Fluoxetine (Prozac) interaction with the mitochondrial voltage‐dependent anion channel and protection against apoptotic cell death
Abstract
Here, we demonstrate that fluoxetine interacted with VDAC and decreased its conductance. Fluoxetine inhibited the opening of the mitochondrial permeability transition pore, the release of cytochrome c, and protected against staurosporine‐induced apoptotic cell death. These findings may explain some of the reported fluoxetine side effects.
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Fluoxetine inhibits the opening of the mitochondrial permeability transition (MPT) pore, the release of cytochrome c, and protects against staurosporine-induced apoptotic cell death.
“Nahon et al. (2005) demonstrated that fluoxetine was able to inhibit the opening of the mitochondrial permeability transition (MPT) pore, the release of cytochrome c (cytC) and protected against staurosporine-induced apoptotic cell death [8].”
From Preclinical and Clinical Evidence of Antioxidant Effects of Antidepressant Agents: Implications for the Pathophysiology of Major Depressive Disorder (2012) · cites this paper as [8]
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- Authors
- Nahon, E., Israelson, A., Abu-Hamad, S., & Shoshan-Barmatz, V.
- Affiliations
- Ben-Gurion University of the Negev (IL)
- ORCID
- Israelson, Adrian
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2005-08-24
- Volume
- 579
- Issue
- 22
- Pages
- 5105-5110
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W1983099105
- Cited by
- 101
- References
- 34
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 4 · 2021: 5 · 2020: 7 · 2019: 5 · 2018: 8 · 2017: 8 · 2016: 7 · 2015: 4 · 2014: 4 · 2013: 6 · 2012: 11
- FWCI
- 1.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
- Keywords
- fluoxetine, mitochondrial voltage-dependent anion channel, voltage-dependent anion channel, mitochondrial permeability transition pore, cytochrome c release, staurosporine-induced apoptosis, apoptosis, adverse drug reactions, serotonin reuptake inhibition
- MeSH terms
- Animals, Cell Line, Enzyme Inhibitors, Fluoxetine, Humans, Mitochondria, Liver, Apoptosis, Selective Serotonin Reuptake Inhibitors, Porins, Staurosporine, Cytochromes c, Voltage-Dependent Anion Channels, Rats
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