@article{mbs:/content/journal/micro/10.1099/mic.0.2008/017228-0, author = "Sapienza, Karen and Bannister, William and Balzan, Rena", title = "Mitochondrial involvement in aspirin-induced apoptosis in yeast", journal= "Microbiology", year = "2008", volume = "154", number = "9", pages = "2740-2747", doi = "https://doi.org/10.1099/mic.0.2008/017228-0", url = "https://www.microbiologyresearch.org/content/journal/micro/10.1099/mic.0.2008/017228-0", publisher = "Microbiology Society", issn = "1465-2080", type = "Journal Article", keywords = "FCCP, carbonylcyanide-p-trifluoromethoxyphenylhydrazone", keywords = "pHi, intracellular pH", keywords = "NAO, 10-N-nonyl acridine orange", keywords = "Rh123, rhodamine 123", keywords = "ROS, reactive oxygen species", keywords = "MnSOD, manganese superoxide dismutase", keywords = "ΔΨm, mitochondrial membrane potential", keywords = "C-SNARF-1-AM, 5-(and-6-)-carboxy-seminaphthorhodafluor-1-acetoxymethyl ester", keywords = "CuZnSOD, copper/zinc superoxide dismutase", abstract = "We have previously reported that aspirin induces apoptosis in manganese superoxide dismutase (MnSOD)-deficient Saccharomyces cerevisiae 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 c and a dramatic drop in the mitochondrial membrane potential (ΔΨm). 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 ΔΨm was not required for aspirin-induced release of cytochrome c, since the initial release of cytochrome c occurred prior to the disruption of the ΔΨm. It is thus possible that cytochrome c release does not involve the early onset of the mitochondrial permeability transition, but only an alteration of the permeability of the outer mitochondrial membrane.", }