver. It was also shown that Ach possesses a stimulating effect on alanine and aspartate aminotransferases. As detected by 31P NMR spectroscopy, continuous liver perfusion with pyruvate and lactate in the presence of Ach leads to a significant decrease of ATP level, implying enhanced energy requirements for gluconeogenesis under these conditions. Elimination of the described effects of Ach by atropine, the antagonist of muscarinic receptors, and identification of the type 3 muscarinic receptors (m3) in isolated hepatocytes as well as in whole liver, imply that Ach may exert its effect on liver metabolism through m3 receptors.

Acetylcholine↗
PubMed2006

Increasing glycolytic flux in Torulopsis glabrata by redirecting ATP production from oxidative phosphorylation to substrate-level phosphorylation.

AIMS: This study aimed at further increasing the pyruvate productivity of a multi-vitamin auxotrophic yeast Torulopsis glabrata by redirecting ATP production from oxidative phosphorylation to substrate-level phosphorylation. METHODS AND RESULTS: We examined two strategies to decrease the activity of F0F1-ATPase. The strategies were to inhibit F0F1-ATPase activity by addition of oligomycin, or to disrupt F0F1-ATPase by screening neomycin-resistant mutant. The addition of 0.05 mmol l(-1) oligomycin to the culture broth of T. glabrata CCTCC M202019 resulted in a significantly decreased intracellular ATP level (35.7%) and a significantly increased glucose consumption rate (49.7%). A neomycin-resistant mutant N07 was screened and selected after nitrosoguanidine mutagenesis of the parent strain T. glabrata CCTCC M202019. Compared with the parent strain, the F0F1-ATPase activity of the mutant N07 decreased about 65%. As a consequence, intracellular ATP level of the mutant N07 decreased by 24%, which resulted in a decreased growth rate and growth yield. As expected, glucose consumption rate and pyruvate productivity of the mutant N07 increased by 34% and 42.9%, respectively. Consistently, the activities of key glycolytic enzymes of the mutant N07, including phosphofructokinase, pyruvate kinase and glyceraldehyde-3-phosphate dehydrogenase, increased by 63.7%, 28.8% and 14.4%, respectively. In addition, activities of the key enzymes involved in electron transfer chain of the mutant N07 also increased. CONCLUSIONS: Impaired oxidative phosphorylation in T. glabrata leads to a decreased intracellular ATP production, thereby increasing the glycolytic flux. SIGNIFICANCE AND IMPACT OF THE STUDY: The strategy of redirecting ATP production from oxidative phosphorylation to substrate-level phosphorylation provides an alternative approach to enhance the glycolytic flux in eukaryotic micro-organisms.

Adenosine Triphosphate↗
PubMed2000

ATP synthesis during low-flow ischemia: influence of increased glycolytic substrate.

BACKGROUND: Our goals were to (1) simulate the degree of low-flow ischemia and mixed anaerobic and aerobic metabolism of an acutely infarcting region; (2) define changes in anaerobic glycolysis, oxidative phosphorylation, and the creatine kinase (CK) reaction velocity; and (3) determine whether and how increased glycolytic substrate alters the energetic profile, function, and recovery of the ischemic myocardium in the isolated blood-perfused rat heart. METHODS AND RESULTS: Hearts had 60 minutes of low-flow ischemia (10% of baseline coronary flow) and 30 minutes of reperfusion with either control or high glucose and insulin (G+I) as substrate. In controls, during ischemia, rate-pressure product and oxygen consumption decreased by 84%. CK velocity decreased by 64%; ATP and phosphocreatine (PCr) concentrations decreased by 51% and 63%, respectively; inorganic phosphate (P(i)) concentration increased by 300%; and free [ADP] did not increase. During ischemia, relative to controls, the G+I group had similar CK velocity, oxygen consumption, and tissue acidosis but increased glycolysis, higher [ATP] and [PCr], and lower [P(i)] and therefore had a greater free energy yield from ATP hydrolysis. Ischemic systolic and diastolic function and postischemic recovery were better. CONCLUSIONS: During low-flow ischemia simulating an acute myocardial infarction region, oxidative phosphorylation accounted for 90% of ATP synthesis. The CK velocity fell by 66%, and CK did not completely use available PCr to slow ATP depletion. G+I, by increasing glycolysis, slowed ATP depletion, maintained lower [P(i)], and maintained a higher free energy from ATP hydrolysis. This improved energetic profile resulted in better systolic and diastolic function during ischemia and reperfusion. These results support the clinical use of G+I in acute MI.

