ArticleRedox biology2016
Induction of mitochondrial reactive oxygen species production by GSH mediated S-glutathionylation of 2-oxoglutarate dehydrogenase.
Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 90 citations in OpenAlex.
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- Comparative chromatin accessibility and transcriptome analyses identify key energy metabolism genes for hypoxia adaptation in embryos of Tibetan chickens.Poultry science · 2026Article
- miR-1343-3p regulating OGDHL/PDHB-pyruvate glucose metabolic reprogramming against gastric cancer cell proliferation.Discover oncology · 2025Article
- Glutaredoxin 2 Protects Lens Epithelial Cells From Ferroptosis by Preventing HNRNPA2B1 S-Glutathionylation in Diabetes-Mediated Cataractogenesis.Investigative ophthalmology & visual science · 2025Article
- A preserved TGFβ cytostatic response through DLD-mediated metabolic modulation undermines anti-TGFβ therapy in gastric cancer.Nature communications · 2025Article
- PET microplastics alter the transcriptome profile and oxidative stress markers in the liver of immature piglets: an in vivo study.Archives of toxicology · 2025Article
- From Carcinogenesis to Drug Resistance: The Multifaceted Role of Oxidative Stress in Head and Neck Cancer.Cancers · 2025Review
- Common food preservatives induce an oxidative stress response inMicrobiology (Reading, England) · 2025Article
- Oxidative stress-induced CDO1 glutathionylation regulates cysteine metabolism and sustains redox homeostasis under ionizing radiation.Redox biology · 2025Article
- Targeted Redox Regulation α-Ketoglutarate Dehydrogenase Complex for the Treatment of Human Diseases.Cells · 2025Review
- ROS and calcium signaling are critical determinant of skin pigmentation.Cell calcium · 2025Review
- Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells.Biology · 2024Review
- Identifying Redox-Sensitive Cysteine Residues in Mitochondria.Antioxidants (Basel, Switzerland) · 2023Article
- Oxidative stress involves phenotype modulation of morbid soreness symptoms in fibromyalgia.RMD open · 2023Article
- Nitric oxide-driven modifications of lipoic arm inhibit α-ketoacid dehydrogenases.Nature chemical biology · 2023Article
- The mechanisms of action of mitochondrial targeting agents in cancer: inhibiting oxidative phosphorylation and inducing apoptosis.Frontiers in pharmacology · 2023Review
- RNA Sequencing Analysis Reveals Divergent Adaptive Response to Hypo- and Hyper-Salinity in Greater Amberjack (Animals : an open access journal from MDPI · 2022Article
- Targeting 2-oxoglutarate dehydrogenase for cancer treatment.American journal of cancer research · 2022Review
- Mechanism Involved in Acute Liver Injury Induced by Intestinal Ischemia-Reperfusion.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
2-Oxoglutarate dehydrogenase (Ogdh) is an important mitochondria redox sensor that can undergo S-glutathionylation following an increase in H2O2 levels. Although S-glutathionylation is required to protect Ogdh from irreversible oxidation while simultaneously modulating its activity it remains unknown if glutathione can also modulate reactive oxygen species (ROS) production by the complex. We report that reduced (GSH) and oxidized (GSSG) glutathione control O2(∙-)/H2O2 formation by Ogdh through protein S-glutathionylation reactions. GSSG (1mM) induced a modest decrease in Ogdh activity which was associated with a significant decrease in O2(∙-)/H2O2 formation. GSH had the opposite effect, amplifying O2(∙-)/H2O2 formation by Ogdh. Incubation of purified Ogdh in 2.5mM GSH led to significant increase in O2(∙-)/H2O2 formation which also lowered NADH production. Inclusion of enzymatically active glutaredoxin-2 (Grx2) in reaction mixtures reversed the GSH-mediated amplification of O2(∙-)/H2O2 formation. Similarly pre-incubation of permeabilized liver mitochondria from mouse depleted of GSH showed an approximately ~3.5-fold increase in Ogdh-mediated O2(∙-)/H2O2 production that was matched by a significant decrease in NADH formation which could be reversed by Grx2. Taken together, our results demonstrate GSH and GSSG modulate ROS production by Ogdh through S-glutathionylation of different subunits. This is also the first demonstration that GSH can work in the opposite direction in mitochondria-amplifying ROS formation instead of quenching it. We propose that this regulatory mechanism is required to modulate ROS emission from Ogdh in response to variations in glutathione redox buffering capacity.
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