ArticleThe Journal of biological chemistry2018
Oxaloacetic acid mediates ADP-dependent inhibition of mitochondrial complex II-driven respiration.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Protonophore uncouplers and the decoupler α,ω-hexadecanedioic acid relieve the succinate-induced blockade of glutamate and malate oxidation in the resting state (state 4).Journal of bioenergetics and biomembranes · 2026Article
- Oxaloacetate damages mitochondria by perturbing MIC60-dependent membrane remodeling.PLoS biology · 2026Article
- Oxaloacetate inhibition of succinate dehydrogenase: mechanism and physiological implications.American journal of physiology. Cell physiology · 2026Review
- Review
- The Post-COVID syndrome caused by excessive inflammation: pathogenesis, potential targets and therapeutic agents.Frontiers in pharmacology · 2026Review
- Sex dimorphism and substrate dependency of liver mitochondrial bioenergetics and HAmerican journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Mitochondrial reactive oxygen species production in lungs of rats with different susceptibilities to hyperoxia-induced acute lung injury.Biochimica et biophysica acta. Bioenergetics · 2025Article
- Deletion of Skeletal Muscle Mitochondrial Glutamic-Oxaloacetic Transaminase (GOT2) Enhances Oxaloacetate Inhibition of Succinate Dehydrogenase and Alters Substrate Selectivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Restoring Homeostasis: Treating Amyotrophic Lateral Sclerosis by Resolving Dynamic Regulatory Instability.International journal of molecular sciences · 2025Article
- GATD3A-deficiency-induced mitochondrial dysfunction facilitates senescence of fibroblast-like synoviocytes and osteoarthritis progression.Nature communications · 2024Article
- L-Arginine and Intermittent Hypoxia Are Stress-Limiting Factors in Male Wistar Rat Models.International journal of molecular sciences · 2024Article
- Effect of the mitochondrial transaminase (GOT2) on membrane potential-sensitive respiration in mitochondria of differentiated C2C12 muscle cells.American journal of physiology. Cell physiology · 2024Article
- Complex II ambiguities-FADHThe Journal of biological chemistry · 2024Review
- Effects of ROS pathway inhibitors and NADH and FADHArchives of biochemistry and biophysics · 2023Article
- Oxaloacetate regulates complex II respiration in brown fat: dependence on UCP1 expression.American journal of physiology. Cell physiology · 2023Article
- Regulation and function of the mammalian tricarboxylic acid cycle.The Journal of biological chemistry · 2023Review
- Metabolic clearance of oxaloacetate and mitochondrial complex II respiration: Divergent control in skeletal muscle and brown adipose tissue.Biochimica et biophysica acta. Bioenergetics · 2023Article
- Computational Modeling of Substrate-Dependent Mitochondrial Respiration and Bioenergetics in the Heart and Kidney Cortex and Outer Medulla.Function (Oxford, England) · 2023Article
- Membrane potential-dependent regulation of mitochondrial complex II by oxaloacetate in interscapular brown adipose tissue.FASEB bioAdvances · 2022Article
- Substrate-dependent differential regulation of mitochondrial bioenergetics in the heart and kidney cortex and outer medulla.Biochimica et biophysica acta. Bioenergetics · 2022Article
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7 authors at 1 institution in 1 country.
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Abstract
We recently reported a previously unrecognized mitochondrial respiratory phenomenon. When [ADP] was held constant ("clamped") at sequentially increasing concentrations in succinate-energized muscle mitochondria in the absence of rotenone (commonly used to block complex I), we observed a biphasic, increasing then decreasing, respiratory response. Here we investigated the mechanism. We confirmed decades-old reports that oxaloacetate (OAA) inhibits succinate dehydrogenase (SDH). We then used an NMR method to assess OAA concentrations (known as difficult to measure by MS) as well as those of malate, fumarate, and citrate in isolated succinate-respiring mitochondria. When these mitochondria were incubated at varying clamped ADP concentrations, respiration increased at low [ADP] as expected given the concurrent reduction in membrane potential. With further increments in [ADP], respiration decreased associated with accumulation of OAA. Moreover, a low pyruvate concentration, that alone was not enough to drive respiration, was sufficient to metabolize OAA to citrate and completely reverse the loss of succinate-supported respiration at high [ADP]. Further, chemical or genetic inhibition of pyruvate uptake prevented OAA clearance and preserved respiration. In addition, we measured the effects of incremental [ADP] on NADH, superoxide, and H
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