scholarly journals Effects of adenine nucleotides and phosphate on adenosine triphosphate sulphurylase from Anabaena cylindrica

1977 ◽  
Vol 164 (1) ◽  
pp. 161-167 ◽  
Author(s):  
S K Sawhney ◽  
D J D Nicholas
Keyword(s):  
Enzyme Activity ◽  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
Adenine Nucleotides ◽  
Anabaena Cylindrica ◽  
Sulphate Assimilation ◽  
Atp Sulphurylase

Production of adenosine 5'-[35S]sulphatophosphate by a partially purified ATP sulphurylase from Anabaena cylindrica was inhibited by AMP, ADP and P1. Decreases in enzyme activity in the presence of these inhibitors were reversed by increasing the concentrations of ATP. The adenine nucleotides inhibited the enzyme competitively with respect to ATP. In the presence of P1, ATP showed a positive co-operative effect on enzyme activity. The inhibition by P1 was enhanced by increasing concentrations of MG2+. The effects of the adenine nucleotides and the interaction of P1 and Mg2+ on ATP sulphurylase activity are discussed in relation to the regulation of sulphate assimilation via the energy metabolism of the alga.

scholarly journals Effects of adenine nucleotides on rice-root adenosine triphosphate sulphurylase activity in vitro

1975 ◽  
Vol 149 (1) ◽  
pp. 301-304 ◽  
Author(s):  
F D Onajobi
Keyword(s):  
Adenosine Triphosphate ◽  
Adenine Nucleotides ◽  
Enzymic Activity ◽  
Rice Root ◽  
Supernatant Fraction ◽  
Atp Sulphurylase

The presence of ATP sulphurylase activity in the 30000g supernatant fraction of rice-root homogenate has been demonstrated. Studies of the effects of adenosine and its nucleotides on the enzymic activity showed that AMP activated but that ADP and adenosine inhibited the enzyme.

Evolutionary Consequences of Tradeoffs between Yield and Rate of ATP Production

2002 ◽  
Vol 216 (1) ◽  
Author(s):  
Thomas Pfeiffer ◽  
Sebastian Bonhoeffer
Keyword(s):  
Game Theory ◽  
Population Dynamics ◽  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
Organic Material ◽  
High Yield ◽  
Atp Production ◽  
Cellular Processes ◽  
Quantitative Properties ◽  
Evolutionary Consequences

Adenosine triphosphate (ATP) is a key compound in the energy metabolism of cells and is required to drive vital biochemical reactions. In heterotrophic organisms ATP production is coupled to the degradation of energy-rich organic material taken up from the environment. In the transfer of the environmental energy to cellular processes heterotrophs face a tradeoff, since the conversion of the environmental energy into ATP cannot be both maximally fast and efficient. Here we show how tradeoffs between rate and yield of ATP production arise firstly from thermodynamical principles, and secondly for the ATP production by respiration and fermentation. Using methods derived from game theory and population dynamics we investigate the evolutionary consequences for both tradeoffs. We show that spatially structured environments enable the evolution of efficient pathways with high yield. The strategies of ATP production realized in a population, however, depend on the quantitative properties of the tradeoffs.

scholarly journals Research Progress of Sirtuin4 in Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Yibing Bai ◽  
Jiani Yang ◽  
Ying Cui ◽  
Yuanfei Yao ◽  
Feng Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Energy Metabolism ◽  
Nicotinamide Adenine Dinucleotide ◽  
Enzyme Activities ◽  
Research Progress ◽  
Diverse Range ◽  
Catalytic Activities ◽  
Cellular Processes ◽  
Dependent Protein

Sirtuins (SIRTs) are members of the silent information regulator-2 family. They are a conserved family of nicotinamide adenine dinucleotide-dependent protein lysine deacylases. SIRTS are involved in intricate cellular processes. There are seven subtypes of SIRTs (1–7) in mammals. SIRT4 is located mainly in mitochondria and has various catalytic activities. These enzyme activities give it a diverse range of important biologic functions, such as energy metabolism, oxidative stress, and aging. Cancer is characterized as reprogramming of energy metabolism and redox imbalance, and SIRT4 can affect tumorigenesis. Here, we review the structure, localization, and enzyme activity of SIRT4 and its role in various neoplasms.

