ArticleBiochimica et biophysica acta2013
Reverse electron flow-mediated ROS generation in ischemia-damaged mitochondria: role of complex I inhibition vs. depolarization of inner mitochondrial membrane.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- The ABA/LANCL1-2 Hormone/Receptors System Controls ROS Production in Cardiomyocytes through ERRα.Biomedicines · 2024Article
- Abscisic Acid and Its Receptors LANCL1 and LANCL2 Control Cardiomyocyte Mitochondrial Function, Expression of Contractile, Cytoskeletal and Ion Channel Proteins and Cell Proliferation via ERRα.Antioxidants (Basel, Switzerland) · 2023Article
- Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases.International journal of molecular sciences · 2023Review
- Substrate-dependent differential regulation of mitochondrial bioenergetics in the heart and kidney cortex and outer medulla.Biochimica et biophysica acta. Bioenergetics · 2022Article
- Calpain-mediated protein targets in cardiac mitochondria following ischemia-reperfusion.Scientific reports · 2022Article
- Article
- Time to Target Mitochondrial Reactive Oxygen Species Generation from Complex I.Function (Oxford, England) · 2022Article
- Preventing Myocardial Injury Following Non-Cardiac Surgery: A Potential Role for Preoperative Antioxidant Therapy with Ubiquinone.Antioxidants (Basel, Switzerland) · 2021Review
- Targeting ER stress and calpain activation to reverse age-dependent mitochondrial damage in the heart.Mechanisms of ageing and development · 2020Review
- Cardiomyocyte specific deletion of p53 decreases cell injury during ischemia-reperfusion: Role of Mitochondria.Free radical biology & medicine · 2020Article
- InactivatedExperimental and therapeutic medicine · 2020Article
- Mitochondrial NADH redox potential impacts the reactive oxygen species production of reverse Electron transfer through complex I.Journal of bioenergetics and biomembranes · 2018Article
- Metformin attenuates ER stress-induced mitochondrial dysfunction.Translational research : the journal of laboratory and clinical medicine · 2017Article
- In Vitro Effects of Cognitives and Nootropics on Mitochondrial Respiration and Monoamine Oxidase Activity.Molecular neurobiology · 2017Article
- Impairment of pH gradient and membrane potential mediates redox dysfunction in the mitochondria of the post-ischemic heart.Basic research in cardiology · 2017Article
- Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex III.The Journal of biological chemistry · 2017Article
- Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies.Annual review of pharmacology and toxicology · 2017Review
- Mitochondrial Metabolism in Aging Heart.Circulation research · 2016Review
- Anticancer potential of Conium maculatum extract against cancer cells in vitro: Drug-DNA interaction and its ability to induce apoptosis through ROS generation.Pharmacognosy magazine · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe reverse electron flow-induced ROS generation (RFIR) is decreased in ischemia-damaged mitochondria. Cardiac ischemia leads to decreased complex I activity and depolarized inner mitochondrial membrane potential (ΔΨ) that are two key factors to affect the RFIR in isolated mitochondria. We asked if a partial inhibition of complex I activity without alteration of the ΔΨ is able to decrease the RFIR.
methodsCardiac mitochondria were isolated from mouse heart (C57BL/6) with and without ischemia. The rate of H2O2 production from mitochondria was determined using amplex red coupled with horseradish peroxidase. Mitochondria were isolated from the mitochondrial-targeted STAT3 overexpressing mouse (MLS-STAT3E) to clarify the role of partial complex I inhibition in RFIR production.
resultsThe RFIR was decreased in ischemia-damaged mouse heart mitochondria with decreased complex I activity and depolarized ΔΨ. However, the RFIR was not altered in the MLS-STAT3E heart mitochondria with complex I defect but without depolarization of the ΔΨ. A slight depolarization of the ΔΨ in wild type mitochondria completely eliminated the RFIR.
conclusionsThe mild uncoupling but not the partially decreased complex I activity contributes to the observed decrease in RFIR in ischemia-damaged mitochondria. GENERAL SIGNIFICANCE: The RFIR is less likely to be a key source of cardiac injury during reperfusion.
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