PubMed Health⌕ Search

Biomedical subjects

G Paradies

Publications and source records attributed to G Paradies.

At least 55 records · Page 3Linked to original sources
PubMed1983

Transport of pyruvate in mitochondria from different tumor cells.

A comparative study of the transport of pyruvate in mitochondria isolated from normal rat liver and from three tumors has been carried out. The Km for net pyruvate uptake in mitochondria isolated from Ehrlich ascites tumor cells is practically equal to that measured in normal rat liver mitochondria while, on the other hand, it is higher in Morris hepatomas 44 and 3924A. The Vmax of pyruvate uptake is depressed in all three types of tumor mitochondria as compared to that in the rat liver mitochondria, with the depression being higher in Morris hepatoma 3924A mitochondria. The lower activity of pyruvate translocator in mitochondria isolated from tumor cells as compared to that in rat liver mitochondria is also shown by depression of the rate of pyruvate-supported oxygen uptake. The results document a decreased activity of the pyruvate translocator in tumor mitochondria which seems to be correlated with the growth rate of the tumor cells.

Animals↗
PubMed1981

A comparative study of the transport of pyruvate in liver mitochondria from normal and diabetic rats.

A comparative study of the transport of pyruvate in liver mitochondria from normal and diabetic rats has been carried out. The Km for the pyruvate uptake in diabetic, ketotic mitochondria is practically equal to that measured in normal mitochondria, while the Vmax is significantly lower. The lower activity of the pyruvate translocator in diabetic mitochondria compared to normal mitochondria is also shown by swelling experiments as well as by following the rate of pyruvate-supported respiration. Pre-exposure of mitochondria from normal rats to the ketone body acetoacetate and to 2-oxobutyrate results in a decrease of the Km for pyruvate uptake. This effect is impaired in mitochondria from diabetic animals. The results indicate that the activity and the properties of the mitochondrial pyruvate translocator are modified in the diabetic, ketotic condition.

3-Hydroxybutyric Acid↗
PubMed1980

[Effect of calcium and other cations on pyruvate transport in rat liver mitochondria].

The effect of Ca2+ and other cations on the initial rate of pyruvate translocation by rat liver mitochondria has been studied. It has been found that added Ca2+ strongly stimulates the rate of pyruvate uptake by non-respiring mitochondria. Mn2+ and to lesser extent Sr2+ could replace Ca2+ whilst Mg2+ has only little effect. The stimulation of pyruvate uptake by Ca2+ is completely abolished by alpha-cyanocinnamate a specific inhibitor of pyruvate translocation but not by lanthanide which inhibits Ca2+ uptake. Direct measurements of the transmembrane delta pH in mitochondria show no appreciable changes following the addition of Ca2+, this excluding the possibility that the Ca2+ dependent stimulation of pyruvate uptake might be due to an increase of transmembrane delta pH. It is therefore conceivable that the effect of Ca2+ can be ascribed to an interaction of this cation with the translocator on the external of the mitochondrial membrane. Although the data obtained do not warrant postulation of the nature of the calcium induced stimulation of mitochondrial pyruvate transport it is likely that this effect may be of a great importance in the regulation of pyruvate transport and metabolism in mitochondria.

Animals↗
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↗
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↗