Impaired energy metabolism in rat myocardium during phosphate depletion

1982 ◽  
Vol 242 (6) ◽  
pp. F699-F704 ◽  
Author(s):  
N. Brautbar ◽  
R. Baczynski ◽  
C. Carpenter ◽  
S. Moser ◽  
P. Geiger ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Inorganic Phosphorus ◽  
High Energy ◽  
Deficient Diet ◽  
Myocardial Energetics ◽  
Phosphate Depletion ◽  
Myocardial Biopsies ◽  
Mitochondrial Capacity

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.

Control mechanisms in blood fluidity: role of adenosine triphosphate

1963 ◽  
Vol 18 (6) ◽  
pp. 1105-1110 ◽  
Author(s):  
L. O. Pilgeram ◽  
D. A. Loegering
Keyword(s):  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
High Energy ◽  
Control Mechanisms ◽  
High Energy Phosphate ◽  
Cellular Mechanisms ◽  
Blood Fluidity ◽  
Phosphate Linkage ◽  
Glass Surfaces

A possible role for cellular energy metabolism in the control of the blood clotting mechanism has been shown. High-energy phosphate was found to strongly inhibit the recalcification time of plasma prepared with siliconized or glass surfaces. The nucleotide, adenosine triphosphate, in crystalline form and chromatographically pure, will inhibit or completely prevent coagulation in vitro. Reactivity is based primarily on the high-energy phosphate linkage and secondarily upon the nucleoside, adenosine. The principal site of action for ATP is on an unidentified precursor of thromboplastin. Available evidence indicates an important role for energy metabolism in the cellular mechanisms which effect a control over thromboplastin generation and its possible thrombotic and arteriosclerotic sequelae. cellular control mechanisms; blood fluidity; thrombosis arteriosclerosis; aging Submitted on July 1, 1963

scholarly journals Hereditary Nonspherocytic Hemolysis With Erythrocyte Phosphofructokinase Deficiency

Blood ◽  
1972 ◽  
Vol 39 (3) ◽  
pp. 415-425 ◽  
Author(s):  
Larry Waterbury ◽  
Eugene P. Frenkel
Keyword(s):  
Enzyme Activity ◽  
Adenosine Triphosphate ◽  
Lactate Production ◽  
Kinetic Studies ◽  
Glycogen Storage ◽  
Muscle Disease ◽  
Phosphofructokinase Activity ◽  
Phosphofructokinase Deficiency

Abstract Hereditary nonspherocytic hemolysis associated with abnormal erythrocyte phosphofructokinase activity was demonstrated in a young man. Enzyme activity in the propositus, his mother, and maternal grandmother was approximately 60% of normal controls. There was markedly increased lability of enzyme activity on in vitro storage. Kinetic studies revealed increased sensitivity to adenosine triphosphate inhibition. Erythrocyte adenosine triphosphate levels were depressed. The absence of muscle disease and the presence of normal in vivo lactate production following ischemic exercise differentiated this kindred from those with Type VII glycogen storage disease.

