scholarly journals OXIDATIVE PHOSPHORYLATION BY A CELL-FREE PARTICULATE SYSTEM FROM UNFERTILIZED ARBACIA EGGS

1950 ◽  
Vol 33 (5) ◽  
pp. 547-553 ◽  
Author(s):  
A. K. Keltch ◽  
C. F. Strittmatter ◽  
C. P. Walters ◽  
G. H. A. Clowes
Keyword(s):  
Oxidative Phosphorylation ◽  
Tricarboxylic Acid Cycle ◽  
High Energy ◽  
Equal Weight ◽  
Maximum Oxygen Consumption ◽  
Arbacia Punctulata ◽  
Particulate System ◽  
Mammalian Liver ◽  
A Cell ◽  
Ph Range

1. A cell-free particulate system capable of effecting oxidative phosphorylation has been prepared from unfertilized eggs of Arbacia punctulata. A substantial increase in phosphorylation can be produced by addition of α-ketoglutarate, oxalacetate, or succinate, the magnitude of the increase being greatest with α-ketoglutarate. The activity of the phosphorylating system is sharply dependent on maintenance of a comparatively narrow pH range during both the preparation of the particulate system and its subsequent incubation with oxidizable substrate. 2. The maximum oxygen consumption of the cell-free particulate system derived from a given weight of unfertilized eggs is about three times that of the same weight of intact unfertilized eggs and approximately the same as that of an equal weight of fertilized eggs. 3. The data indicate that generation of high-energy phosphate bonds in the Arbacia egg is coupled, as it is in mammalian liver or kidney, with the functioning of the tricarboxylic acid cycle.

scholarly journals ACTION OF NITRO- AND HALOPHENOLS UPON OXYGEN CONSUMPTION AND PHOSPHORYLATION BY A CELL-FREE PARTICULATE SYSTEM FROM ARBACIA EGGS

1950 ◽  
Vol 33 (5) ◽  
pp. 555-561 ◽  
Author(s):  
G. H. A. Clowes ◽  
A. K. Keltch ◽  
C. F. Strittmatter ◽  
C. P. Walters
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Oxidative Phosphorylation ◽  
High Energy ◽  
Substituted Phenols ◽  
High Energy Phosphate ◽  
Particulate System ◽  
A Cell ◽  
Phosphate Groups ◽  
Stimulation Of

1. The ability of 4,6-dinitrocresol and eight other substituted phenols to stimulate oxygen uptake and inhibit phosphorylation by a cell-free particulate system from unfertilized Arbacia eggs has been determined. Five of those agents can produce both stimulation of oxygen consumption and inhibition of phosphorylation; one inhibits both oxygen consumption and phosphorylation; and two have no effect on either oxygen consumption or phosphorylation. In every case the effects of these substituted phenols upon the cell-free particulate systems parallel those upon oxygen consumption and cleavage in the intact fertilized Arbacia eggs. 2. The data suggest that energy for cleavage of the Arbacia egg is provided at least in part by oxidative phosphorylation and that substituted phenols may block cleavage by interfering with generation and transfer of high-energy phosphate groups.

scholarly journals The ATP Synthase Deficiency in Human Diseases

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 325
Author(s):  
Chiara Galber ◽  
Stefania Carissimi ◽  
Alessandra Baracca ◽  
Valentina Giorgio
Keyword(s):  
Oxidative Phosphorylation ◽  
Atp Synthase ◽  
Mitochondrial Protein ◽  
High Energy ◽  
Neurocognitive Disorders ◽  
Human Diseases ◽  
Age Related ◽  
Muscle Tissues ◽  
Mitochondrial Atp Synthase ◽  
Genes Encoding

Human diseases range from gene-associated to gene-non-associated disorders, including age-related diseases, neurodegenerative, neuromuscular, cardiovascular, diabetic diseases, neurocognitive disorders and cancer. Mitochondria participate to the cascades of pathogenic events leading to the onset and progression of these diseases independently of their association to mutations of genes encoding mitochondrial protein. Under physiological conditions, the mitochondrial ATP synthase provides the most energy of the cell via the oxidative phosphorylation. Alterations of oxidative phosphorylation mainly affect the tissues characterized by a high-energy metabolism, such as nervous, cardiac and skeletal muscle tissues. In this review, we focus on human diseases caused by altered expressions of ATP synthase genes of both mitochondrial and nuclear origin. Moreover, we describe the contribution of ATP synthase to the pathophysiological mechanisms of other human diseases such as cardiovascular, neurodegenerative diseases or neurocognitive disorders.

