scholarly journals The Effect of Nitrogen Mustard on the Life Cycle of Ehrlich Ascites Tumour Cells In Vivo

1964 ◽  
Vol 18 (1) ◽  
pp. 150-158 ◽  
Author(s):  
J P Layde ◽  
R Baserga
Keyword(s):  
Life Cycle ◽  
Nitrogen Mustard ◽  
Tumour Cells ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

scholarly journals Regulation of glutathione metabolism in Ehrlich ascites tumour cells

1992 ◽  
Vol 286 (1) ◽  
pp. 257-262 ◽  
Author(s):  
J M Estrela ◽  
R Hernandez ◽  
P Terradez ◽  
M Asensi ◽  
I R Puertes ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Tumour Cells ◽  
Glutathione Metabolism ◽  
Glutathione S Transferase ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

Glutathione metabolism was studied in cancer cells during the growth of an Ehrlich ascites tumour. GSH, but not GSSG, content decreases when cell proliferation and the rate of protein synthesis in the tumour decrease. This change correlates with a decrease in the rate of GSH synthesis and an increase in glutathione peroxidase and glutathione S-transferase activities. Glutathione efflux from tumour cells seems to co-ordinate with the rate of GSH synthesis. Cysteine, and not methionine, promotes GSH synthesis in tumour cells. However, changes in the rate of GSH synthesis are not due to limitations in the supply of blood cysteine or to changes in the intracellular amino acid pool of the cancer cells. Our data suggest that changes in protein metabolism accompanying tumour growth in vivo can modulate glutathione content in cancer cells.

scholarly journals Some properties of adenosine kinase from Ehrlich ascites-tumour cells

1968 ◽  
Vol 106 (2) ◽  
pp. 549-555 ◽  
Author(s):  
A. W. Murray
Keyword(s):  
Maximum Velocity ◽  
Enzymic Activity ◽  
Tumour Cells ◽  
Adenosine Kinase ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

1. Adenosine kinase was measured in dialysed extracts from Ehrlich ascites-tumour cells by a chromatographic procedure. 2. In the absence of added Mg2+ the Km values for ATP and adenosine were 0·22mm and 2·8μm respectively. 3. The maximum velocity of adenosine kinase with free ATP was about three times that with the Mg2+–ATP complex. Free Mg2+ was a non-competitive inhibitor of the reaction. A small amount of added Mg2+, Mn2+ or Ca2+ was required for maximum adenosine kinase activity after cation bound to the enzyme had been released by treatment with p-chloromercuribenzoate and then removed by dialysis. 4. GTP, ITP, deoxy-ATP, deoxy-GTP, CTP, xanthosine triphosphate, UTP and thymidine triphosphate could partially or completely replace ATP as a phosphate donor. 5. The reaction of ATP with adenosine kinase was competitively inhibited by AMP, GMP, IMP, ADP, deoxy-ADP and IDP (Ki 0·2, 1·1, 5·9, 1·2, 0·5 and 0·78mm respectively). Enzymic activity was markedly affected by the relative concentrations of AMP, ADP and ATP in assay mixtures. 6. The results are discussed in terms of possible mechanisms regulating the rate of adenosine kinase in vivo.

Characterisation of multidrug-resistant Ehrlich ascites tumour cells selected in vivo for resistance to etoposide

2000 ◽  
Vol 60 (3) ◽  
pp. 353-361 ◽  
Author(s):  
Dorte Nielsen ◽  
Christian Maare ◽  
Jens Eriksen ◽  
Thomas Litman ◽  
Ellen Friche ◽  
...  
Keyword(s):  
Multidrug Resistant ◽  
Tumour Cells ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

scholarly journals Some inhibitory effects of (−)-emetine on growth of Ehrlich ascites carcinoma

1974 ◽  
Vol 140 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Randall K. Johnson ◽  
W. Robert Jondorf
Keyword(s):  
Tumour Cells ◽  
Survival Times ◽  
New Host ◽  
Ascites Tumour ◽  
Ehrlich Ascites ◽  
Ehrlich Ascites Tumour ◽  
Ascites Tumour Cells ◽  
Ehrlich Ascites Tumour Cells

(−)-Emetine has little or no effect on O2 consumption of Ehrlich ascites-cell suspensions or on the viability of transplanted Ehrlich ascites-tumour cells exposed to, or incubated with, the drug in vitro before inoculation into new-host mice. (−)-Emetine administered as a single injection to mice bearing Ehrlich ascites-tumour cells slows the growth rate of the tumour. The subcutaneous or intraperitoneal injection of the drug depresses protein and DNA synthesis of the tumour cells in vivo in a reversible manner. Mice bearing ascitic sarcoma 180 or Ehrlich ascites-tumour cells when given a course of treatment with (−)-emetine or (−)-O-methyltubulosine have a substantially lower tumour load than untreated controls and correspondingly longer survival times.

Sign in / Sign up

Export Citation Format

Share Document