Sulforaphane is a Nrf2-independent inhibitor of mitochondrial fission
O'Mealey GB, Berry WL, Plafker SM
Redox biology · 66 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- Oklahoma Center for the Advancement of Science and Technology
- Government
- National Institutes of Health
- Government
- National Institute of General Medical Sciences
- Government
- NIGMS NIH HHS
- Grants
- Oklahoma Center for the Advancement of Science and Technology (HR13-182); National Institutes of Health (R01 GM092900); National Institute of General Medical Sciences (R01GM092900)
Based on 4 listed funder(s).
Publication
- Published
- 2016-11-21 · Redox Biol · vol. 11 · pp. 103–110
- Publisher
- Elsevier BV
- Cited
- 79 citations · more than 92% of similar papers · 3.1× the field average
- Impact
- Top 10% most cited in its field
- References
- 61 works
- Access
- Open access (journal) · CC-BY-NC-ND
- Research areas
- Genomics, phytochemicals, and oxidative stress · Glutathione Transferases and Polymorphisms · Redox biology and oxidative stress
- Keywords
- Sulforaphane, KEAP1, Cytoprotection, Staurosporine, Mitochondrion, Oxidative stress, Cell biology, Mitochondrial fission, Apoptosis, Chemistry, Biology, Biochemistry, Signal transduction, Transcription factor, Protein kinase C
- MeSH
- mitochondria, humans, isothiocyanates, sulfoxides, dynamins, carboxylic ester hydrolases, antioxidants, signal transduction, apoptosis, oxidative stress, nf-e2-related factor 2, retinal pigment epithelium, mitochondrial dynamics, kelch-like ech-associated protein 1
3 authors
From US
- Gary B. O'MealeyOklahoma Medical Research Foundation
- William L. BerryUniversity of Oklahoma Health Sciences Center
- Scott M. Plafker · correspondingOklahoma Medical Research Foundation
Abstract
The KEAP1-Nrf2-ARE antioxidant system is a principal means by which cells respond to oxidative and xenobiotic stresses. Sulforaphane (SFN), an electrophilic isothiocyanate derived from cruciferous vegetables, activates the KEAP1-Nrf2-ARE pathway and has become a molecule-of-interest in the treatment of diseases in which chronic oxidative stress plays a major etiological role. We demonstrate here that the mitochondria of cultured, human retinal pigment epithelial (RPE-1) cells treated with SFN undergo hyperfusion that is independent of both Nrf2 and its cytoplasmic inhibitor KEAP1. Mitochondrial fusion has been reported to be cytoprotective by inhibiting pore formation in mitochondria during apoptosis, and consistent with this, we show Nrf2-independent, cytoprotection of SFN-treated cells exposed to the apoptosis-inducer, staurosporine. Mechanistically, SFN mitigates the recruitment and/or retention of the soluble fission factor Drp1 to mitochondria and to peroxisomes but does not affect overall Drp1 abundance. These data demonstrate that the beneficial properties of SFN extend beyond activation of the KEAP1-Nrf2-ARE system and warrant further interrogation given the current use of this agent in multiple clinical trials.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY-NC-ND).
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