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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Substrate specificity of monoamine oxidase (MAO) of the A type from rat brain and liver tissues was altered after exposure of rats to an increased oxygen pressure [4 ati O2, 1 hr]. Simultaneously with a decrease in monoamine deaminating activity the enzyme acquired an ability to deaminate several substances, which are not MAO substrates in normal state, in particular, aminosugars. Activity of MAO of the B type was not altered in brain under hyperoxia. Alterations in catalytic properties of MAO of the A type were apparently important in development of the oxygen intoxication.
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PMID:[Type A and B monoamine oxidase activity in hyperbaric oxygenation]. 45 1

The causes of the adenosine monophosphate (AMP) deamination increase in rat brain mitochondria under conditions of hyperoxia, hypoxia and cold stress were studied. Data from the inhibitory analysis suggest that the increased intensity of AMP deamination under hypoxia is conditioned by the alterations in the substrate specificity of type A monoamine oxidase which acquires the ability to deaminate AMP. The enhancement of AMP deamination under hyperoxia and cold stress is due to the activation of true AMP deaminase in the mitochondrial fraction. The cytoplasmic AMP deaminase activity remains unchanged thereby. The effects of the AMP deaminase specific effectors, ATP and inorganic phosphate, were investigated.
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PMID:[Deamination of adenosine monophosphate in the rat brain in hyperoxia, hypoxia, and cold stress]. 152 39

Toxicity to the central nervous system (CNS) by hyperbaric oxygen (HBO) presumably relates to increased production of reactive oxygen species. The sites of generation of reactive oxygen species during HBO, however, have not been fully characterized in the brain. We investigated the relationship between regional generation of hydrogen peroxide (H2O2) in the brain in the presence of an irreversible inhibitor of catalase, aminotriazole (ATZ), and protection from CNS O2 toxicity by a monoamine oxidase (MAO) inhibitor, pargyline. At 6 ATA of oxygen, pargyline significantly protected rats from CNS O2 toxicity whereas ATZ enhanced O2 toxicity. In animals pretreated with ATZ, HBO inactivated 21-40% more catalase than air exposure in the six brain regions studied. Because ATZ-mediated inactivation of catalase was H2O2 dependent, the decrease in catalase activity during hyperoxia was proportional to the intracellular production of H2O2. Pargyline, administered 30 min before HBO, inhibited MAO by greater than 90%, prevented ATZ inhibition of catalase activity during HBO, and reversed the augmentation of CNS O2 toxicity by ATZ. These findings indicate that H2O2 generated by MAO during hyperoxia is important to the pathogenesis of CNS O2 toxicity in rats.
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PMID:Prevention of H2O2 generation by monoamine oxidase protects against CNS O2 toxicity. 175 1

It has been established that white rats adapted to the low temperature of the environment (45 days 2-4 degrees C) in contrast to the animals undergoing such action during 3 days (cold stress) show resistance to the toxic action of the high oxygen pressure. The considerable removal of convulsions under the action of oxygen, the absence of increase of erythrocyte membrane permeability in the preconvulsive stage of hyperoxia and prevention of changes in the substrate specificity of type A monoamine oxidase both in preconvulsive and convulsive periods of oxygen intoxication are their characteristics.
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PMID:[Biochemical indices of the sensitivity of cold-adapted animals to hyperoxic exposure]. 343 32

Under conditions of hyperoxia mitochondrial monoamine oxidase (MAO) of the A type from rat brain proved to be able to deaminate gamma-aminobutyric acid (GABA); the transformation in the enzymatic properties appears to be responsible for a decrease in content of the intermediator in brain. Preadministration of chlorgiline (inhibitor of MAO of the A type) into animals before hyperoxygenation prevented completely the GABA content decrease, not affecting the glutamate decarboxylase activity, which was decreased in hyperoxia. At the same time, chlorgiline exhibited the total protective effect increasing 2-fold the period before oxygen convulsions.
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PMID:[Monoamine oxidase activity and gamma-aminobutyric acid levels in hyperoxia. The effect of clorgyline]. 370 20

During hyperoxia monoamine oxidase type A acquires the ability to deaminate polyamines and histamine. A preliminary injection of clorgyline (a monoamine oxidase type A inhibitor) before hyperoxic exposure leads to a significant removal of oxygen seizures and prevents changes in the cerebral spermidine and histamine content observed in the unprotected animals. The data confirm the important role of modification of catalytic properties in monoamine oxidase in the mechanism of oxygen intoxication.
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PMID:[Monoamine oxidase activity and effect of clorgyline on the polyamine level during hyperoxia in rats]. 372 40

Administration of monoamine oxidase type A inhibitor clorgyline to rats before hyperoxia prevented oxygen-induced increase in diene conjugate and Shiff's base brain and plasma levels in hyperoxia. This was due to antioxidative effect of clorgyline which resulted in stabilization of blood cellular membranes. Clorgyline had a normalizing effect on extraerythrocyte hemoglobin level, total peroxidase activity and glucose-6-phosphate dehydrogenase activity in the serum.
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PMID:[Effect of clorgyline on the intensity of lipid peroxidation and on erythrocyte membrane stability in hyperoxia]. 380 52

Chlorgyline, an inhibitor of type A monoamine oxidase, administered to rats prevented oxygen-induced decrease in gamma-aminobutyric acid brain content in hyperoxia. At the same time chlorgyline had an overall protective effect, increasing two-fold the period prior to the development of oxygen convulsions. The data suggest an important role of the modification of monoamine oxidase catalytic properties in the development of oxygen-induced intoxication and, particularly, in the decrease of gamma-aminobutyric acid content in hyperoxia.
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PMID:[Effect of chlorgyline on gamma-aminobutyric acid levels in hyperoxia]. 394 14

An over two-fold decrease in the affinity of mitochondrial MAO to serotonin was found under hyperoxia, hypoxia and cold stress. At the same time serotonin deaminase and glucosamine deaminase activity was detected in the supernatant obtained after precipitation of the mitochondria. The data obtained indicate that the modification of the catalytic properties of MAO is caused both by alteration of the molecular properties of the enzyme and structural derangement of the mitochondrial membranes.
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PMID:[Possible mechanism of the change in the catalytic properties of brain monoamine oxidase in rats]. 401 57

1 The uptake of 5-hydroxytryptamine (5-HT) and beta-phenylethylamine (PEA) and their deamination by monoamine oxidase (MAO) were studied in perfused lung from male and female rats exposed to 100% O(2) at 1 ATA for up to 60 h.2 The uptake and metabolism of 5-HT in lungs from both male and female rats was not changed by exposure to O(2).3 The uptake and metabolism of PEA by lungs from male rats was unchanged. Uptake of PEA by lungs from female rats was inhibited 20% and 62% after 37 h and 50 h exposure respectively.4 MAO activity, both in vitro and in perfused lung, was increased towards PEA after 35 h of hyperoxia.5 Metabolism of PEA in perfused lung, measured over 30 min, was inhibited 52% after 50 h of O(2) hyperoxia.6 These results show that exposure to high concentrations of O(2) damages lung, resulting in inhibition of uptake of PEA and consequently in inhibition of metabolism of PEA.7 These results also indicate that, in lung from female rats, MAO-type B is more susceptible to changes in O(2) tension than MAO type A.
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PMID:Effect of hyperoxia on uptake and metabolism of 5-hydroxytryptamine and beta-phenylethylamine in rat lung: a sex difference. 723 95


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