| Autor: |
Lenzen, Sigurd, Brünig, Heike, Münster, Wilfried |
| Zdroj: |
Molecular & Cellular Biochemistry; Oct1992, Vol. 116 Issue 2, p141-151, 11p |
| Abstrakt: |
Alloxan at millimolar concentrations slightly inhibited the velocity of Ca uptake by isolated rat liver mitochondria irrespective of the free Ca concentration between 1 and 10 µM and was an effective concentration-dependent stimulator of mitochondrial Ca efflux. Ninhydrin also slightly inhibited the velocity of mitochondrial Ca uptake but only at free Ca concentrations above 5 µM. However, ninhydrin was a strong stimulator of mitochondrial Ca efflux even at micromolar concentrations, 10-50 times more potent than alloxan. The mitochondrial membrane potential was reduced 10-20% at most by alloxan and ninhydrin. Alloxan and ninhydrin also stimulated Ca efflux from isolated permeabilized liver cells. When isolated intact liver cells had been pre-incubated with alloxan or ninhydrin before permeabilization of the cells the ability of spermine to induce mitochondrial Ca uptake was abolished. Glucose provided the typical protection against the effects of alloxan on mitochondrial Ca transport only in experiments with intact cells but not in experiments with permeabilized cells or isolated mitochondria. Therefore glucose protection is apparently due to inhibition of alloxan uptake into the cell. Glucose provided no protection against effects of ninhydrin under any of the experimental conditions. Thus both alloxan and ninhydrin are potent stimulators of Ca efflux by isolated mitochondria but very weak inhibitors of the velocity of mitochondrial Ca uptake. The direct effects of ninhydrin on mitochondrial Ca efflux may contribute to the cytotoxic action of this agent whereas the direct effects of alloxan on mitochondrial Ca transport require concentrations which are too high to be of relevance for the induction of the typical pancreatic B-cell toxic effects of alloxan. However, the effects on mitochondrial Ca transport during incubation of intact cells which may result from the generation of cytotoxic intermediates during alloxan xenobiotic metabolism may well contribute to the pancreatic B-cell toxic effect of alloxan. Mol Cell Biochem 118: 141-151, 1992) [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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