High-energy phosphate compounds and some glycolytic substrates in the rat brain during hypoxia

1979 ◽  
Vol 4 (4) ◽  
pp. 261-264 ◽  
Author(s):  
Barbara Broniszewska-Ardelt ◽  
Marianna Sikorska
Keyword(s):  
Rat Brain ◽  
High Energy ◽  
High Energy Phosphate ◽  
Phosphate Compounds

DIVERSITY OF METABOLIC PATTERNS IN HUMAN BRAIN TUMORS?I. HIGH ENERGY PHOSPHATE COMPOUNDS AND BASIC COMPOSITION

1977 ◽  
Vol 29 (6) ◽  
pp. 959-977 ◽  
Author(s):  
O. H. Lowry ◽  
S. J. Berger ◽  
M. M.-Y. Chi ◽  
J. G. Carter ◽  
A. Blackshaw ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Human Brain ◽  
High Energy ◽  
High Energy Phosphate ◽  
Basic Composition ◽  
Human Brain Tumors ◽  
Phosphate Compounds

Cerebral high-energy compounds: changes in anoxia

1962 ◽  
Vol 202 (1) ◽  
pp. 77-79 ◽  
Author(s):  
Richard N. Lolley ◽  
Frederick E. Samson
Keyword(s):  
Ion Exchange ◽  
Rat Brain ◽  
Adenosine Triphosphate ◽  
Energy Flow ◽  
Inorganic Phosphate ◽  
High Energy ◽  
High Energy Phosphate ◽  
Guanosine Triphosphate ◽  
Inosine Monophosphate ◽  
Flow Through

Acid-soluble phosphates of rat brain during anoxia were determined by ion-exchange and chemical procedures. There is a general shift during anoxia of triphosphate nucleotides to monophosphates and a very rapid breakdown of phosphoryl-creatine. However, total phosphate leaving the high-energy phosphate pool is not equal to the changes in inorganic phosphate; inorganic phosphate change is much larger than high-energy phosphate change in early anoxia and much smaller in extended anoxia. The patterns of guanosine triphosphate and uridine triphosphate changes are more complex than adenosine triphosphate changes. Nicotinamideadenine dinucleotide levels are steady until late anoxia, at which time they decrease slightly. Cytidine monophosphate is the only cytidine nucleotide detected. Inosine nucleotide concentrations in control animals were below the limit of the method, but in late anoxia inosine monophosphate appeared. The data show that the energy flow through the phosphates in brain is rapid and involves phosphate compounds other than the acid-soluble nucleotides and phosphoryl-creatine.

Depletion of high energy phosphate compounds in the tumor-bearing state and reversal after tumor resection

Surgery ◽  
1996 ◽  
Vol 120 (3) ◽  
pp. 534-541 ◽  
Author(s):  
Steven N. Hochwald ◽  
Lawrence E. Harrison ◽  
Jeffrey L. Port ◽  
David Blumberg ◽  
Murray F. Brennan ◽  
...  
Keyword(s):  
Tumor Resection ◽  
High Energy ◽  
High Energy Phosphate ◽  
Tumor Bearing ◽  
Phosphate Compounds

Effect of cyclocreatine feeding on levels of amino acids in rat hearts before and after an ischemic episode

1991 ◽  
Vol 261 (6) ◽  
pp. H1919-H1926
Author(s):  
M. Osbakken ◽  
D. N. Zhang ◽  
D. Nelson ◽  
M. Erecinska
Keyword(s):  
Amino Acids ◽  
High Energy ◽  
Global Ischemia ◽  
Sprague Dawley ◽  
High Energy Phosphate ◽  
Rat Hearts ◽  
Before And After ◽  
Reperfusion Period ◽  
Phosphate Compounds

Feeding Sprague-Dawley rats for 3 wk a diet containing 1% by weight of cyclocreatine increased the reservoir of the high-energy phosphate compounds but also caused alterations in the levels of the two key amino acids, aspartate and glutamate. Both were decreased by approximately 50% in the presence of an unaltered content of glutamine. In vitro exposure of these hearts to sequential perfusion, global ischemia, and reperfusion in the absence of added amino acids resulted in changes in aspartate, glutamate, and glutamine that were different from those in hearts from control rats. In the cyclocreatine-fed group, aspartate concentration ([aspartate]) and [glutamate] fell after global ischemia, whereas [glutamine] was unaltered. [Glutamine] decreased, however, in the reperfusion period. In control hearts, the predominant effect was a steady decline in glutamine, which was accompanied by either less than 10% (after global ischemia) or 30-50% fall (after reperfusion) in [aspartate] and [glutamate]. The concentration of tissue Pi was smaller in hearts from cyclocreatine-fed rats and appeared to increase more slowly during ischemia. In the presence of rotenone and aminooxyacetate, heart homogenates catalyzed production of glutamate from glutamine, which was markedly stimulated by Pi and inhibited by H+. It is postulated that 1) phosphate-activated glutaminase is an important enzyme that determines cardiac [glutamate], 2) lower [phosphate] in hearts from rats fed cyclocreatine is responsible for the apparently lesser activity of glutaminase, 3) breakdown of the high-energy phosphate compounds and consequent rise in Pi activates glutaminase, and 4) slow breakdown of glutamine during global ischemia is a result of inhibition of glutaminase by H+.

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