ArticlePloS one2013
Hyperoxia decreases glycolytic capacity, glycolytic reserve and oxidative phosphorylation in MLE-12 cells and inhibits complex I and II function, but not complex IV in isolated mouse lung mitochondria.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Analysis of variable metabolites in preterm infants with bronchopulmonary dysplasia: a systematic review and meta-analysis.Italian journal of pediatrics · 2024Pooled it
- Oxygen physiology and mechanisms of oxygen toxicity: a narrative review.Medical gas research · 2026Review
- Computational modeling of substrate-dependent lung mitochondrial respiration and bioenergetics in rats with different susceptibility to hyperoxia-induced ARDS.American journal of physiology. Cell physiology · 2026Article
- How hyperoxia affects systemic redox state: insights from PULSE-Ox, a randomised double-blind mechanistic feasibility trial.BJA open · 2026Article
- Sex-specific differences in lung mitochondrial function and injury in rats exposed to hyperoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- SLC25A28 Ameliorates Hyperoxic Lung Injury by Improving Mitochondrial Oxidative Phosphorylation in Alveolar Epithelial Cells.International journal of molecular sciences · 2026Article
- PKM2 Promotes Glycolysis in Alveolar Macrophages and Induces Inflammation in Bronchopulmonary Dysplasia.Inflammation · 2026Article
- High-fat diet obesity exacerbates acute lung injury-induced dysregulation of fatty acid oxidation in alveolar epithelial type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Ferroptosis and hyperoxic lung injury: insights into pathophysiology and treatment approaches.Frontiers in pharmacology · 2025Review
- Longitudinal transcriptomic analysis of the hyperoxia-exposed preterm rabbit as a model of BPD.Frontiers in pediatrics · 2025Article
- Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.Frontiers in physiology · 2025Article
- Caffeine, MitoQ, and GABA Prophylaxis of Mitochondrial Dysfunction Induced in Human Pulmonary Cells by Normobaric-Hyperoxia and Hyperbaric-Hyperoxia.Oxidative medicine and cellular longevity · 2025Article
- L-carnitine: new perspectives on the management of preterm infants.Frontiers in nutrition · 2025Review
- Activated DRP1 promotes mitochondrial fission and induces glycolysis in ATII cells under hyperoxia.Respiratory research · 2024Article
- MicroRNA-210 mediates hypoxia-induced pulmonary hypertension by targeting mitochondrial bioenergetics and mtROS flux.Acta physiologica (Oxford, England) · 2024Article
- Metabolic changes inmBio · 2024Article
- Hypoxia-induced pulmonary hypertension in adults and newborns: implications for drug development.Drug discovery today · 2024Review
- Visualization of the relationship between metabolism and lung diseases from the perspective of bibliometric analysis: research trends and future prospects.Frontiers in medicine · 2024Article
- High-physiological and supra-physiological 1,2-Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
High levels of oxygen (hyperoxia) are frequently used in critical care units and in conditions of respiratory insufficiencies in adults, as well as in infants. However, hyperoxia has been implicated in a number of pulmonary disorders including bronchopulmonary dysplasia (BPD) and adult respiratory distress syndrome (ARDS). Hyperoxia increases the generation of reactive oxygen species (ROS) in the mitochondria that could impair the function of the mitochondrial electron transport chain. We analyzed lung mitochondrial function in hyperoxia using the XF24 analyzer (extracellular flux) and optimized the assay for lung epithelial cells and mitochondria isolated from lungs of mice. Our data show that hyperoxia decreases basal oxygen consumption rate (OCR), spare respiratory capacity, maximal respiration and ATP turnover in MLE-12 cells. There was significant decrease in glycolytic capacity and glycolytic reserve in MLE-12 cells exposed to hyperoxia. Using mitochondria isolated from lungs of mice exposed to hyperoxia or normoxia we have shown that hyperoxia decreased the basal, state 3 and state3 μ (respiration in an uncoupled state) respirations. Further, using substrate or inhibitor of a specific complex we show that the OCR via complex I and II, but not complex IV was decreased, demonstrating that complexes I and II are specific targets of hyperoxia. Further, the activities of complex I (NADH dehydrogenase, NADH-DH) and complex II (succinate dehydrogenase, SDH) were decreased in hyperoxia, but the activity of complex IV (cytochrome oxidase, COX) remains unchanged. Taken together, our study show that hyperoxia impairs glycolytic and mitochondrial energy metabolism in in tact cells, as well as in lungs of mice by selectively inactivating components of electron transport system.
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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.