ArticleThe Journal of biological chemistry2012
A refined analysis of superoxide production by mitochondrial sn-glycerol 3-phosphate dehydrogenase.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
80 citing papers in PubMed, 163 citations in OpenAlex.
- Linking cellular metabolism to mitochondrial outer membrane potential.Mitochondrion · 2026Article
- Experimental workflows for the accurate identification of mitochondrial redox events.Redox biology · 2026Review
- Reply to Lemieux et al.: Integration does not preclude essentiality of mitochondrial glycerol-3-phosphate dehydrogenase.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Adaptation of mitochondrial bioenergetics to coenzyme Q deficiency in human endothelial cells after chronic exposure to bisphosphonates.Scientific reports · 2025Article
- Reactive oxygen species in the pathogenesis of sarcopenia.Free radical biology & medicine · 2025Review
- Article
- Understanding coenzyme Q.Physiological reviews · 2024Review
- Mitochondrial Calcium Regulation of Cardiac Metabolism in Health and Disease.Physiology (Bethesda, Md.) · 2024Review
- Mitochondrial Physiology of Cellular Redox Regulations.Physiological research · 2024Review
- Membrane depolarization kills dormant Bacillus subtilis cells by generating a lethal dose of ROS.Nature communications · 2024Article
- Glycerol 3-phosphate dehydrogenases (1 and 2) in cancer and other diseases.Experimental & molecular medicine · 2024Review
- Mitochondrial Cristae Morphology Reflecting Metabolism, Superoxide Formation, Redox Homeostasis, and Pathology.Antioxidants & redox signaling · 2023Review
- Changes in the Mitochondria in the Aging Process-Can α-Tocopherol Affect Them?International journal of molecular sciences · 2023Review
- Mitochondrial calcium and reactive oxygen species in cardiovascular disease.Cardiovascular research · 2023Review
- Site IQ in mitochondrial complex I generates S1QEL-sensitive superoxide/hydrogen peroxide in both the reverse and forward reactions.The Biochemical journal · 2023Article
- Non-bioenergetic roles of mitochondrial GPD2 promote tumor progression.Theranostics · 2023Article
- The bridge between cell survival and cell death: reactive oxygen species-mediated cellular stress.EXCLI journal · 2023Review
- Effects of sugars, fatty acids and amino acids on cytosolic and mitochondrial hydrogen peroxide release from liver cells.Free radical biology & medicine · 2022Article
- Production of Carotenoids and Phospholipids byMarine drugs · 2022Article
- Mitochondrial Phenotype as a Driver of the Racial Dichotomy in Obesity and Insulin Resistance.Biomedicines · 2022Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The oxidation of sn-glycerol 3-phosphate by mitochondrial sn-glycerol 3-phosphate dehydrogenase (mGPDH) is a major pathway for transfer of cytosolic reducing equivalents to the mitochondrial electron transport chain. It is known to generate H(2)O(2) at a range of rates and from multiple sites within the chain. The rates and sites depend upon tissue source, concentrations of glycerol 3-phosphate and calcium, and the presence of different electron transport chain inhibitors. We report a detailed examination of H(2)O(2) production during glycerol 3-phosphate oxidation by skeletal muscle, brown fat, brain, and heart mitochondria with an emphasis on conditions under which mGPDH itself is the source of superoxide and H(2)O(2). Importantly, we demonstrate that a substantial portion of H(2)O(2) production commonly attributed to mGPDH originates instead from electron flow through the ubiquinone pool into complex II. When complex II is inhibited and mGPDH is the sole superoxide producer, the rate of superoxide production depends on the concentrations of glycerol 3-phosphate and calcium and correlates positively with the predicted reduction state of the ubiquinone pool. mGPDH-specific superoxide production plateaus at a rate comparable with the other major sites of superoxide production in mitochondria, the superoxide-producing center shows no sign of being overreducible, and the maximum superoxide production rate correlates with mGPDH activity in four different tissues. mGPDH produces superoxide approximately equally toward each side of the mitochondrial inner membrane, suggesting that the Q-binding pocket of mGPDH is the major site of superoxide generation. These results clarify the maximum rate and mechanism of superoxide production by mGPDH.
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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.