scholarly journals GATA6 Is Essential for Embryonic Development of the Liver but Dispensable for Early Heart Formation

2005 ◽  
Vol 25 (7) ◽  
pp. 2622-2631 ◽  
Author(s):  
Roong Zhao ◽  
Alistair J. Watt ◽  
Jixuan Li ◽  
Jennifer Luebke-Wheeler ◽  
Edward E. Morrisey ◽  
...  
Keyword(s):  
Cell Fate ◽  
Wild Type ◽  
Gata Factor ◽  
Extraembryonic Endoderm ◽  
Integral Role ◽  
Mammalian Liver ◽  
Septum Transversum ◽  
A Cell ◽  
Heart Formation ◽  
Bud Growth

ABSTRACT Several lines of evidence suggest that GATA6 has an integral role in controlling development of the mammalian liver. Unfortunately, this proposal has been impossible to address directly because mouse embryos lacking GATA6 die during gastrulation. Here we show that the early embryonic deficiency associated with GATA6-knockout mice can be overcome by providing GATA6-null embryos with a wild-type extraembryonic endoderm with the use of tetraploid embryo complementation. Analysis of rescued Gata6 − / − embryos revealed that, although hepatic specification occurs normally, the specified cells fail to differentiate and the liver bud does not expand. Although GATA6 is expressed in multiple tissues that impact development of the liver, including the heart, septum transversum mesenchyme, and vasculature, all are relatively unaffected by loss of GATA6, which is consistent with a cell-autonomous requirement for GATA6 during hepatogenesis. We also demonstrate that a closely related GATA factor, GATA4, is expressed transiently in the prehepatic endoderm during hepatic specification and then lost during expansion of the hepatic primordium. Our data support the proposal that GATA4 and GATA6 are functionally redundant during hepatic specification but that GATA6 alone is available for liver bud growth and commitment of the endoderm to a hepatic cell fate.

scholarly journals Permeability of a Cell Membrane Junction

1969 ◽  
Vol 53 (4) ◽  
pp. 498-515 ◽  
Author(s):  
A. L. Politoff ◽  
S. J. Socolar ◽  
W. R. Loewenstein
Keyword(s):  
Salivary Gland ◽  
Energy Metabolism ◽  
Cell Membrane ◽  
Oxidative Phosphorylation ◽  
Ion Permeability ◽  
Intracellular Injection ◽  
Gland Cells ◽  
Salivary Gland Cells ◽  
Junctional Permeability ◽  
A Cell

The ion permeability of the membrane junctions between Chironomus salivary gland cells is strongly depressed by treatments that are generally known to inhibit energy metabolism. These treatments include prolonged cooling at 6°–8°C, and exposure to dinitrophenol, cyanide, oligomycin, and N-ethylmaleimide. Intracellular injection of ATP appears to prevent depression of junctional permeability by dinitrophenol or to reverse it. Ouabain, azide, p-chloromercuriphenylsulfonic acid, reserpine, and acetazolamide fail to depress junctional permeability. Thus the ion permeability of the junctional membranes appears to depend on energy provided by oxidative phosphorylation. Possible energy-linked processes for maintaining junctional permeability are discussed, including processes involving transport of permeability-modifying species such as Ca++.

scholarly journals Impaired Cerebral Mitochondrial Oxidative Phosphorylation Function in a Rat Model of Ventricular Fibrillation and Cardiopulmonary Resuscitation

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Jun Jiang ◽  
Xiangshao Fang ◽  
Yue Fu ◽  
Wen Xu ◽  
Longyuan Jiang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Cardiopulmonary Resuscitation ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Rat Model ◽  
Mitochondrial Function ◽  
High Energy ◽  
Mitochondrial Morphology ◽  
High Energy Phosphates

