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Am J Physiol Regul Integr Comp Physiol
2013 Jun 01;30411:R1009-16. doi: 10.1152/ajpregu.00563.2012.
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Low Po₂ conditions induce reactive oxygen species formation during contractions in single skeletal muscle fibers.
Zuo L
,
Shiah A
,
Roberts WJ
,
Chien MT
,
Wagner PD
,
Hogan MC
.
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Contractions in whole skeletal muscle during hypoxia are known to generate reactive oxygen species (ROS); however, identification of real-time ROS formation within isolated single skeletal muscle fibers has been challenging. Consequently, there is no convincing evidence showing increased ROS production in intact contracting fibers under low Po₂ conditions. Therefore, we hypothesized that intracellular ROS generation in single contracting skeletal myofibers increases during low Po₂ compared with a value approximating normal resting Po₂. Dihydrofluorescein was loaded into single frog (Xenopus) fibers, and fluorescence was used to monitor ROS using confocal microscopy. Myofibers were exposed to two maximal tetanic contractile periods (1 contraction/3 s for 2 min, separated by a 60-min rest period), each consisting of one of the following treatments: high Po₂ (30 Torr), low Po₂ (3-5 Torr), high Po₂ with ebselen (antioxidant), or low Po₂ with ebselen. Ebselen (10 μM) was administered before the designated contractile period. ROS formation during low Po₂ treatment was greater than during high Po₂ treatment, and ebselen decreased ROS generation in both low- and high-Po₂ conditions (P < 0.05). ROS accumulated at a faster rate in low vs. high Po₂. Force was reduced >30% for each condition except low Po₂ with ebselen, which only decreased ~15%. We concluded that single myofibers under low Po₂ conditions develop accelerated and more oxidative stress than at Po₂ = 30 Torr (normal human resting Po₂). Ebselen decreases ROS formation in both low and high Po₂, but only mitigates skeletal muscle fatigue during reduced Po₂ conditions.
Barclay,
Modelling diffusive O(2) supply to isolated preparations of mammalian skeletal and cardiac muscle.
2005, Pubmed
Barclay,
Modelling diffusive O(2) supply to isolated preparations of mammalian skeletal and cardiac muscle.
2005,
Pubmed
Boveris,
The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen.
1973,
Pubmed
Cadenas,
Production of superoxide radicals and hydrogen peroxide by NADH-ubiquinone reductase and ubiquinol-cytochrome c reductase from beef-heart mitochondria.
1977,
Pubmed
Chance,
Hydroperoxide metabolism in mammalian organs.
1979,
Pubmed
Costa,
Active oxygen species in the liver of rats submitted to chronic hypobaric hypoxia.
1993,
Pubmed
Damerau,
Generation of free radicals in Langendorff and working hearts during normoxia, hypoxia, and reoxygenation.
1993,
Pubmed
Davies,
Free radicals and tissue damage produced by exercise.
1982,
Pubmed
Dröge,
Free radicals in the physiological control of cell function.
2002,
Pubmed
Edman,
Contractile performance of striated muscle.
2010,
Pubmed
Hempel,
Dihydrofluorescein diacetate is superior for detecting intracellular oxidants: comparison with 2',7'-dichlorodihydrofluorescein diacetate, 5(and 6)-carboxy-2',7'-dichlorodihydrofluorescein diacetate, and dihydrorhodamine 123.
1999,
Pubmed
Hogan,
NAD(P)H fluorescence imaging of mitochondrial metabolism in contracting Xenopus skeletal muscle fibers: effect of oxygen availability.
2005,
Pubmed
,
Xenbase
Hogan,
Phosphorescence quenching method for measurement of intracellular PO2 in isolated skeletal muscle fibers.
1999,
Pubmed
,
Xenbase
Jackson,
Free radicals generated by contracting muscle: by-products of metabolism or key regulators of muscle function?
2008,
Pubmed
Jamieson,
The relation of free radical production to hyperoxia.
1986,
Pubmed
Ji,
Modulation of skeletal muscle antioxidant defense by exercise: Role of redox signaling.
2008,
Pubmed
Ji,
Glutathione and antioxidant enzymes in skeletal muscle: effects of fiber type and exercise intensity.
1992,
Pubmed
Kindig,
Effect of extracellular PO2 on the fall in intracellular PO2 in contracting single myocytes.