Adenosine Triphosphate↗
PubMed1986

Inhibition of ureogenesis in isolated rat liver cells by a non-steroidal anti-inflammatory drug (butibufen).

The effect of a non-steroidal anti-inflammatory drug (butibufen) on ureogenesis in isolated rat hepatocytes has been studied. Butibufen at 0.4 mM, and particularly at 2 mM, strongly inhibited urea synthesis. The drug at these concentrations also inhibited markedly carbamoylphosphate synthetase activity. In addition, 2 mM butibufen lowered ATP concentrations of the cells and enhanced oxygen consumption in isolated liver mitochondria. The results suggest that the inhibition by 0.4 mM butibufen on carbamoylphosphate synthetase activity can account for the entire inhibition of ureogenesis, whereas the decreased cellular ATP concentration at 2 mM butibufen might be at least partly responsible for low carbamoylphosphate synthesis and thus, for reduced urea production. The decrease in ATP levels probably results from uncoupling effects of butibufen on oxidative phosphorylation.

Adenosine Triphosphate↗
PubMed2002

The role of mitochondrial and sarcolemmal K(ATP) channels in canine ethanol-induced preconditioning in vivo.

UNLABELLED: Chronic consumption of small doses of ethanol protects myocardium from ischemic injury. We tested the hypothesis that mitochondrial and sarcolemmal adenosine triphosphate-dependent potassium (K(ATP)) channels mediate these beneficial effects. Dogs (n = 76) were fed with ethanol (1.5 g/kg) or water mixed with dry food bid for 6 or 12 wk, fasted overnight before experimentation, and instrumented for measurement of hemodynamics. Dogs received intracoronary saline (vehicle), 5-hydroxydecanoate (a mitochondrial K(ATP) channel antagonist; 6.75 mg/kg over 45 min), or HMR-1098 (a sarcolemmal K(ATP) channel antagonist; 45 microg/kg over 45 min) and were subjected to a 60 min coronary artery occlusion followed by 3 h of reperfusion. A final group of dogs was pretreated with ethanol and chow for 6 wk before occlusion and reperfusion. Myocardial infarct size and transmural coronary collateral blood flow were measured with triphenyltetrazolium chloride staining and radioactive microspheres, respectively. The area at risk of infarction was similar between groups. A 12-wk pretreatment with ethanol significantly reduced infarct size to 13% +/- 2% (mean +/- SEM; n = 8) of the area at risk compared with control experiments (25% +/- 2%; n = 8), but a 6-wk pretreatment did not (21% +/- 2%; n = 8). 5-hydroxydecanoate and HMR-1098 abolished the protective effects of 12-wk ethanol pretreatment (24% +/- 2% and 29% +/- 3%, respectively; n = 8 for each group) but had no effect in dogs that did not receive ethanol (22% +/- 2% and 23% +/- 4%, respectively; n = 8 for each group). No differences in hemodynamics or transmural coronary collateral blood flow were observed between the groups. The results indicate that mitochondrial and sarcolemmal K(ATP) channels mediate ethanol-induced preconditioning in dogs independent of alterations in systemic hemodynamics or coronary collateral blood flow. IMPLICATIONS: Mitochondrial and sarcolemmal K(ATP) channels mediate ethanol-induced preconditioning independent of alterations in systemic hemodynamics or coronary collateral perfusion in vivo.

Adenosine Triphosphate↗
PubMed1984

O2 consumption, aerobic glycolysis and tissue phosphagen content during activation of the Na+/K+ pump in rat portal vein.