Enzyme activity patterns of energy metabolism in skiers of different performance levels (M. quadriceps femoris)

1982 ◽  
Vol 48 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Eva V. Macková ◽  
Arnošt Bass ◽  
štĚpánka šprynarová ◽  
Jan Teisinger ◽  
Karel Vondra ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Energy Metabolism ◽  
Activity Patterns ◽  
Quadriceps Femoris ◽  
Performance Levels

Effects of Bupivacaine on Mitochondrial Energy Metabolism in Heart of Rats following Exposure to Chronic Hypoxia

2002 ◽  
Vol 97 (6) ◽  
pp. 1507-1511 ◽  
Author(s):  
Karine Nouette-Gaulain ◽  
François Forestier ◽  
Monique Malgat ◽  
Roger Marthan ◽  
Jean-Pierre Mazat ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Energy Metabolism ◽  
Left Ventricle ◽  
Adenosine Triphosphate ◽  
Hypobaric Hypoxia ◽  
Chronic Hypoxia ◽  
Left Ventricular ◽  
Mitochondrial Energy Metabolism ◽  
Hypoxic Heart ◽  
The Right

Background Adaptation to chronic exposure to hypoxia alters energy metabolism in the heart, particularly in the left ventricle, which undergoes a loss in oxidative capacity. Highly lipophilic local anesthetics interfere with mitochondrial energy metabolism. The purpose of this study was to compare the effects of bupivacaine on mitochondrial energy metabolism in heart of rats subjected to normoxic or hypoxic environments. Methods Male Wistar rats (n = 10) were subjected to hypobaric hypoxia (simulated altitude = 5,000 m, 380 mmHg) for 2 weeks. Control rats (n = 10) were maintained in an ambient normoxic environment. Mitochondrial metabolism (oxygen consumption and adenosine triphosphate synthesis) was assessed using saponin-skinned ventricular fibers. Bupivacaine (0-5 mM) was tested on both left and right ventricles of normoxic or hypoxic heart. Results In animals exposed to hypobaric hypoxia for 14 days, cardiac mass significantly increased, and the right-to-left ventricular ratio was approximately twofold (0.48 +/- 0.11 vs. 0.22 +/- 0.04, P < 0.05). Oxygen consumption and adenosine triphosphate synthesis were significantly lower in the hypoxic left ventricles but not in the right ones. The uncoupling effect of bupivacaine was more pronounced in the left ventricle from hypoxic heart than in the right ventricle; the bupivacaine-induced decrease in the adenosine triphosphate synthesis rate and in the adenosine triphosphate-to-oxygen ratio was significantly greater in the hypoxic left ventricle than in the normoxic one. Conclusions Chronic hypoxia impairs cardiac energy metabolism in left ventricles and enhances the depressant effects of bupivacaine on mitochondrial functions.

scholarly journals Creatine deficiency and heart failure

2021 ◽  
Author(s):  
Annamaria Del Franco ◽  
Giuseppe Ambrosio ◽  
Laura Baroncelli ◽  
Tommaso Pizzorusso ◽  
Andrea Barison ◽  
...  
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
Creatine Supplementation ◽  
Energy Deficit ◽  
Clinical Value ◽  
Comprehensive Overview ◽  
Cardiac Energy Metabolism ◽  
Creatine Deficiency ◽  
Cardiac Energy

AbstractImpaired cardiac energy metabolism has been proposed as a mechanism common to different heart failure aetiologies. The energy-depletion hypothesis was pursued by several researchers, and is still a topic of considerable interest. Unlike most organs, in the heart, the creatine kinase system represents a major component of the metabolic machinery, as it functions as an energy shuttle between mitochondria and cytosol. In heart failure, the decrease in creatine level anticipates the reduction in adenosine triphosphate, and the degree of myocardial phosphocreatine/adenosine triphosphate ratio reduction correlates with disease severity, contractile dysfunction, and myocardial structural remodelling. However, it remains to be elucidated whether an impairment of phosphocreatine buffer activity contributes to the pathophysiology of heart failure and whether correcting this energy deficit might prove beneficial. The effects of creatine deficiency and the potential utility of creatine supplementation have been investigated in experimental and clinical models, showing controversial findings. The goal of this article is to provide a comprehensive overview on the role of creatine in cardiac energy metabolism, the assessment and clinical value of creatine deficiency in heart failure, and the possible options for the specific metabolic therapy.

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