scholarly journals P-glycoprotein expression in Ehrlich ascites tumour cells after in vitro and in vivo selection with daunorubicin

1998 ◽  
Vol 78 (9) ◽  
pp. 1175-1180 ◽  
Author(s):  
D Nielsen ◽  
J Eriksen ◽  
C Maare ◽  
AH Jakobsen ◽  
T Skovsgaard
Keyword(s):  
Tumour Cells ◽  
In Vivo Selection ◽  
Ascites Tumour ◽  
P Glycoprotein ◽  
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.

Calcium Exchanges of Ehrlich Ascites Tumour Cells of Mice in vitro

Nature ◽  
1958 ◽  
Vol 182 (4638) ◽  
pp. 809-809
Author(s):  
DOREEN THOMASON ◽  
RAYMOND SCHOFIELD
Keyword(s):  
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.

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