Related Experiment Video
Updated: Jul 2, 2026
Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
Mitochondrial involvement in aspirin-induced apoptosis in yeast
Karen Sapienza1, William Bannister1, Rena Balzan1
1Department of Physiology and Biochemistry, University of Malta, Msida MSD 2080, Malta.
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 (DeltaPsi(m)). 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 DeltaPsi(m) was not required for aspirin-induced release of cytochrome c, since the initial release of cytochrome c occurred prior to the disruption of the DeltaPsi(m). 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.
Insights
Aspirin triggers programmed cell death (apoptosis) in yeast by disrupting cellular respiration and releasing cytochrome c from mitochondria. This occurs independently of mitochondrial membrane potential loss, suggesting outer membrane alterations.
Area of Science:
- Biochemistry
- Cell Biology
- Yeast Genetics
Background:
- Aspirin is known to induce apoptosis in specific yeast models.
- Manganese superoxide dismutase (MnSOD)-deficient Saccharomyces cerevisiae cells are sensitive to aspirin-induced apoptosis on ethanol medium.
Purpose of the Study:
- To investigate the role of mitochondria in aspirin-induced apoptosis in MnSOD-deficient yeast.
- To elucidate the sequence of events leading to cytochrome c release and cell death.
Main Methods:
- Cultivation of MnSOD-deficient Saccharomyces cerevisiae on ethanol medium.
- Measurement of cellular respiration, mitochondrial membrane potential (DeltaPsi(m)), and intracellular cytosolic pH.
- Analysis of mitochondrial cytochrome c release.
Main Results:
- Aspirin inhibited cellular respiration and reduced mitochondrial membrane potential.
- Aspirin induced the release of mitochondrial cytochrome c into the cytosol.
- Cytochrome c release preceded the loss of mitochondrial membrane potential, and cytosolic pH drop was not the initial trigger.
Conclusions:
- Mitochondrial dysfunction, specifically cytochrome c release via outer membrane permeability changes, is central to aspirin-induced apoptosis in this yeast model.
- The loss of mitochondrial membrane potential is not a prerequisite for initial cytochrome c release.
