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Regulation of hypoxia responses by flavin adenine dinucleotide-dependent modulation of HIF-1α protein stability.
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Oxygen deprivation induces a range of cellular adaptive responses that enable to drive cancer progression. Here, we report that lysine-specific demethylase 1 (LSD1) upregulates hypoxia responses by demethylating RACK1 protein, a component of hypoxia-inducible factor (HIF) ubiquitination machinery,
The pathway of adenine nucleotide catabolism and its control in isolated rat hepatocytes subjected to anoxia.
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1. The breakdown of the adenine nucleotide pool provoked by the replacement of the O(2)/CO(2) gas phase by N(2)/CO(2) was studied in isolated rat hepatocytes with the purpose of defining the pathway of the catabolism of AMP in anoxic conditions. 2. Approx. 40% of the adenine nucleotide pool was lost
Preclinical evidence of mitochondrial nicotinamide adenine dinucleotide as an effective alarm parameter under hypoxia.
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Early detection of tissue hypoxia in the intensive care unit is essential for effective treatment. Reduced nicotinamide adenine dinucleotide (NADH) has been suggested to be the most sensitive indicator of tissue oxygenation at the mitochondrial level. However, no experimental evidence comparing the
The influence of hypoxia and anoxia on distribution of adenine nucleotides in isolated hepatocytes.
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Isolated hepatocytes incubated under conditions of "chemical hypoxia" (KCN + iodoacetic acid) exhibited a marked dephosphorylation of the cytoplasmic and mitochondrial adenine nucleotides to AMP. Cytoplasmic adenine nucleotide levels (ATP + ADP + AMP) were decreased by 40%. There was no significant
Effects of hypobaric hypoxia on adenine nucleotide pools, adenine nucleotide transporter activity and protein expression in rat liver.
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OBJECTIVE
To explore the effect of hypobaric hypoxia on mitochondrial energy metabolism in rat liver.
METHODS
Adult male Wistar rats were exposed to a hypobaric chamber simulating 5,000 m high altitude for 23 h every day for 0 (H0), 1 (H1), 5 (H5), 15 (H15) and 30 d (H30) respectively. Rats were
[Content of adenine nucleotides and creatinephosphate in brain, myocardium, liver and skeletal muscle under combined action of hypercapnia, hypoxia and cooling].
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Cooling of rats under conditions of hypercapina and hypoxia induced no changes in the content of adenine nucleotides in the brain and skeletal muscles and decreased their concentration in the liver and myocardium. The content of creatine phosphate increased in the brain, but had no changes in the
Influence of hypoxanthine, allopurinol and adenine on resistance of rats and hamsters to hypobaric hypoxia.
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The survival time of rats and hamsters in lethal hypoxia was measured after a sublethal exposure and a normoxia break, at the beginning of which purines were administered intraperitoneally in the following dosages: 25 mg/kg hypoxanthine, 50 mg/kg allopurinol, 25 mg/kg adenine. In rats,
Renal cellular hypoxia in adenine-induced chronic kidney disease.
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We determined whether adenine-induced chronic kidney disease (CKD) in rats is associated with renal tissue hypoxia. Adenine (100 mg) or its vehicle was administered to male Sprague-Dawley rats, daily by oral gavage, over a 15-day period. Renal function was assessed before, and 7 and 14 days after,
[Characteristics of adenine nucleotide translocator in mitochondria of rat cerebral cortex during hypobaric hypoxia exposure].
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The purpose of the present study was to explore the effects of hypoxic exposure on mitochondrial adenine nucleotide translocator (ANT) activity and its characteristics. Male Wistar rats were exposed to hypoxia in a hypobaric chamber simulating high altitude at 5 000 m for 1, 5, 15 and 30 d. Control
Effect of propionyl carnitine on energy charge and adenine nucleotide content of cardiac endothelial cells during hypoxia.
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Adenine mucleotide metabolism is very active in endothelial cells. These cells are very rich in xanthine oxidase which may produce oxygen reactive species during ischaemia and reperfusion when a high amount of adenine nucleotides may be catabolized to hypoxanthine. We investigated the effect of
Adenine nucleotides, glutamate and respiratory function of heart mitochondria during acute hypoxia.
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The effect of acute hypoxia on adenine nucleotides, glutamate, aspartate, alanine and respiration of heart mitochondria was studied in rats. The losses of intramitochondrial adenine nucleotides (ATP+ADP+AMP) during hypoxia were related to depression of state 3 respiration supported by glutamate and
Energy metabolism following prolonged hepatic cold preservation: benefits of interrupted hypoxia on the adenine nucleotide pool in rat liver.
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The ability of brief hypothermic reperfusion (HtR) to restore hepatic energy metabolism following periods of cold hypoxic preservation was studied in isolated rat livers after storage times of 5, 10, and 24 h. In addition, investigations were performed on the effects of HtR used to restore liver
Catabolism of cytoplasmic and intramitochondrial adenine nucleotides in C2C12 skeletal myotube under chemical hypoxia.
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Loss of adenosine-5'-triphosphate (ATP) and accumulation of inosine-5'-monophosphate (IMP) are the major purine metabolic changes in the skeletal muscle during hypoxia. This study addressed whether chemical metabolic inhibition reflects those changes in cultured skeletal myotube. For this aim,
Mechanisms whereby exogenous adenine nucleotides improve rabbit renal proximal function during and after anoxia.
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When a suspension of rabbit proximal tubules is subjected to anoxia, ATP falls by 80-90% during 40 min of anoxia, and upon reoxygenation (reox) the cells only recover 25-50% of their initial ATP. Addition of Mg-ATP (magnesium chloride-treated ATP), Mg-ADP, or Mg-AMP (five aliquots of 200 nmol/ml
[14C-adenine incorporation into neurons and glia of the cerebral cortex of rats after hypoxia and transplantation of embryonal nerve tissue].
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Incorporation of 14C-adenine (imp/min per mg) into RNA of brain tissue and into fractions of neurones and glial cells of cerebral cortex was studied rats with diffuse damage (hypoxia), with local injury of brain tissue and after transplantation of embryonal nervous tissue. The diffuse damage
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