Oxygen consumption, lactate production and tissue contents of ATP, phosphocreatine (PCr) and lactate were measured following readdition of K+ to K+-depleted rat portal veins, in order to study the energy turnover associated with Na+/K+ pumping. During incubation in K+-free medium at 37 degrees C spontaneous contractions disappeared in 10-20 min. Readdition of K+ (5.9 mM) after 40 min K+-free incubation caused hyperpolarization of the cell membrane for the first 5-10 min and then gradual depolarization with return of spontaneous action potentials and contractions by 10-20 min. During the first 4-6 min after K+ readdition aerobic lactate production was about doubled and then gradually returned to the original level (0.17 mumol/min g) at about 20 min. The increase in glycolytic rate was prevented by 1 mM ouabain. In contrast, O2 consumption (in K+-free medium, 0.38 mumol/min g) rose by about 10% when K+ was added and this increase lasted about 5 min. By 8 min after K+ addition the increased glycolysis and oxidative phosphorylation had accounted for each about the same amount of extra ATP generation over that extrapolated from the steady rate before K+ addition. The average total increase in ATP turnover in the first 8 min was 15%. During this period there was no change in the cellular content of ATP, PCr, or extractable ADP. The results indicate that Na+/K+ pumping utilizes a relatively small share of the total energy turnover in the vascular smooth muscle but is to a large extent dependent on aerobic glycolysis and therefore a major site of carbohydrate usage.

Aerobiosis↗
PubMed2002

ATP-sensitive K(+) channels in the brain: sensors of hypoxic conditions.

Rapid minimization of energy consumption in excitable tissues is effective protection from lethal effects of extreme metabolic stress. The ATP-sensitive K(+) channels in the brain respond in ATP-depleted metabolic states such as hypoxia and may be involved in the protection mechanism against energy-consuming generalized seizure.

Adenosine Triphosphate↗
PubMed1994

Myocardial energetics and blood flow in acute rapid ventricular pacing.

The mechanism whereby chronic rapid ventricular pacing induces severe heart failure is unclear, but the phenomenon is associated with a reduction in left ventricular ATP levels. Accordingly, the current study was undertaken to evaluate the acute effects of rapid ventricular pacing on hemodynamics, left ventricular adenine nucleotide levels, myocardial blood flow, and oxygen consumption. Anesthetized dogs (n = 7) were studied in sinus rhythm and during 30 min of pacing at 250 beats/min. Pacing caused a significant (means +/- SD, all p < 0.001) decrease in cardiac output (3.0 +/- 0.6 to 2.0 +/- 0.6 L/min) and peak left ventricular systolic pressure (133 +/- 14 to 82 +/- 10 mmHg (1 mmHg = 133.3 Pa)) and an increase in pulmonary wedge pressure (10 +/- 2 to 18 +/- 3 mmHg). Following pacing, the peak first derivative of left ventricular pressure and the relaxation time constant, tau, remained unchanged compared with baseline values. Myocardial blood flow and oxygen consumption both increased by 70% with pacing. The transmural distribution of myocardial blood flow and myocardial lactate consumption remained unchanged. There was no change in left ventricular ATP or ADP levels with the observed increase in myocardial oxygen consumption. Therefore, the hemodynamic deterioration associated with acute rapid ventricular pacing, in contrast to that of chronic pacing, is not associated with perturbed myocardial energetics.

Adenine Nucleotides↗
PubMed1990

Relation between the O2 supply:demand ratio, MVO2, and adenosine formation in hearts stimulated with inotropic agents.

Mooted controllers of adenosine formation in heart are the oxygen supply:demand ratio, myocardial oxygen consumption (MVO2), the cytosolic phosphorylation potential (log[ATP]/[ADP][Pi]). The relationship between these parameters and purine release (adenosine + inosine) into the venous effluent was examined in isovolumic rat hearts perfused at 20 and 12 mL.min-1.g-1 with a glucose containing crystalloid buffer and stimulated with inotropic agents (isoproterenol, norepinephrine, 3-isobutyl-1-methylxanthine, and ouabain). The oxygen supply:demand ratio and MVO2 were continuously determined using an oxygen electrode to monitor oxygen supply and consumption. The phosphorylation potential was calculated from phosphorus metabolite levels determined by 31P-NMR spectroscopy and HPLC analysis. Left ventricular function was assessed as the rate-pressure product. All inotropic agents increased the rate-pressure product, with increases in function being greater in the hearts perfused at 20 mL.min-1.g-1. MVO2 was linearly related to the rate-pressure product at each flow rate; however, the hearts perfused at 20 mL.min-1.g-1 exhibited approximately twofold greater MVO2 values for similar rate-pressure product values. All inotropic agents increased adenosine release into the venous effluent. While there was a significant linear relation between adenosine formation and MVO2 in hearts perfused at both flow rates and stimulated with drugs, the relations differed with adenosine release being approximately fourfold greater in hearts perfused at 12 mL.min-1.g-1 under similar conditions of MVO2. Adenosine formation correlated exponentially with the ratio of oxygen supply:demand under all conditions (r = 0.97) and the relation did not differ significantly between hearts perfused at different rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1987

Platelet storage lesion in second-generation containers: correlation with platelet ATP levels.

