1887

Abstract

We have previously reported that aspirin induces apoptosis in manganese superoxide dismutase (MnSOD)-deficient cells when cultivated on the non-fermentable carbon source ethanol. Here, we investigated the role of mitochondria in aspirin-induced apoptosis. We report that aspirin had an inhibitory effect on cellular respiration, and caused the release of most of the mitochondrial cytochrome and a dramatic drop in the mitochondrial membrane potential (ΔΨ). Also, aspirin reduced the intracellular cytosolic pH in the MnSOD-deficient cells growing in ethanol medium, but this did not seem to be the initial trigger that committed these cells to aspirin-induced apoptosis. Furthermore, loss of ΔΨ was not required for aspirin-induced release of cytochrome , since the initial release of cytochrome occurred prior to the disruption of the ΔΨ. It is thus possible that cytochrome release does not involve the early onset of the mitochondrial permeability transition, but only an alteration of the permeability of the outer mitochondrial membrane.

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2008-09-01
2024-04-18
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