ArticleOncotarget2016
Apoptosis inducing factor (AIF) mediates lethal redox stress induced by menadione.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
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- Pyrazoline B Induces Oxidative Stress Mediated Toxicity, Cell Cycle Arrest, and Caspase-Independent Apoptosis in BT-474 Human Breast Cancer Cells.Journal of experimental pharmacology · 2025Article
- Antioxidant and Anti-Inflammatory Potential ofJournal of inflammation research · 2025Article
- Loss of WDR23 proteostasis impacts mitochondrial homeostasis in the mouse brain.Cellular signalling · 2024Article
- Antioxidant, Antiinflammation, and Antifibrotic Activity of Ciplukan (Journal of inflammation research · 2024Article
- Modulators reducing the efficiency of oxidative ATP synthesis in mitochondria: protonophore uncouplers, cyclic redox agents, and decouplers.Biophysical reviews · 2023Review
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- Combination of Ascorbic Acid and Menadione Induces Cytotoxic Autophagy in Human Glioblastoma Cells.Oxidative medicine and cellular longevity · 2022Article
- Autophagy: A Player in response to Oxidative Stress and DNA Damage.Oxidative medicine and cellular longevity · 2019Article
- IMMP2L: a mitochondrial protease suppressing cellular senescence.Cell research · 2018Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial apoptosis inducing factor (AIF) is a redox-active enzyme that participates to the biogenesis/maintenance of complex I of the respiratory chain, yet also contributes to catabolic reactions in the context of regulated cell death when AIF translocates to the cytosol and to the nucleus. Here we explore the contribution of AIF to cell death induced by menadione (2-methyl-1,4-naphtoquinone; also called vitamin K3) in conditions in which this pro-oxidant does not cause the mitochondrial release of AIF, yet causes caspase-independent cell killing. Depletion of AIF from human cancer cells reduced the cytotoxicity of menadione. This cytoprotective effect was accompanied by the maintenance of high levels of reduced glutathione (GSH), which are normally depleted by menadione. In addition, AIF depletion reduced the arylation of cellular proteins induced by menadione. This menadione-triggered arylation, which can be measured by a fluorescence assay, is completely suppressed by addition of exogenous glutathione or N-acetyl cysteine. Complex I inhibition by Rotenone did not mimic the cytoprotective action of AIF depletion. Altogether, these results are compatible with the hypothesis that mitochondrion-sessile AIF facilitates lethal redox cycling of menadione, thereby precipitating protein arylation and glutathione depletion.
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