The nature of platelet lesion occurring with storage of platelet concentrates (PC) in second-generation containers was investigated using various storage media and storage periods up to 14 days. In CPD-plasma (control medium), the changes which occurred progressively during storage were loss of discoid shape, microscopic platelet aggregate formation, fragmentation and the appearance of disintegrated, 'balloon' forms. By day 14 less than 10% of the platelets were discoid in shape, the platelet count had decreased by 23%, and there was a 5-fold increase in the amount of lactate dehydrogenase in plasma. Associated with this was a decrease in the platelet oxygen consumption rate, D(O2), loss of cellular ATP and extent of ADP-induced shape change, and a decrease in the hypotonic shock response. These parameters decreased at a similar rate, with a 50% decrease (t1/2) at days 7-9. They correlated highly with each other during storage and also with a fall in pH. At day 14 of storage, mean pH was 6.1 +/- 0.3. To evaluate the effect of pH stabilization during storage, 4 mEq sodium bicarbonate was added to PC in CPD-plasma. Although pH maintenance was much improved, 7.2-6.6 during 14 days of storage, the same in vitro lesions developed, although more slowly. The t1/2 of the same parameters was prolonged for approximately two days. When PC were stored in a plasma-free physiologic salt solution whose salt composition was similar to CPD-plasma, the t1/2 of the parameters increased to 11-15 days of storage, although the platelets eventually developed the same in vitro lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1986

On the interaction between anthralin and mitochondria: a revision.

Anthralin is an inhibitor of oxidative phosphorylation at concentrations found in vivo. ADP-stimulated oxygen consumption is diminished. Consequently, the rate of ATP synthesis is reduced and mitochondrial ATP content declines. Neither the isolated ATPase (F1F0-ATPase), nor the mitochondrial membrane-bound ATPase are influenced by the drug. Respiration under resting conditions is not affected. The experimental data unequivocally indicate that anthralin is not an uncoupler of oxidative phosphorylation, as previously stated. Furthermore, the interpretation that respiratory deficiency induced in yeast strains by anthralin is a consequence of petite mutations has to be reconsidered. Under in vivo conditions, anthralin inhibits respiration per se. Our experiments, including the electron spin resonance spectroscopy, reveal that anthralin alters mitochondrial membrane structure and function simultaneously. A redox or free-radical mediated step may be involved. In consequence, inhibition of ATP production occurs which may become the limiting factor for increased cellular metabolism in psoriasis.

Adenine Nucleotides↗
PubMed1989

Impaired energy metabolism in platelets from patients with Wiskott-Aldrich syndrome.

The platelet function defect seen in patients with Wiskott-Aldrich syndrome (WAS) has been ascribed to abnormal mitochondrial energy generation. The present study reveals a reduced energy content and low adenylate energy charge in platelets from two WAS-patients. Energy consumption in the resting platelets is slightly beyond the normal range, especially when ATP-resynthesis is primarily glycolytic. When platelets are stimulated with thrombin, the increase in energy consumption is 40-60% lower than in controls, both when energy is produced in glycolysis as when the mitochondria supply most of the energy. Analysis of the electron transport chain reveals no abnormalities. In contrast, the balance between glycolytic and mitochondrial ATP resynthesis is disturbed with a lowered contribution of oxidative ATP production. No such abnormalities are found in two WAS-carriers with the exception of a slight impairment in energy consumption during stimulation with thrombin. Thus, the platelet malfunction in WAS may be caused by a defect in the regulation of energy generation.

Adenosine Diphosphate↗
PubMed1995

Effect of substrate on mitochondrial NADH, cytosolic redox state, and phosphorylated compounds in isolated hearts.

