ArticleAmerican journal of physiology. Cell physiology2015
Thiol-based antioxidants elicit mitochondrial oxidation via respiratory complex III.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Phase II trial of cytarabine and mitoxantrone with devimistat in acute myeloid leukemia.Nature communications · 2022Trial
- The Reductive Stress Nexus: Integrated Pathways of Metabolic Dysregulation, Senescence and Blood-Brain Barrier Failure in Neurodegenerative Disease and Brain Aging.Cell biochemistry and biophysics · 2026Review
- Impact of mitochondrial reductive stress due to respiratory chain limitation on cancer via posttranslational modifications.Redox biology · 2026Review
- Early ADME and Preliminary Toxicity Studies of I-152, anChemical research in toxicology · 2026Article
- Cysteine induces mitochondrial reductive stress in glioblastoma through hydrogen peroxide production.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- CHCHD2 mediates glioblastoma cell proliferation, mitochondrial metabolism, hypoxia‑induced invasion and therapeutic resistance.International journal of oncology · 2023Article
- Expected and Unexpected Effects of Pharmacological Antioxidants.International journal of molecular sciences · 2023Review
- Antiproliferative effects of mitochondria-targeted N-acetylcysteine and analogs in cancer cells.Scientific reports · 2023Article
- Induction of Premature Cell Senescence Stimulated by High Doses of Antioxidants Is Mediated by Endoplasmic Reticulum Stress.International journal of molecular sciences · 2021Article
- Neuron Activity Dependent Redox Compartmentation Revealed with a Second Generation Red-Shifted Ratiometric Sensor.ACS chemical neuroscience · 2020Article
- Taurine Reverses Oxidative Damages and Restores the Muscle Function in Overuse of Exercised Muscle.Frontiers in physiology · 2020Review
- High doses of synthetic antioxidants induce premature senescence in cultivated mesenchymal stem cells.Scientific reports · 2019Article
- Extending roGFP Emission via Förster-Type Resonance Energy Transfer Relay Enables Simultaneous Dual Compartment Ratiometric Redox Imaging in Live Cells.ACS sensors · 2017Article
- N‑acetylcysteine induces apoptosis via the mitochondria‑dependent pathway but not via endoplasmic reticulum stress in H9c2 cells.Molecular medicine reports · 2017Article
- Comparison of neurons derived from mouse P19, rat PC12 and human SH-SY5Y cells in the assessment of chemical- and toxin-induced neurotoxicity.BMC pharmacology & toxicology · 2017Article
- Distinct responses of compartmentalized glutathione redox potentials to pharmacologic quinones targeting NQO1.Biochemical and biophysical research communications · 2017Article
- Live-cell imaging approaches for the investigation of xenobiotic-induced oxidant stress.Biochimica et biophysica acta · 2016Review
- An unexplored role for Peroxiredoxin in exercise-induced redox signalling?Redox biology · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Excessive oxidation is widely accepted as a precursor to deleterious cellular function. On the other hand, an awareness of the role of reductive stress as a similar pathological insult is emerging. Here we report early dynamic changes in compartmentalized glutathione (GSH) redox potentials in living cells in response to exogenously supplied thiol-based antioxidants. Noninvasive monitoring of intracellular thiol-disulfide exchange via a genetically encoded biosensor targeted to cytosol and mitochondria revealed unexpectedly rapid oxidation of the mitochondrial matrix in response to GSH ethyl ester or N-acetyl-l-cysteine. Oxidation of the probe occurred within seconds in a concentration-dependent manner and was attenuated with the membrane-permeable ROS scavenger tiron. In contrast, the cytosolic sensor did not respond to similar treatments. Surprisingly, the immediate mitochondrial oxidation was not abrogated by depolarization of mitochondrial membrane potential or inhibition of mitochondrial GSH uptake. After detection of elevated levels of mitochondrial ROS, we systematically inhibited multisubunit protein complexes of the mitochondrial respiratory chain and determined that respiratory complex III is a downstream target of thiol-based compounds. Disabling complex III with myxothiazol completely blocked matrix oxidation induced with GSH ethyl ester or N-acetyl-l-cysteine. Our findings provide new evidence of a functional link between exogenous thiol-containing antioxidants and mitochondrial respiration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.