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ubiquinone/hypoxie
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Effect of experimental hypoxia on the ubiquinone level of skeletal muscle in rabbits.
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Rabbits were kept for 2 and 4 hours in a chamber containing a gas mixture of 92% N2 and 8% O2. The ubiquinone level in the musculus quadriceps femoris of the animals was determined. Rabbits after 4 hours hypoxia were retaken into normal conditions for 2 hours before killing. Biochemical findings
[Ubiquinone and vitamin E content in rat tissues in experimental focal myocarditis and hypoxic hypoxia].
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The content of ubiquinone and vitamin E in liver, heart, kidney and muscle tissues has been found to vary in experimental focal myocarditis and acute hypoxic hypoxia. These compounds have been demonstrated to accumulate in myocardial mitochondria, which is likely to be related to both interstitial
Effect of anoxia/reperfusion on the reversible active/de-active transition of NADH-ubiquinone oxidoreductase (complex I) in rat heart.
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The multi-subunit mammalian NADH-ubiquinone oxidoreductase (complex I) is part of the mitochondrial electron transport chain and physiologically serves to reduce ubiquinone with NADH as the electron donor. The three-dimensional structure of this enzyme complex remains to be elucidated and also
Chronic hypoxia-induced Cirbp hypermethylation attenuates hypothermic cardioprotection via down-regulation of ubiquinone biosynthesis.
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Therapeutic hypothermia is commonly used during cardiopulmonary bypass (CPB) to protect the heart against myocardial injury in cardiac surgery. Patients who suffer from chronic hypoxia (CH), such as those with certain heart or lung conditions, are at high risk of severe myocardial injury after
Anoxia-induced gene expression in turtle heart. Upregulation of mitochondrial genes for NADH-ubiquinone oxidoreductase subunit 5 and cytochrome c oxidase subunit 1.
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A cDNA library constructed from heart of anoxia-exposed adult turtles (Trachemys scripta elegans) was differentially screened with 32P-labeled single-stranded cDNA probes from heart of control versus anoxic animals to clone genes induced by anoxia stress. Four cDNA clones, pBTaR20, pBTaR34, pBTaR63
[The concentration and bisynthesis of ubiquinone-9 in the liver of white rats adapted to altitude hypoxia].
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The content and biosynthesis of ubiquinone-9 in the thin slices of the liver of rats was studied during altitude adaptation. There was a three-fold acceleration of ubiquinone biosynthesis during the first period of altitude adaptation. Acceleration of biosynthesis of ubiquinone-9 in rat liver was
[Effects of ubiquinone (CoQ10) on hypoxic hypoxia].
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Effect of chronic hypobaric hypoxia on ubiquinone levels in heart muscle.
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Effect of chronic hypoxia on myoglobin, cytochromes and ubiquinone levels in the rat.
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Recombinant human interleukin (IL)-1 beta-mediated regulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha) stabilization, nuclear translocation and activation requires an antioxidant/reactive oxygen species (ROS)-sensitive mechanism.
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Cytokine-mediated regulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha) non-hypoxic stabilization, translocation and activation is not well characterized. Furthermore, evidence that reactive oxygen species (ROS) signaling mediates interleukin (IL)-1 beta-dependent regulation of HIF-1 alpha
Preservation of complex I function during hypoxia-reoxygenation-induced mitochondrial injury in proximal tubules.
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Inhibition of complex I has been considered to be an important contributor to mitochondrial dysfunction in tissues subjected to ischemia-reperfusion. We have investigated the role of complex I in a severe energetic deficit that develops in kidney proximal tubules subjected to hypoxia-reoxygenation
Cloning and characterization of hypoxia-inducible factor-1 subunits from Ascaris suum - a parasitic nematode highly adapted to changes of oxygen conditions during its life cycle.
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The parasitic nematode Ascaris suum successfully adapts to a significant decrease in oxygen availability during its life cycle by altering its metabolic system dramatically. However, little is known about the regulatory mechanisms of adaptation to hypoxic environments in A. suum. In multicellular
Effects of hypoxia-reoxygenation stress on mitochondrial proteome and bioenergetics of the hypoxia-tolerant marine bivalve Crassostrea gigas.
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Mitochondria are key intracellular targets of hypoxia-reoxygenation (H/R) stress due to their central role in generation of ATP and reactive oxygen species (ROS). Intertidal oysters Crassostrea gigas are adapted to frequent H/R cycles and maintain aerobic function despite frequent oxygen
Mitochondrial mechanisms underlying tolerance to fluctuating oxygen conditions: Lessons from hypoxia-tolerant organisms.
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Oxygen (O2) is essential for most metazoan life due to its central role in in mitochondrial oxidative phosphorylation (OXPHOS), which generates >90% of the cellular ATP. Oxygen fluctuations are an ultimate mitochondrial stressor resulting in mitochondrial damage, energy deficiency and cell death.
Coenzyme q10 confers cardiovascular protection against acute mevinphos intoxication by ameliorating bioenergetic failure and hypoxia in the rostral ventrolateral medulla of the rat.
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Coenzyme Q10 (CoQ10, ubiquinone) is a highly mobile electron carrier in the mitochondrial respiratory chain that also acts as an antioxidant. We evaluated the cardiovascular protective efficacy of CoQ10 at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone
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