ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
Forward operation of adenine nucleotide translocase during F0F1-ATPase reversal: critical role of matrix substrate-level phosphorylation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- Localization of SUCLA2 and SUCLG2 subunits of succinyl CoA ligase within the cerebral cortex suggests the absence of matrix substrate-level phosphorylation in glial cells of the human brain.Journal of bioenergetics and biomembranes · 2015Trial
- Re-evaluating the rationale for targeting oxidative phosphorylation in acute myeloid leukemia.The Biochemical journal · 2026Review
- Complex I preserves mitochondrial polarization during infection of human macrophages by secretion-competent bacteria.Infection and immunity · 2026Article
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
- Measuring mitochondrial membrane potential.The EMBO journal · 2025Article
- Oxidative Phosphorylation in Uncoupled Mitochondria.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The Warburg hypothesis and the emergence of the mitochondrial metabolic theory of cancer.Journal of bioenergetics and biomembranes · 2025Review
- Acute myeloid leukemia mitochondria hydrolyze ATP to support oxidative metabolism and resist chemotherapy.Science advances · 2025Article
- Complex I activity in hypoxia: implications for oncometabolism.Biochemical Society transactions · 2024Review
- Impact of Lysine Succinylation on the Biology of Fungi.Current issues in molecular biology · 2024Review
- Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia.Scientific reports · 2024Article
- Amino Acid and Glucose Fermentation Maintain ATP Content in Mouse and Human Malignant Glioma Cells.ASN neuro · 2024Article
- Viability of HepG2 and MCF-7 cells is not correlated with mitochondrial bioenergetics.Scientific reports · 2023Article
- How much (ATP) does it cost to build a trypanosome? A theoretical study on the quantity of ATP needed to maintain and duplicate a bloodstream-form Trypanosoma brucei cell.PLoS pathogens · 2023Article
- Article
- Proline Oxidation Supports Mitochondrial ATP Production When Complex I Is Inhibited.International journal of molecular sciences · 2022Article
- Endoplasmic reticulum stress induces mitochondrial dysfunction but not mitochondrial unfolded protein response in SH-SY5Y cells.Molecular and cellular biochemistry · 2022Article
- Energy metabolism design of the striated muscle cell.Physiological reviews · 2021Review
- The Mystery of Extramitochondrial Proteins Lysine Succinylation.International journal of molecular sciences · 2021Review
- Beyond mitochondria: Alternative energy-producing pathways from all strata of life.Metabolism: clinical and experimental · 2021Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
In pathological conditions, F(0)F(1)-ATPase hydrolyzes ATP in an attempt to maintain mitochondrial membrane potential. Using thermodynamic assumptions and computer modeling, we established that mitochondrial membrane potential can be more negative than the reversal potential of the adenine nucleotide translocase (ANT) but more positive than that of the F(0)F(1)-ATPase. Experiments on isolated mitochondria demonstrated that, when the electron transport chain is compromised, the F(0)F(1)-ATPase reverses, and the membrane potential is maintained as long as matrix substrate-level phosphorylation is functional, without a concomitant reversal of the ANT. Consistently, no cytosolic ATP consumption was observed using plasmalemmal K(ATP) channels as cytosolic ATP biosensors in cultured neurons, in which their in situ mitochondria were compromised by respiratory chain inhibitors. This finding was further corroborated by quantitative measurements of mitochondrial membrane potential, oxygen consumption, and extracellular acidification rates, indicating nonreversal of ANT of compromised in situ neuronal and astrocytic mitochondria; and by bioluminescence ATP measurements in COS-7 cells transfected with cytosolic- or nuclear-targeted luciferases and treated with mitochondrial respiratory chain inhibitors in the presence of glycolytic plus mitochondrial vs. only mitochondrial substrates. Our findings imply the possibility of a rescue mechanism that is protecting against cytosolic/nuclear ATP depletion under pathological conditions involving impaired respiration. This mechanism comes into play when mitochondria respire on substrates that support matrix substrate-level phosphorylation.
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