Postcardiac arrest brain injury significantly contributes to mortality and morbidity in patients suffering from cardiac arrest (CA). Evidence that shows that mitochondrial dysfunction appears to be a key factor in tissue damage after ischemia/reperfusion is accumulating. However, limited data are available regarding the cerebral mitochondrial dysfunction during CA and cardiopulmonary resuscitation (CPR) and its relationship to the alterations of high-energy phosphate. Here, we sought to identify alterations of mitochondrial morphology and oxidative phosphorylation function as well as high-energy phosphates during CA and CPR in a rat model of ventricular fibrillation (VF). We found that impairment of mitochondrial respiration and partial depletion of adenosine triphosphate (ATP) and phosphocreatine (PCr) developed in the cerebral cortex and hippocampus following a prolonged cardiac arrest. Optimal CPR might ameliorate the deranged phosphorus metabolism and preserve mitochondrial function. No obvious ultrastructural abnormalities of mitochondria have been found during CA. We conclude that CA causes cerebral mitochondrial dysfunction along with decay of high-energy phosphates, which would be mitigated with CPR. This study may broaden our understanding of the pathogenic processes underlying global cerebral ischemic injury and provide a potential therapeutic strategy that aimed at preserving cerebral mitochondrial function during CA.

scholarly journals IN VITRO EFFECTS OF FLUORIDE ON TRICARBOXYLIC ACID CYCLE DEHYDROGENASES AND OXIDATIVE PHOSPHORYLATION: PART I

1967 ◽  
Vol 15 (4) ◽  
pp. 195-201 ◽  
Author(s):  
C. JAMES LOVELACE ◽  
GENE W. MILLER
Keyword(s):  
Oxidative Phosphorylation ◽  
Competitive Inhibition ◽  
Tricarboxylic Acid Cycle ◽  
Succinic Dehydrogenase ◽  
Tricarboxylic Acid ◽  
Initial Increase ◽  
Acid Cycle ◽  
Oxidase System ◽  
Vitro Effect

Studies were conducted on the in vitro effect of fluoride on the succinic oxidase system utilizing mitochondria obtained from cauliflower. Preincubation of mitochondria with fluoride did not increase inhibition of succinic oxidase. Various other tricarboxylic acid cycle substrates were used to determine their sensitivity to fluoride; only succinate oxidation was affected. A series of succinate concentrations in the presence and in the absence of fluoride showed increased activity of succinic dehydrogenase, which indicated competitive inhibition. Various concentrations of phosphate in the absence of fluoride showed that phosphate had only slight effects on the succinic 2,6-dichlorophenolindophenol reductase component of the succinic oxidase system. In the absence of phosphate, various concentrations of fluoride showed an initial increase in activity followed by a decrease in activity of succinic 2,6-dichlorophenolindophenol reductase. In the presence of phosphate, fluoride caused marked inhibition of succinic 2,6-dichlorophenolindophenol reductase. It is believed that this inhibition results from an enzyme-fluorophosphate complex which has a lower dissociation constant than that of the enzyme-substrate complex. An oxidative phosphorylation study indicated that both respiration and phosphorylation were inhibited.

Oxidative phosphorylation and respiratory control in mitochondria from Aspergillus oryzae

1969 ◽  
Vol 15 (8) ◽  
pp. 975-977 ◽  
Author(s):  
K. Watson ◽  
W. Paton ◽  
J. E. Smith
Keyword(s):  
Bovine Serum Albumin ◽  
Oxidative Phosphorylation ◽  
Aspergillus Oryzae ◽  
Reaction Medium ◽  
Respiratory Control ◽  
Adenosine Diphosphate ◽  
Yeast Mitochondria ◽  
Active Oxidation ◽  
Isolated Mitochondria ◽  
Ph Range

Mitochondria isolated from Aspergillus oryzae exhibited respiratory control with a range of substrates. Bovine serum albumin was required in the reaction medium to observe adenosine diphosphate (ADP) controlled respiration. The mitochondria carried out active oxidation and phosphorylation with citrate as substrate in the pH range 6–7 and showed a slight optimum for oxidative phosphorylation at pH 6.5. The respiratory properties of the isolated mitochondria were similar to those reported for A. niger and yeast mitochondria.

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