The effect of metabolic substrates on the relation among cytosolic redox state (NADHc/NAD+) mitochondrial NADH (NADHm), and [ATP]/([ADP] x [Pi]) was studied in isolated working rabbit hearts. Substrates were varied from 5.6 mM glucose alone to glucose in combination with 10 mM lactate and/or 10 mM pyruvate while afterload and preload were held constant. Changes in NADHm were determined from epicardial NADH fluorescence. The ratio of glycerol 3-phosphate (G-3-P) to dihydroxyacetone phosphate (DHAP), determined from tissue extracts, was used as an index of cytosolic redox. Myocardial 31P metabolites were measured using nuclear magnetic resonance spectroscopy. The addition of pyruvate to the perfusion medium caused increases in myocardial oxygen consumption (MVo2), NADHm fluorescence, phosphocreatine (PCr), and [ATP]/([ADP] x [Pi]) and a decrease in NADHc/NADc+ (decreased G-3-P/DHAP). Although the addition of lactate to the perfusion medium caused an increase in NADHm similar to pyruvate, MVo2 and PCr did not change significantly, [ATP]/([ADP] x [Pi]) increased less than with pyruvate, and there was an increase in NADHc/NADc+. The findings suggest that variations in the cytosolic redox state do not necessarily result in obligatory changes in either the mitochondrial redox state or in the [ATP]/([ADP] x [Pi]). This implies that under the conditions of this study an equilibrium is not maintained between [ATP]/([ADP] x [Pi]) and NADHc/NADc+. Furthermore, similar levels of NADHm can be associated with different values for [ATP]/([ADP] x [Pi]) and MVo2, depending on the substrates available to the heart.

Adenosine Diphosphate↗
PubMed2025

Dominant negative ATP5F1A variants disrupt oxidative phosphorylation causing neurological disorders.

ATP5F1A encodes the &#x3b1;-subunit of complex V of the respiratory chain, which is responsible for mitochondrial ATP synthesis. We describe 6 probands with heterozygous de novo missense ATP5F1A variants that presented with developmental delay, intellectual disability, and movement disorders. All variants were located at the contact points between the &#x3b1;- and &#x3b2;-subunits. Functional studies in C. elegans revealed that the variants were damaging via a dominant negative genetic mechanism. Biochemical and proteomics studies of proband-derived cells showed a marked reduction in complex V abundance and activity. Mitochondrial physiology studies revealed increased oxygen consumption, yet decreased mitochondrial membrane potential and ATP levels indicative of uncoupled oxidative phosphorylation as a pathophysiologic mechanism. Our findings contrast with the previously reported ATP5F1A variant, p.Arg207His, indicating a different pathological mechanism. This study expands the phenotypic and genotypic spectrum of ATP5F1A-associated conditions and highlights how functional studies can provide an&#xa0;understanding of the genetic, molecular, and cellular mechanisms of ATP5F1A variants of uncertain significance. With 12 heterozygous individuals now reported, ATP5F1A is the most frequent nuclear genome cause of complex V deficiency.

Humans↗
PubMed1985

Effect of sulfite on the energy metabolism of mammalian tissues in correlation to sulfite oxidase activity.

Mammalian tissues show significant differences in the activity of sulfite oxidase (EC 1.8.3.1) which detoxifies sulfite by oxidation to sulfate. Lung tissue and phagocytic cells such as alveolar macrophages, peritoneal macrophages, Kupffer cells and granulocytes show very low activities of sulfite oxidase. Liver tissue and hepatocytes, however, exhibit high activities of sulfite oxidase. Lung tissue and macrophages show an almost 100% decrease of the intracellular ATP levels when incubated with 1 mM sulfite at pH 6 for 30 min. In addition, the O2 consumption of lung tissue is inhibited by 1 mM sulfite at pH 6 by more than 80%. This sulfite-induced decrease of the ATP level and of the O2 consumption of lung tissue is enhanced between pH 6.0 and pH 7.4 with decreasing pH value of the incubation medium. In contrast, the ATP levels in liver tissue and hepatocytes are not affected by 1 mM sulfite at pH 6. The O2 consumption of liver tissue and hepatocytes is significantly increased by sulfite due to the high activities of sulfite oxidase. Therefore, the activity of the 'sulfite-detoxifying enzyme' sulfite oxidase and the sensitivity of the energy metabolism to sulfite show a reciprocal relationship in the tissues and cells studied.

Adenosine Triphosphate↗