scholarly journals Dual inhibition of glycolysis and autophagy as a therapeutic strategy in the treatment of Ehrlich ascites carcinoma

2020 ◽  
Vol 34 (7) ◽  
Author(s):  
Mohammed A. Mansour ◽  
Wafaa M. Ibrahim ◽  
Mona M. Salama ◽  
Afrah F. Salama
Keyword(s):  
Therapeutic Strategy ◽  
Ehrlich Ascites Carcinoma ◽  
Ehrlich Ascites ◽  
Inhibition Of Glycolysis ◽  
Dual Inhibition

scholarly journals Dual inhibition of glycolysis and glutaminolysis as a therapeutic strategy in the treatment of ovarian cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (38) ◽  
pp. 63551-63561 ◽  
Author(s):  
Li Sun ◽  
Yajie Yin ◽  
Leslie H. Clark ◽  
Wenchuan Sun ◽  
Stephanie A. Sullivan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Therapeutic Strategy ◽  
Inhibition Of Glycolysis ◽  
Dual Inhibition

scholarly journals Selective inhibition of mitochondrial respiration and glycolysis in human leukaemic leucocytes by methylglyoxal

1997 ◽  
Vol 323 (2) ◽  
pp. 343-348 ◽  
Author(s):  
Swati BISWAS ◽  
Manju RAY ◽  
Sanjoy MISRA ◽  
D. P. DUTTA ◽  
Subhankar RAY
Keyword(s):  
Oxygen Consumption ◽  
Mitochondrial Respiration ◽  
Complex I ◽  
Electron Flow ◽  
Mitochondrial Respiratory Chain ◽  
Ehrlich Ascites Carcinoma ◽  
Selective Inhibition ◽  
Ehrlich Ascites ◽  
Inhibition Of Glycolysis ◽  
Flow Through

The effect of methylglyoxal on the oxygen consumption of mitochondria of both normal and leukaemic leucocytes was tested by using different respiratory substrates and complex specific artificial electron donors and inhibitors. The results indicate that methylglyoxal strongly inhibits mitochondrial respiration in leukaemic leucocytes, whereas, at a much higher concentration, methylglyoxal fails to inhibit mitochondrial respiration in normal leucocytes. Methylglyoxal strongly inhibits ADP-stimulated α-oxoglutarate and malate plus NAD+-dependent respiration, whereas, at a higher concentration, methylglyoxal fails to inhibit succinate and α-glycerophosphate-dependent respiration. Methylglyoxal also fails to inhibit respiration which is initiated by duroquinone and cannot inhibit oxygen consumption when the N,N,N´,N´-tetramethyl-p-phenylenediamine by-pass is used. NADH oxidation by sub-mitochondrial particles of leukaemic leucocytes is also inhibited by methylglyoxal. Lactaldehyde, a catabolite of methylglyoxal, can exert a protective effect on the inhibition of leukaemic leucocyte mitochondrial respiration by methylglyoxal. Methylglyoxal also inhibits l-lactic acid formation by intact leukaemic leucocytes and critically reduces the ATP level of these cells, whereas methylglyoxal has no effect on normal leucocytes. We conclude that methylglyoxal inhibits glycolysis and the electron flow through mitochondrial complex I of leukaemic leucocytes. This is strikingly similar to our previous studies on mitochondrial respiration, glycolysis and ATP levels in Ehrlich ascites carcinoma cells [Ray, Dutta, Halder and Ray (1994) Biochem. J. 303, 69–72; Halder, Ray and Ray (1993) Int. J. Cancer 54, 443–449], which strongly suggests that the inhibition of electron flow through complex I of the mitochondrial respiratory chain and inhibition of glycolysis by methylglyoxal may be common characteristics of all malignant cells.

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

Antioxidant, cytotoxic and apoptotic potentials of seeds of Momordica subangulata subsp. renigera inhibit the growth of Ehrlich ascites carcinoma in mice

2019 ◽  
Vol 13 (4) ◽  
pp. 3049-3059
Author(s):  
Polash Chandra Karmakar ◽  
Rumana Yesmin ◽  
Hanif Ali ◽  
M. Rowshanul Habib ◽  
Dhirendra Nath Barman ◽  
...  
Keyword(s):  
Ehrlich Ascites Carcinoma ◽  
Ehrlich Ascites

Tumor cell metabolism in vitro: a study of incubation media

1970 ◽  
Vol 48 (4) ◽  
pp. 517-519 ◽  
Author(s):  
I. C. Caldwell ◽  
Marianne F. Chan
Keyword(s):  
Nucleic Acid ◽  
Structural Integrity ◽  
Cell Metabolism ◽  
Ehrlich Ascites Carcinoma ◽  
Leukemic Cells ◽  
Prolonged Incubation ◽  
Ehrlich Ascites ◽  
Eac Cells ◽  
Rna And Dna

A number of incubation media which have been used in studies of the metabolism of Ehrlich ascites carcinoma (EAC) cells in vitro have been examined with respect to their abilities to support the incorporation of radioactive precursors into nucleotides and nucleic acids, and to maintain the structural integrity and tumor-inducing abilities of EAC cells. Cells incubated in the chemically-defined "Fischer's medium for leukemic cells of mice" were able to produce lethal tumors in mice after more than 16 h of incubation, maintained their structural integrity on prolonged incubation, and catalyzed high rates of incorporation of exogenously added substrates into nucleotides, RNA, and DNA. However, cells incubated in balanced salts solutions supplemented with glucose had these characteristics: (a) were unable to produce lethal tumors after 4 h of incubation, (b) released large amounts of nucleotide, nucleic acid, and protein material into the medium after less than 2 h of incubation, and (c) catalyzed the incorporation of radioactive precursors into nucleotides and RNA at much lower rates than did cells incubated in Fischer's medium, and were virtually unable to catalyze the incorporation of adenine-14C into DNA.

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