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P32 Incorporation by Ehrlich ascites cells in vitro.
13
Citations
14
References
1959
Year
GlycobiologyAscites CellsMetabolic RemodelingRedox BiologyCellular PhysiologyTumor BiologyOxidative StressCell SignalingHealth SciencesAdenosine PhosphatesBiochemistryAdenosine TriphosphateCellular BiologyCell BiologyP32 IncorporationEnergy MetabolismMitochondrial FunctionPhysiologyCatabolismCellular BiochemistryMetabolismMedicine
I t was shown by in 19~9 (8) that addition of glucose to tumor slices led to a decrease in their respiratory activity, and this fact has been confirmed (6, 10). The inhibitory effect of glucose on the respiratory activity of ascites cells is much greater and may approach 40 per cent (for reviews of the Crabtree or reversed effect in ascites tumor cells, the recent papers by Bloch-Frankenthal and Weinhouse [3] and by Ibsen, Coe, and McKee [13] should be consulted). The mechanism of this effect has been studied by Racker (~1) and by Chance and Hess (7), both of whom seem to favor some form of imbalance of the adenine nudeotides through the interplay of cytoplasmic glycolysis and mitochondrial respiration. However, the results of Aisenberg, Reinafarje, and Potter (1) and Aisenberg and Potter (~) indicate that, in a system consisting of a mixture of a glycolyzing preparation with liver mitochondria, the phenomenon of the Pasteur effect may be observed but there is no detectable change in the levels of each of the three adenosine phosphates. On the other hand, the observations and calculations of Quastel and Bickis (19) suggest that the depletion of adenosine triphosphate (ATP) resulting from the inhibition of respiration by glucose is exactly counterbalanced by the yield of ATP from aerobic glycolysis. A similar series of sparing actions has been described by Medes and Weinhouse (16), who observed that added substrates such as acetate and other fa t ty acids may spare the oxidation of endogenous carbon compounds and that added glucose was a preferred substrate for oxidation by ascites cells. I t was felt that a detailed study of the rate of turnover of p82 in the various acid-soluble components of Ehrlich ascites cells would shed some light on the effects of glucose in this system. Such in vitro studies of p3~ turnover have been carried out by Harrington and Lavik (11, 1~) and by Thomson, Smellie, and Davidson (~4) using Ehrlich ascites cells. Similar studies have
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