2003,
Pubmed
,
Xenbase
Kolbeck,
Increased superoxide production during fatigue in the perfused rat diaphragm.
1997,
Pubmed
Mach,
Consequences of hyperoxia and the toxicity of oxygen in the lung.
2011,
Pubmed
McArdle,
Intracellular generation of reactive oxygen species by contracting skeletal muscle cells.
2005,
Pubmed
Mohanraj,
Antioxidants protect rat diaphragmatic muscle function under hypoxic conditions.
1998,
Pubmed
Moylan,
Oxidative stress, chronic disease, and muscle wasting.
2007,
Pubmed
Murphy,
Hydroxyl radical and glutathione interactions alter calcium sensitivity and maximum force of the contractile apparatus in rat skeletal muscle fibres.
2008,
Pubmed
Münzel,
Role for NADPH/NADH oxidase in the modulation of vascular tone.
1999,
Pubmed
Niess,
Response and adaptation of skeletal muscle to exercise--the role of reactive oxygen species.
2007,
Pubmed
Pattwell,
Measurement of free radical production by in vivo microdialysis during ischemia/reperfusion injury to skeletal muscle.
2001,
Pubmed
Pellegrino,
Redox homeostasis, oxidative stress and disuse muscle atrophy.
2011,
Pubmed
Powers,
Influence of exercise and fiber type on antioxidant enzyme activity in rat skeletal muscle.
1994,
Pubmed
Reid,
Reactive oxygen in skeletal muscle. II. Extracellular release of free radicals.
1992,
Pubmed
Reid,
Reactive oxygen in skeletal muscle. I. Intracellular oxidant kinetics and fatigue in vitro.
1992,
Pubmed
Sies,
Ebselen as a glutathione peroxidase mimic and as a scavenger of peroxynitrite.
1997,
Pubmed
Sies,
Ebselen, a selenoorganic compound as glutathione peroxidase mimic.
1993,
Pubmed
St-Pierre,
Topology of superoxide production from different sites in the mitochondrial electron transport chain.
2002,
Pubmed
Stary,
Resistance to fatigue of individual Xenopus single skeletal muscle fibres is correlated with mitochondrial volume density.
2004,
Pubmed
,
Xenbase
Sun,
Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor-Ca2+ release channel by NADPH oxidase 4.
2011,
Pubmed
Supinski,
Extracellular calcium modulates generation of reactive oxygen species by the contracting diaphragm.
1999,
Pubmed
Tsan,
Superoxide dismutase and pulmonary oxygen toxicity: lessons from transgenic and knockout mice (Review).
2001,
Pubmed
Vanden Hoek,
Significant levels of oxidants are generated by isolated cardiomyocytes during ischemia prior to reperfusion.
1997,
Pubmed
Viña,
Mechanism of free radical production in exhaustive exercise in humans and rats; role of xanthine oxidase and protection by allopurinol.
2000,
Pubmed
Wagner,
Muscle intracellular oxygenation during exercise: optimization for oxygen transport, metabolism, and adaptive change.
2012,
Pubmed
Westerblad,
Cellular mechanisms of fatigue in skeletal muscle.
1991,
Pubmed
Whitehead,
Skeletal muscle NADPH oxidase is increased and triggers stretch-induced damage in the mdx mouse.
2010,
Pubmed
Zuo,
Detection of reactive oxygen and nitrogen species in tissues using redox-sensitive fluorescent probes.
2002,
Pubmed
Zuo,
Sources for superoxide release: lessons from blockade of electron transport, NADPH oxidase, and anion channels in diaphragm.
2003,
Pubmed
Zuo,
The radical trap 5,5-dimethyl-1-pyrroline N-oxide exerts dose-dependent protection against myocardial ischemia-reperfusion injury through preservation of mitochondrial electron transport.
2009,
Pubmed
Zuo,
Reactive oxygen species formation in the transition to hypoxia in skeletal muscle.
2005,
Pubmed
Zuo,
Particulate matter exposure exacerbates high glucose-induced cardiomyocyte dysfunction through ROS generation.
2011,
Pubmed
Zuo,
Reactive oxygen species formation during tetanic contractions in single isolated Xenopus myofibers.
2011,
Pubmed
,
Xenbase
Zuo,
Intra- and extracellular measurement of reactive oxygen species produced during heat stress in diaphragm muscle.
2000,
Pubmed
