Interrelationships of metabolic pathways in the Ehrlich ascites carcinoma cells I. Glycolysis and respiration (Crabtree Effect)

Ibsen, Kenneth H.; Coe, Elmon L.; McKee, Ralph W.

doi:10.1016/0006-3002(58)90064-7

Cited by 96 publications

(19 citation statements)

References 50 publications

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“…Thus, state-3 oxidation would be curtailed for want of ADP, analogous to the results obtained in experiments with isolated mitochondria (8, 16). However, Ibsen et al subsequently observed that respiratory inhibition began when ADP was present in excess of the capacity of both the respiratory chain or glycolysis to phosphorylate it (17). Hess and Chance later reported that the ratio of ATP to ADP (ATP/ADP) in glycolyzing (metabolizing glucose) cells was usually lower than the ratio in nonglycolyzing controls (19).…”

Section: Observations On the Crabtree Effectmentioning

confidence: 66%

“…The hexokinase reaction, which utilizes the cells' complement of adenosine triphosphate (ATP) to phosphorylate the added glucose, yields ADP, the phosphate acceptor for oxidative phosphorylation, or state-3 oxidation (16). There can be little doubt that this is correct because as soon as glucose is added a large decrease in cellular ATP occurs simultaneously with an increase in ADP (17,18).…”

Section: Observations On the Crabtree Effectmentioning

confidence: 99%

“…1); thus the respiratory chain could have access to all the ADP produced by hexose phosphorylation (20). However, an equally plausible interpretation would be that the competition for (17). This indicated that the hexose phosphorylation reaction might be sufficient for induction of respiratory inhibition.…”

Section: Inhibition Of the Crabtree Effectmentioning

confidence: 99%

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Phosphate Mediation of the Crabtree and Pasteur Effects

Koobs

1972

Science

136

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The enhanced capacity of tumors to metabolize glucose (glycolysis) was observed in vivo by the Coris in 1925 (1). Four years later Henry Crabtree reported the phenomenon of glucoseinduced respiratory inhibition in slices of solid sarcomas and carcinomas. He also made the observation that tumors were not the only tissues capable of enhanced aerobic glycolysis (2). A list of normal tissues, including blood cells, having more than the usual glycolytic capacity was presented by Ibsen in his history and discussion of the Crabtree effect (3). The ability of tumors to fulfill energy requirements by

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Section: Observations On the Crabtree Effectmentioning

confidence: 66%

Section: Observations On the Crabtree Effectmentioning

confidence: 99%

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Phosphate Mediation of the Crabtree and Pasteur Effects

Koobs

1972

Science

136

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“…In addition, 2DOG-6-P does not inhibit hexokinase activity (22) as does G-6-P. Since 2DOG does not lead to the formation of pyruvic and lactic acids, it does not complicate the interpretation of mitochondrial respiratory state with respect to the arrival of ADP at the mitochondria and does not lead to a lowering of intracellular pH as does glucose (9) . Use of 2DOG has permitted us to monitor changes in the redox state of pyridine nucleotide of the mitochondria in intact ascites tumor cells by fluorescence emission (15) uncomplicated by glycolytic-induced changes in pyridin nucleotide in the cytosol .…”

Section: Ultrastructural Transformation Related To Partial and Complementioning

confidence: 99%

Oxidative Phosphorylation and Ultrastructural Transformation in Mitochondria in the Intact Ascites Tumor Cell

Hackenbrock

Rehn

Weinbach

et al. 1971

The Journal of Cell Biology

164

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We have examined the ultrastructure of mitochondria as it relates to energy metabolism in the intact cell . Oxidative phosphorylation was induced in ultrastructurally intact Ehrlich ascites tumor cells by rapidly generating intracellular adenosine diphosphate from endogenous adenosine triphosphate by the addition of 2-deoxyglucose . The occurrence of oxidative phosphorylation was ascertained indirectly by continuous and synchronous monitoring of respiratory rate, fluorescence of pyridine nucleotide, and 90° light-scattering . Oxidative phosphorylation was confirmed by direct enzymatic analysis of intracellular adenine nucleotides and by determination of intracellular inorganic orthophosphate . Microsamples of cells rapidly fixed for electron microscopy revealed that, in addition to oxidative phosphorylation, an orthodox -> condensed ultrastructural transformation occurred in the mitochondria of all cells in less than 6 sec after the generation of adenosine diphosphate by 2-deoxyglucose . A 90° light-scattering increase, which also occurs at this time, showed a t 12 of only 25 sec which agreed temporally with a slower orthodox ---> maximally condensed mitochondrial transformation . Neither oxidative phosphorylation nor ultrastructural transformation could be initiated in mitochondria in intact cells by the intracellular generation of adenosine diphosphate in the presence of uncouplers of oxidative phosphorylation . Partial and complete inhibition of oxidative phosphorylation by oligomycin resulted in a positive relationship to partial and complete inhibition of 2-deoxyglucose-induced ultrastructural transformation in the mitochondria in these cells . The data presented reveal that an orthodox -* condensed ultrastructural transformation is linked to induced oxidative phosphorylation in mitochondria in the intact ascites tumor cell.

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“…to its translocation from the cytosol to the mitochondrial fraction of tumour cells). Since, according to Ibsen et al, (1958) and Thompson and Bachelard (1977) the mitochondrionbound hexokinase develops an ATPaselike stimulatory action on cell respiration through activation of the intramitochondrial ATP, the subcellular translocation of hexokinase could explain the increased 02 consumption of leukaemic cells.…”

Section: Discussionmentioning

confidence: 99%

Regulation of glycolysis and oxygen consumption in lymph-node cells of normal and leukaemic mice

Arany¹,

Rady²,

Kertai³

1981

Br J Cancer

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Summary.-Lymph-node cells of (AKR x C3H) F1 leukaemic mice showed a considerable increase of glycolytic activity and 02 consumption. The glycolytic enzymes phosphofructokinase, pyruvate kinase, aldolase and lactic acid dehydrogenase showed increased activities in leukaemic conditions. Studies on permeabilized leukaemic and normal lymph-node cells, and assays on partially purified phosphofructokinase and pyruvate kinase enzymes, revealed that the enhanced glycolysis of the tumour cells was due to the predominance of glycolytic isoenzymes relatively insensitive to the natural metabolic inhibitors. The glycolytic enzyme hexokinase showed decreased activity in leukaemic conditions, owing to a subcellular translocation of its bulk from the cytosol to the mitochondrial fraction. Association of hexokinase with the mitochondria accounted for an ATPase-like stimulatory action on cell respiration which can explain the increased 02 uptake of leukaemic cells.

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Interrelationships of metabolic pathways in the Ehrlich ascites carcinoma cells I. Glycolysis and respiration (Crabtree Effect)

Cited by 96 publications

References 50 publications

Phosphate Mediation of the Crabtree and Pasteur Effects

Phosphate Mediation of the Crabtree and Pasteur Effects

Oxidative Phosphorylation and Ultrastructural Transformation in Mitochondria in the Intact Ascites Tumor Cell

Regulation of glycolysis and oxygen consumption in lymph-node cells of normal and leukaemic mice

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