Ehrlich-Ascites tumour cells

The first step of this sequence, which is not unique to de novo purine nucleotide biosynthesis, is the synthesis of 5-phosphoribosylpyrophosphate (PRPP) from ribose-5-phosphate and adenosine triphosphate. Phosphoribosyl-pyrophosphate synthetase, the enzyme that catalyses this reaction [278], is under feedback control by adenosine triphosphate [279]. Cordycepin interferes with thede novo pathway [229, 280, 281), and cordycepin triphosphate inhibits the synthesis of PRPP in extracts from Ehrlich ascites tumour cells [282]. Formycin [283], probably as the triphosphate, 9-0-D-xylofuranosyladenine [157] triphosphate, and decoyinine (LXXlll) [284-286] (p. 89) also inhibit the synthesis of PRPP in tumour cells, and this is held to be the blockade most important to their cytotoxic action. It has been suggested but not established that tubercidin (triphosphate) may also be an inhibitor of this reaction [193]. 

Although both orotic acid and uracil are utilized by Ehrlich ascites tumour cells in mice [52], the presence of orotic acid completely inhibits the incorporation of bicarbonate into C2 of the acid-soluble nucleotides in the same tumour system [181]. 

Woerdenbag and coworkers reported on the cytotoxicity of artemisinin endoperoxides to Ehrlich ascites tumour cells . Artemisinin had an IC50 of 29.8 p.M, whereas arteether, artemether, artelininc acid and sodium artesunate all had more potent activities, ranging from 12.2 to 19.9 p.M. It was found that opening of the lactone ring of artemisinin dramatically reduced the cytotoxicity. An ether dimer of dihydroartemisinin 106, prepared by... 

Kuznicki J, Filipek A, Hunziker PE, Huber S, Heizmann CW. 1989b. Calcium-binding protein from mouse Ehrlich ascites-tumour cells is homologous to human calcyclin. Biochem J 263(3) 951-956. 

Parry EW (1981) Cycloheximide treatment modifies the pattern of metastasis following intravenous injection of ehrlich ascites tumour cells. Gann 72 464—467. 

AflBnity Labellii. —Of a large number of 5-substituted-2 -deoxyuridine 5 -mono-phosphates prepared as potential inhibitors of thymidylate kinase, 5-formyl-dUMP was found to be a potent non-competitive inhibitor of the enzyme from calf thymus, and 5-azidomethyl-dUMP irreversibly inactivated both this enzyme and the enzyme from Ehrlich ascites tumour cells. Protection by cofactor addition could only be demonstrated for the latter case, however. 5-Iodoacetamidomethyl-dUMP (68) irreversibly inactivates the tumour enzyme more rapidly than the calf thymus enzyme, and protection could also be demonstrated in this case it has therefore been claimed that (68) is isozyme-specific for the tumour enzyme. ... 

The above described rationale of SAR can be exemplified by the bioactivities of the bromotyrosine derivatives, aeroplysinin-1 and dienone, as well as their complicated molecular substrates aerophobin-1 and isofistularin-3, isolated from the Mediterranean sponge, Aplysina aerophoba. Aeroplysinin-1 and dienone exhibit pronounced biological activity whereas aerophobin-1 and isofistularin-3 were always inactive when tested in equimolar concentrations [23]. Aeroplysinin-1 and dienone are antibiotically active against a broad spectrum of marine bacteria such as Vibrio, Micrococcus, and Alteromonas species [24] and are also cytotoxic to Ehrlich ascites tumour cells and HeLa tumour cells in the microculture tetrazolium (MTT) and clonogenic assays [25]. In these assays, it has been demonstrated that the free radical transformation of aeroplysinin-1 and dienone to its semiquinone structures are responsible for the cytotoxicity [25], Aeroplysinin-1 and dienone are the pharmacophores of aerophobin-1 and isofistularin-3. 

Moderately active against Ehrlich ascites tumour cells (231)... 

Besides yeast and muscle, glycolytic oscillations have also been observed in Ehrlich ascites tumour cells (Ibsen Schiller, 1967) an insect, the blowfly Phormia terraenovae, for which age-dependent changes in the oscillations have been described (Collatz Horning, 1990 Horning Collatz, 1990) pancreatic p-cells (Chou et al., 1992) and, very recently, heart cells (O Rourke et al., 1994). 

M14. Murray, A. W., and Friedrichs, B., Inhibition of 5-nucleotidase from Ehrlich ascites tumour cells by nucleotide triphosphates. Biochem. J. Ill, 83 (1969). 

Lactate dehydrogenase Cytoplasmic malate dehydrogenase Mitochondrial malate dehydrogenase Ehrlich ascites tumour cells... 

Human fibroblast and leukocyte interferons show a strong affinity for the copper chelate of bis-carboxymethylaminoagarose. Human leukocyte interferon adsorbs non-specifically to immobilized hyperimmune serum immunoglobulin The interferon can be recovered by washing the adsorbent with 1,2-dihydroxyethane. An improved procedure for the isolation of interferons produced by mouse Ehrlich ascites tumour cells infected with Newcastle disease virus provides interferons of three size classes (mol. wts. 3.3 X lO", 2.6x10, ... 

The Na -glucose symporter has been studied most intensively in intestine, but similar translocation catalysts appear to occur in a number of other tissues, for example, in kidney in diaphragm in leucocytes and possibly in Ehrlich ascites tumour cells . 

Inhibitor of Purine metab. in Ehrlich ascites tumour cells in vitro. 

Daily intraperitoneal administration of pantothenic acid (100 mg/kg) for 5 days conferred significant protection against the peroxidative actions of a 0.5 ml/kg intraperitoneal dose of CCh in rats (Nagiel-Ostaszewski and Lau-Cam 1990). lipid peroxidation by incubation of Ehrlich ascites tumour cells with FeClj -i- HjOj was partly prevented by preincubation with D-pantothenate, 4 -phospho-pantothenate, D-pantothenol, or pantethine (Sly-SHENOv et al. 1995). Rats exposed to y radiation from a Co source, receiving 0.25 Gy at weekly intervals were protected from the deleterious effects by 26 mg pantothenol/kg x day given for 2 d before each irradiation (Slyshenov et al. 1998). 

The glycocalyx (cell coat) of Ehrlich ascites tumour cells, which is rich in glycoproteins and glycosaminoglycans, contains only one fraction (mol. wt. 1.3 X 10 ) which interacts with I-concanavalin A. ... 

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