scholarly journals Transfer of intestine-derived diamines into tumour cells during treatment of Ehrlich-ascites—carcinoma-bearing mice with polyamine anti-metabolites

1984 ◽  
Vol 218 (2) ◽  
pp. 641-644 ◽  
Author(s):  
A Kallio ◽  
P Nikula ◽  
J Jänne
Keyword(s):  
General Circulation ◽  
Diamine Oxidase ◽  
Ehrlich Ascites Carcinoma ◽  
Tumour Cells ◽  
Carcinoma Cells ◽  
Ehrlich Ascites

Treatment of Ehrlich-ascites-carcinoma-bearing mice with methylglyoxal bis(guanylhydrazone) alone or in combination with 2-difluoromethylornithine greatly enhanced the transfer of intragastrically administered radioactive putrescine and cadaverine into the carcinoma cells. Difluoromethylornithine alone did not have any effect on the accumulation of intestine-derived diamines in the tumour cells. The frequently reported restoration of difluoromethylornithine-induced polyamine depletion on administration of methylglyoxal bis(guanylhydrazone) is in all likelihood attributable to a profound inhibition of intestinal diamine oxidase (EC 1.4.3.6), resulting in an enhanced entry of intestinal (bacterial) diamines into general circulation and finally into tumour cells.

scholarly journals Tumourigenicity, cell-surface glycoprotein changes and ornithine decarboxylase gene pattern in Ehrlich ascites-carcinoma cells

1985 ◽  
Vol 229 (3) ◽  
pp. 711-715 ◽  
Author(s):  
L Alhonen-Hongisto ◽  
A Kallio ◽  
R Sinervirta ◽  
O A Jänne ◽  
C G Gahmberg ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cell Line ◽  
Ornithine Decarboxylase ◽  
Ehrlich Ascites Carcinoma ◽  
Tumour Cells ◽  
Carcinoma Cells ◽  
Surface Glycoprotein ◽  
Cell Surface Glycoprotein ◽  
Phenotypic Changes ◽  
Ehrlich Ascites

We selected a 2-difluoromethylornithine-resistant Ehrlich ascites-carcinoma cell line that grows in the presence of 20 mM-difluoromethylornithine. These cells contain 10-20 times the normal amount of hybridizable sequences for ornithine decarboxylase (EC 4.1.1.17) in their genomic DNA. We used these gene-amplified cells, their revertant counterparts (grown in the absence of the drug after an established gene amplification) and tumour cells grown in the presence of putrescine to investigate the changes of ornithine decarboxylase gene pattern and simultaneously occurring phenotypic changes, such as tumourigenicity and the expression of cell-surface glycoproteins. In the tumour cells reverted back to the normal gene frequency, not only did the amplified sequences disappear, but there were also signs of gene re-arrangements seen as a ‘gene jump’, when a signal evidently moved to a heavier restriction fragment. Similar gene re-arrangement likewise occurred in cells exposed to putrescine. Although the wild-type tumour cells and the gene-amplified cells readily grew in the peritoneal cavity of mice, the revertant cells and the putrescine-treated cells had lost their tumourigenicity in mice. Gene-amplified tumour cells and the revertant cells showed distinct changes in their surface glycoprotein pattern in comparison with the parental cell line. These findings indicate that alterations of ornithine decarboxylase gene pattern/dosage may be associated with phenotypic changes possibly related to the tumourigenicity of these carcinoma cells.

scholarly journals Intracellular putrescine and spermidine deprivation induces increased uptake of the natural polyamines and methylglyoxal bis(guanylhydrazone)

1980 ◽  
Vol 192 (3) ◽  
pp. 941-945 ◽  
Author(s):  
L Alhonen-Hongisto ◽  
P Seppänen ◽  
J Jänne
Keyword(s):  
Transport System ◽  
Culture Medium ◽  
Ehrlich Ascites Carcinoma ◽  
Tumour Cells ◽  
Carcinoma Cells ◽  
Polyamine Synthesis ◽  
Ascites Tumour ◽  
Proliferative Effect ◽  
Ehrlich Ascites ◽  
Ascites Tumour Cells

Inhibition of polyamine synthesis by alpha-difluoromethylornithine in cultured Ehrlich ascites-carcinoma cells rapidly enhanced the uptake of exogenous putrescine, spermidine and spermine from the culture medium. In tumour cells exposed to the drug for 2 days, the intracellular concentration of spermidine was decreased to less than 10% of that found in untreated cells. However, the strikingly stimulated transport system brought the concentration of spermidine to the control values in less than 2h after supplementation of the cells with micromolar concentrations of the polyamine. In the absence of polyamine deprivation, tumour cells did not accumulate extracellular polyamines to any appreciable extent. Ascites-tumour cells deprived of putrescine and spermidine likewise concentrated methylglyoxal bis(guanylhydrazone) [1,1′-[methylethanedylidine)dinitrilo]diguanidine] at a greatly enhanced rate. A previous “priming of tumour cells with difluoromethylornithine followed by an exposure of the cells to methylglyoxal bis(guanylhydrazone) resulted in a marked and rapid anti-proliferative effect.

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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