Isolation of fatty acids from the mycelium ofPenicillium stipitatum thom and their effect on ehrlich ascites carcinoma cells

1974 ◽  
Vol 19 (4) ◽  
pp. 301-306 ◽  
Author(s):  
J. Fuska ◽  
I. Kuhr ◽  
V. Koman
Keyword(s):  
Fatty Acids ◽  
Ehrlich Ascites Carcinoma ◽  
Carcinoma Cells ◽  
Ehrlich Ascites

THE OXIDATION OF LEUCINE BY EHRLICH ASCITES CARCINOMA CELLS

1965 ◽  
Vol 43 (7) ◽  
pp. 977-991 ◽  
Author(s):  
P. G. Scholefield
Keyword(s):  
Fatty Acids ◽  
Mouse Liver ◽  
Ehrlich Ascites Carcinoma ◽  
Inhibitory Effect ◽  
Carcinoma Cells ◽  
Effective Inhibitor ◽  
Leucine Oxidation ◽  
Liver Slices ◽  
Ehrlich Ascites ◽  
Keto Acids

The oxidation of leucine-1-14C to14CO2by Ehrlich ascites carcinoma cells was inhibited on addition of pyruvate and other α-keto acids, a maximum inhibitory effect being attained with 1 mM pyruvate. The only compound, among those tested, which reversed this inhibition was malonate. Oxidation of leucine-2-14C to14CO2occurred at a rate which was 1% of that observed with leucine-1-14C and was sensitive to the presence of fatty acids as well as to pyruvate. Glutamine was a particularly effective inhibitor of leucine oxidation. The inhibition produced by isoleucine was competitive, the KIvalue being 0.13 mM compared with the KMvalue of 0.2 mM. It is suggested that the inhibition by pyruvate is due to a competition between pyruvate and the α-ketoisovaleric acid derived from leucine for the cofactors required for the oxidation of the α-keto acids. In contrast, oxidation of leucine-1-14C by mouse liver slices was increased approximately threefold by pyruvate.

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

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.

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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