ArticleJournal of applied physiology (Bethesda, Md. : 1985)2011
Differential responses of targeted lung redox enzymes to rat exposure to 60 or 85% oxygen.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- 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
- Lung uptake of two SPECT markers identifies sensitivity to hyperoxia-induced acute respiratory distress syndrome in rats.Frontiers in physiology · 2025Article
- Mitochondrial function in lungs of rats with different susceptibilities to hyperoxia-induced acute lung injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Effect of low-to-moderate hyperoxia on lung injury in preclinical animal models: a systematic review and meta-analysis.Intensive care medicine experimental · 2023Review
- 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
- Article
- Biomarkers for Radiation Pneumonitis Using Noninvasive Molecular Imaging.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2016Article
- 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
- 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
- Optical imaging of tissue mitochondrial redox state in intact rat lungs in two models of pulmonary oxidative stress.Journal of biomedical optics · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Rat exposure to 60% O(2) (hyper-60) or 85% O(2) (hyper-85) for 7 days confers susceptibility or tolerance, respectively, of the otherwise lethal effects of exposure to 100% O(2). The objective of this study was to determine whether activities of the antioxidant cytosolic enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1) and mitochondrial complex III are differentially altered in hyper-60 and hyper-85 lungs. Duroquinone (DQ), an NQO1 substrate, or its hydroquinone (DQH(2)), a complex III substrate, was infused into the arterial inflow of isolated, perfused lungs, and the venous efflux rates of DQH(2) and DQ were measured. Based on inhibitor effects and kinetic modeling, capacities of NQO1-mediated DQ reduction (V(max1)) and complex III-mediated DQH(2) oxidation (V(max2)) increased by ∼140 and ∼180% in hyper-85 lungs, respectively, compared with rates in lungs of rats exposed to room air (normoxic). In hyper-60 lungs, V(max1) increased by ∼80%, with no effect on V(max2). Additional studies revealed that mitochondrial complex I activity in hyper-60 and hyper-85 lung tissue homogenates was ∼50% lower than in normoxic lung homogenates, whereas mitochondrial complex IV activity was ∼90% higher in only hyper-85 lung tissue homogenates. Thus NQO1 activity increased in both hyper-60 and hyper-85 lungs, whereas complex III activity increased in hyper-85 lungs only. This increase, along with the increase in complex IV activity, may counter the effects the depression in complex I activity might have on tissue mitochondrial function and/or reactive oxygen species production and may be important to the tolerance of 100% O(2) observed in hyper-85 rats.
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