Effects of Metabolic Inhibitors on Energy Metabolism of Ehrlich Ascites Carcinoma Cells

Nature ◽  
1965 ◽  
Vol 205 (4966) ◽  
pp. 44-46 ◽  
Author(s):  
I. J. BICKIS ◽  
J. H. QUASTEL
Keyword(s):  
Energy Metabolism ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Metabolic Inhibitors ◽  
Ehrlich Ascites

STUDIES ON THE BIOSYNTHESIS OF NUCLEOTIDES IN EHRLICH ASCITES CARCINOMA CELLS IN VITRO

1965 ◽  
Vol 43 (2) ◽  
pp. 209-224 ◽  
Author(s):  
B. I. Uppin ◽  
P. G. Scholefield
Keyword(s):  
Exchange Reaction ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
The Other ◽  
Metabolic Inhibitors ◽  
Ehrlich Ascites ◽  
Oxidative Pathway ◽  
Time Courses ◽  
Oxidation Of Glucose

Studies have been made of the effects of metabolic inhibitors on the oxidation and incorporation of radioactivity into nucleotides of glucose labelled in the 1, 2, and 6 positions. The results indicate that in Ehrlich ascites carcinoma cells the predominant oxidative pathway is the hexosemonophosphate shunt. Investigation of the time courses of oxidation of the labelled glucose molecules confirms this conclusion. The pattern of incorporation of radioactivity initially suggests that nucleotide ribose is not formed via this pathway. However, it is shown that the coupling of an active transketolase system with the other enzymes of the hexosemonophosphate shunt provides a sufficient explanation of all the experimental observations. The conclusion is reached that pentose is formed by oxidation of glucose through the shunt but that the labelling pattern is largely established as the result of the exchange reaction catalyzed by transketolase.

AMINO ACID ACCUMULATION IN EHRLICH ASCITES CARCINOMA CELLS

1960 ◽  
Vol 38 (1) ◽  
pp. 1311-1326 ◽  
Author(s):  
A. Tenenhouse ◽  
J. H. Quastel
Keyword(s):  
Amino Acids ◽  
Steady State ◽  
Amino Acid ◽  
Active Transport ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Ion Concentration ◽  
Metabolic Inhibitors ◽  
Ehrlich Ascites ◽  
Glycine Transport

Measurements of the transport of amino acids into Ehrlich ascites carcinoma cells have shown that the following relationship exists between the intracellular steady-state concentration of the amino acid (Cx) and the extracellular concentration (C0):[Formula: see text]where Cm is the maximum intracellular concentration (formed when C0 is large) and Em is a constant. It is shown that Em is identical with Km, the Michaelis constant, if a carrier enzyme is involved in the process of active transport and is, therefore, a measure of the affinity of the amino acid for the effective agent involved in the transport phenomenon.The ratio of the steady-state intracellular and extracellular concentrations of amino acids exceeds unity with all amino acids examined. The responses of L-S-ethylcysteine transport to changes of potassium ion concentration and to changes of temperature differ from those of glycine transport and indicate that different carriers are involved in the active transport of these amino acids into Ehrlich ascites cells. This conclusion is supported by the fact that, whereas glycine and L-serine compete with each other for concentrative uptake, such mutual competition does not occur between S-ethylcysteine and glycine or L-serine or L-leucine.Effects of the metabolic inhibitors, 2,4-dinitrophenol, iodoacetate, and stilbestrol show that these substances exercise inhibitory effects on active transport of amino acids by suppression of respiratory or glycolytic energy. Stilbestrol, which is a particularly potent inhibitor, is more effective under aerobic conditions (in the absence of glucose) than under anaerobic conditions (in the presence of glucose). It is reasonable to account for these results on the hypothesis that the carrier responsible for amino acid transport is ATP dependent and that the carrier breaks down, and is no longer available for amino acid transfer, if the ATP content of the cell is depleted.

AMINO ACID ACCUMULATION IN EHRLICH ASCITES CARCINOMA CELLS

1960 ◽  
Vol 38 (11) ◽  
pp. 1311-1326 ◽  
Author(s):  
A. Tenenhouse ◽  
J. H. Quastel
Keyword(s):  
Amino Acids ◽  
Steady State ◽  
Amino Acid ◽  
Active Transport ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Ion Concentration ◽  
Metabolic Inhibitors ◽  
Ehrlich Ascites ◽  
Glycine Transport

Measurements of the transport of amino acids into Ehrlich ascites carcinoma cells have shown that the following relationship exists between the intracellular steady-state concentration of the amino acid (Cx) and the extracellular concentration (C0):[Formula: see text]where Cm is the maximum intracellular concentration (formed when C0 is large) and Em is a constant. It is shown that Em is identical with Km, the Michaelis constant, if a carrier enzyme is involved in the process of active transport and is, therefore, a measure of the affinity of the amino acid for the effective agent involved in the transport phenomenon.The ratio of the steady-state intracellular and extracellular concentrations of amino acids exceeds unity with all amino acids examined. The responses of L-S-ethylcysteine transport to changes of potassium ion concentration and to changes of temperature differ from those of glycine transport and indicate that different carriers are involved in the active transport of these amino acids into Ehrlich ascites cells. This conclusion is supported by the fact that, whereas glycine and L-serine compete with each other for concentrative uptake, such mutual competition does not occur between S-ethylcysteine and glycine or L-serine or L-leucine.Effects of the metabolic inhibitors, 2,4-dinitrophenol, iodoacetate, and stilbestrol show that these substances exercise inhibitory effects on active transport of amino acids by suppression of respiratory or glycolytic energy. Stilbestrol, which is a particularly potent inhibitor, is more effective under aerobic conditions (in the absence of glucose) than under anaerobic conditions (in the presence of glucose). It is reasonable to account for these results on the hypothesis that the carrier responsible for amino acid transport is ATP dependent and that the carrier breaks down, and is no longer available for amino acid transfer, if the ATP content of the cell is depleted.

Trichosanthes dioica seed lectin inhibits Ehrlich ascites carcinoma cells growth in vivo in mice by inducing G 0 /G 1 cell cycle arrest

2021 ◽  
Author(s):  
Shaikh Shohidul Islam ◽  
Md. Rezaul Karim ◽  
A. K. M. Asaduzzaman ◽  
A. H. M. Khurshid Alam ◽  
Zahid Hayat Mahmud ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Cycle Arrest ◽  
Ehrlich Ascites ◽  
Trichosanthes Dioica

COMPETITION BETWEEN AMINO ACIDS FOR TRANSPORT INTO EHRLICH ASCITES CARCINOMA CELLS

1961 ◽  
Vol 39 (11) ◽  
pp. 1717-1735 ◽  
Author(s):  
P. G. Scholefield
Keyword(s):  
Carbon Dioxide ◽  
Amino Acids ◽  
Amino Acid ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Transport Systems ◽  
Radioactive Carbon ◽  
Ehrlich Ascites ◽  
Competitive Inhibitors ◽  
Amino Acid Analogues

The cumulative entry of amino acids into Ehrlich ascites carcinoma cells is due to the presence of active transport systems, each with its own specific range of substrates. Several amino acids and amino acid analogues may have an affinity for the same transport system and thus may inhibit transport of other amino acids by acting as competitive inhibitors or competitive substrates. Loss of methionine from ascites cells takes place by a diffusion process which obeys Fick's law. Leucine accumulation by ascites cells is small and is increased on addition of certain other amino acids. The increase is not due to inhibition of leucine oxidation as increase in the rate of production of radioactive carbon dioxide from labeled leucine also occurs. Kinetic aspects of these results are discussed.

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