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M L Eboli

Publications and source records attributed to M L Eboli.

25 records · Page 2Linked to original sources
PubMed1977

Pyruvate transport in tumour-cell mitochondria.

Tumour-cell mitochondria contain a pyruvate-transporting system exhibiting the same general properties as those described in rat liver mitochondria. The Km for net pyruvate uptake in tumour-cell mitochondria is practically similar to that measured in rat liver mitochondria but the V is lower. This difference is also shown by swelling experiments. The possible implication of these observations in the context of lactate accumulation in tumour-cell is discussed.

Animals↗
PubMed1977

NAD(P)H utilization in the reduction of pyruvate to lactate in a glycogen-containing subline of Ehrlich ascites tumour cells.

The possible pathways of utilization of glucose-6-phosphate (G-6-P) produced from glycogen breakdown have been investigated in a glycogen-containing subline of Ehrlich ascites tumour cells. Addition of either mitochondrial inhibitors or pyruvate to ascites cells metabolizing endogenous substrates enhances the rate of lactate production. However, only in the former condition such effect is abolished by iodoacetate (IAA). In pyruvate-supplemented cells mitochondrial inhibitors cause a further increase in lactate production which becomes insensitive to IAA when the cells are depleted of endogenous substrates. Measurements of the glycogen content show that either in the presence of mitochondrial inhibitors or pyruvate there is a stimulation of glycogenolysis. Significant changes (about 10--20 fold increase) of the G-6-P level are observed only in the presence of both mitochondrial inhibitors and IAA, irrespective of pyruvate addition. However, with pyruvate the accumulation of G-6-P becomes lower if the cells are starved. The results obtained indicate that in our conditions G-6-P which is produced during glycogenolysis may be oxidized either through the Embden-Meyerhof pathway or the phosphogluconate pathway. Indeed, whereas mitochondrial inhibitors promote the utilization of this metabolite through the first route by enhancing the activity of phosphofructokinase, added pyruvate favours the other route by lowering the cytosolic NADPH/NADP+ ratio.

Anaerobiosis↗
PubMed1976

Transport of anionic substrates and glutamate metabolism in mitochondria from ascites tumor cells.

A study is presented of alpha-oxoglutarate and glutamate transport and of glutamate oxidation in ascites tumor cell mitochondria. Kinetics analysis of alpha-oxoglutarate transport in mitochondria from two strains of Ehrlich ascites tumor cells, the hyperdiploid and the hyperdiploid Lettré mutant, shows that the activity of the alpha-oxoglutarate carrier and its affinityfor substrates are higher in the mutant than in the wild strain. Evidence is presented showing the occurrence of carrier mediated glutamate-OH-exchange-diffusion in mitochondria from both strains. The activity of the glutamate carrier is apparently higher in the hyperdiploid Lettré mutant. Glutamate oxidation occurs mainly through transamination to asparatate in both tumor stains. The rate of deamination in the two strains correlates directly with the level of glutamide dehydrogenase (EC 1.4.1.3.), which is higher in the wild than in the mutant strain. Thus glutamate dehydrogenase per se, and not glutamate penetration, constitutes the control step for gluttochondria of glutamate with externally added oxaloacetate (arsenite present) that exclude an obligatory transport of oxaloacetate on the alpha-oxoglutarate carrier.

Animals↗