We have studied the role of changes in mitochondrial membrane potential (DeltaPsi) in two widely-used models of apoptosis, such as dexamethasone-treated rat thymocytes and U937 human cells treated with tumor necrosis factor-alpha and cycloheximide. To dissipate DeltaPsi, we used low concentrations of valinomycin, unable per se to induce apoptosis, and demonstrated that the decline in DeltaPsi exerts opposite effects in the two models. Indeed, in U937 cells, depolarization of mitochondria increased apoptosis, which decreased in rat thymocytes.
View Article and Find Full Text PDFThe effect of the in vivo thyroid status on mitochondrial membrane potential (delta psi(m)) in isolated rat hepatocytes was studies by means of a cytofluorimetric technique and the delta psi(m)-specific probe JC-1. It is shown that the delta psi(m) level decreases in the order hypothyroid > euthyroid > hyperthyroid. Polarographic measurement of the hepatocyte respiratory rates revealed an opposite trend of values: the highest respiratory rate in hepatocytes from hyperthyroid animals, the lowest in those from hypothyroid ones.
View Article and Find Full Text PDFThe present paper describes the possibility of determination of mitochondrial membrane potential (Deltapsi) in isolated hepatocytes making use of a Deltapsi-sensitive dye, i.e., the lipophilic cationic probe 5,5',6,6'-tetrachloro-1,1',3, 3'-tetraethylbenzimidazolcarbocyanine iodide (JC-1) and of cytofluorimetry.
View Article and Find Full Text PDFBiochem Mol Biol Int
March 1997
The specific involvement of cardiolipin in modulating and/or controlling the activity of a number of mitochondrial carriers, enzymes and receptors is well documented; however, comparatively less understood is its role for the integrated functions of intact mitochondria. The aim of the present research was to get a better insight into this problem by investigating the effect of in vitro addition of cardiolipin on the properties of isolated liver mitochondria. The results obtained show that cardiolipin induces extensive structural and functional perturbations at the level of the inner mitochondrial membrane.
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