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Mitochondrial ATP‐sensitive K+ channel opening decreases reactive oxygen species generation
Open accessAbstract
Mitochondrial ATP‐sensitive K+ channel (mitoK ATP) opening was shown previously to slightly increase respiration and decrease the membrane potential by stimulating K+ cycling across the inner membrane. Here we show that mitoK ATP opening reduces reactive oxygen species generation in heart, liver and brain mitochondria. Decreased H 2 O 2 release is observed when mitoK ATP is active both with respiration stimulated by oxidative phosphorylation and when ATP synthesis is inhibited. In addition, decreased H 2 O 2 release is observed when mitochondrial ΔpH is enhanced, an effect expected to occur when mitoK ATP is open. We conclude that mitoK ATP is an effective pathway to trigger mild uncoupling, preventing reactive oxygen species release.
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“This might explain why a ROS-increasing effect of diazoxide has not been detected in the presence of NADH-generating substrates or when complex III was not inhibited [129,138,139].”
From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [138]
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Metadata
- Authors
- Ferranti, R., da Silva, M. M., & Kowaltowski, A. J.
- Affiliations
- Universidade de São Paulo (BR)
- Corresponding author
- Kowaltowski, Alicia J
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2003-01-15
- Volume
- 536
- Issue
- 1-3
- Pages
- 51-55
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2039868368
- Cited by
- 136
- References
- 25
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 1 · 2021: 4 · 2020: 3 · 2019: 1 · 2018: 4 · 2017: 2 · 2016: 2 · 2015: 6 · 2014: 5 · 2013: 8 · 2012: 6
- FWCI
- 4.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fundação de Amparo à Pesquisa do Estado de São Paulo
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- mitochondrial ATP-sensitive potassium channel, reactive oxygen species, hydrogen peroxide release, mitochondrial uncoupling, mitochondrial membrane potential, oxidative phosphorylation, ATP synthesis inhibition, heart mitochondria, liver mitochondria, brain mitochondria, mitochondrial respiration
- MeSH terms
- Adenosine Triphosphate, Animals, Brain, Hydrogen Peroxide, Mitochondria, Mitochondria, Heart, Mitochondria, Liver, Oxidative Phosphorylation, Potassium, Potassium Channels, Ion Transport, Reactive Oxygen Species
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