ArticleJournal of applied physiology (Bethesda, Md. : 1985)2008
Coenzyme Q1 redox metabolism during passage through the rat pulmonary circulation and the effect of hyperoxia.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2008. 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, 27 citations in OpenAlex.
- Sex-specific differences in lung mitochondrial function and injury in rats exposed to hyperoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Article
- Biomarkers of lung alveolarization and microvascular maturation in response to intermittent hypoxia and/or early antioxidant/fish oil supplementation in neonatal rats.Pediatric pulmonology · 2023Article
- In vivo molecular imaging stratifies rats with different susceptibilities to hyperoxic acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Depolarized mitochondrial membrane potential and protection with duroquinone in isolated perfused lungs from rats exposed to hyperoxia.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Quantification of mitochondrial membrane potential in the isolated rat lung using rhodamine 6G.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Combined inhibition of glycolysis, the pentose cycle, and thioredoxin metabolism selectively increases cytotoxicity and oxidative stress in human breast and prostate cancer.Redox biology · 2015Article
- Depleted energy charge and increased pulmonary endothelial permeability induced by mitochondrial complex I inhibition are mitigated by coenzyme Q1 in the isolated perfused rat lung.Free radical biology & medicine · 2013Article
- Novel Flurometric Tool to Assess Mitochondrial Redox State of Isolated Perfused Rat Lungs after Exposure to Hyperoxia.IEEE journal of translational engineering in health and medicine · 2013Article
- Surface fluorescence studies of tissue mitochondrial redox state in isolated perfused rat lungs.Annals of biomedical engineering · 2013Article
- Differential lung uptake of 99mTc-hexamethylpropyleneamine oxime and 99mTc-duramycin in the chronic hyperoxia rat model.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2012Article
- Role of glutathione in lung retention of 99mTc-hexamethylpropyleneamine oxime in two unique rat models of hyperoxic lung injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
- Coenzyme Q(1) as a probe for mitochondrial complex I activity in the intact perfused hyperoxia-exposed wild-type and Nqo1-null mouse lung.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Optical imaging of tissue mitochondrial redox state in intact rat lungs in two models of pulmonary oxidative stress.Journal of biomedical optics · 2012Article
- Differential responses of targeted lung redox enzymes to rat exposure to 60 or 85% oxygen.Journal of applied physiology (Bethesda, Md. : 1985) · 2011Article
- Quantifying mitochondrial and plasma membrane potentials in intact pulmonary arterial endothelial cells based on extracellular disposition of rhodamine dyes.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Genetic evidence for NAD(P)H:quinone oxidoreductase 1-catalyzed quinone reduction on passage through the mouse pulmonary circulation.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Characterization of the threshold for NAD(P)H:quinone oxidoreductase activity in intact sulforaphane-treated pulmonary arterial endothelial cells.Free radical biology & medicine · 2011Article
- Distribution of capillary transit times in isolated lungs of oxygen-tolerant rats.Annals of biomedical engineering · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The objective was to evaluate the pulmonary disposition of the ubiquinone homolog coenzyme Q(1) (CoQ(1)) on passage through lungs of normoxic (exposed to room air) and hyperoxic (exposed to 85% O(2) for 48 h) rats. CoQ(1) or its hydroquinone (CoQ(1)H(2)) was infused into the arterial inflow of isolated, perfused lungs, and the venous efflux rates of CoQ(1)H(2) and CoQ(1) were measured. CoQ(1)H(2) appeared in the venous effluent when CoQ(1) was infused, and CoQ(1) appeared when CoQ(1)H(2) was infused. In normoxic lungs, CoQ(1)H(2) efflux rates when CoQ(1) was infused decreased by 58 and 33% in the presence of rotenone (mitochondrial complex I inhibitor) and dicumarol [NAD(P)H-quinone oxidoreductase 1 (NQO1) inhibitor], respectively. Inhibitor studies also revealed that lung CoQ(1)H(2) oxidation was via mitochondrial complex III. In hyperoxic lungs, CoQ(1)H(2) efflux rates when CoQ(1) was infused decreased by 23% compared with normoxic lungs. Based on inhibitor effects and a kinetic model, the effect of hyperoxia could be attributed predominantly to 47% decrease in the capacity of complex I-mediated CoQ(1) reduction, with no change in the other redox processes. Complex I activity in lung homogenates was also lower for hyperoxic than for normoxic lungs. These studies reveal that lung complexes I and III and NQO1 play a dominant role in determining the vascular concentration and redox status of CoQ(1) during passage through the pulmonary circulation, and that exposure to hyperoxia decreases the overall capacity of the lung to reduce CoQ(1) to CoQ(1)H(2) due to a depression in complex I activity.
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