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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo production of nitrous oxide (N(2)O) by earthworms is due to their gut microbiota, and it is hypothesized that the microenvironment of the gut activates ingested N(2)O-producing soil bacteria. In situ measurement of N(2)O and O(2) with microsensors demonstrated that the earthworm gut is anoxic and the site of N(2)O production. The gut had a pH of 6.9 and an average water content of approximately 50%. The water content within the gut decreased from the anterior end to the posterior end. In contrast, the concentration of N(2)O increased from the anterior end to the mid-gut region and then decreased along the posterior part of the gut. Compared to the soil in which worms lived and fed, the gut of the earthworm was highly enriched in total carbon, organic carbon, and total nitrogen and had a C/N ratio of 7 (compared to a C/N ratio of 12 in soil). The aqueous phase of gut contents contained up to 80 mM glucose and numerous compounds that were indicative of anaerobic metabolism, including up to 9 mM formate, 8 mM acetate, 3 mM lactate, and 2 mM succinate. Compared to the soil contents, nitrite and ammonium were enriched in the gut up to 10- and 100-fold, respectively. The production of N(2)O by soil was induced when the gut environment was simulated in anoxic microcosms for 24 h (the approximate time for passage of soil through the earthworm). Anoxia, high osmolarity, nitrite, and nitrate were the dominant factors that stimulated the production of N(2)O. Supplemental organic carbon had a very minimal stimulatory effect on the production of N(2)O, and addition of buffer or ammonium had essentially no effect on the initial N(2)O production rates. However, a combination of supplements yielded rates greater than that obtained mathematically for single supplements, suggesting that the maximum rates observed were due to synergistic effects of supplements. Collectively, these results indicate that the special microenvironment of the earthworm gut is ideally suited for N(2)O-producing bacteria and support the hypothesis that the in situ conditions of the earthworm gut activate ingested N(2)O-producing soil bacteria during gut passage.
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PMID:The earthworm gut: an ideal habitat for ingested N2O-producing microorganisms. 1262 Aug 57

Eutrophication has decreased the O(2) content and increased the NH(4)(+) availability in freshwaters. These changes may affect carbon and nitrogen transformation processes and the production of CH(4) and N(2)O, which are important greenhouse gases. We studied release of CH(4) and N(2)O from a eutrophic lake sediment under varying O(2) and NH(4)(+) conditions. Intact sediment cores were incubated in a laboratory microcosm with a continuous anoxic or oxic water flows containing 0, 50, 500, 5,000, or 15000 microM NH(4)(+). With the anoxic flow, the sediment released CH(4), up to 7.9 mmol m(-2)d(-1). With the oxic flow, the CH(4) emissions were small indicating limited CH(4) production and/or effective CH(4) oxidation. Addition of NH(4)(+) did not affect sediment CH(4) release, evidence that the CH(4) oxidizing bacteria were not disturbed by the extra NH(4)(+). The release of N(2)O from the sediment was highest, up to 7.6 micromol m(-2)d(-1), with the oxic flow without NH(4)(+) addition. Oxygen was the key factor regulating the production of NO(3)(-), which enabled denitrification and production of N(2)O. However, the highest NH(4)(+) addition increased nitrification and associated O(2) consumption causing a decrease in sediment O(2) content and in accumulation of NO(3)(-) and N(2)O, which were effectively reduced to N(2) in denitrification. In summary, sediment CH(4) and N(2)O dynamics are regulated more by the availability of O(2) than extra NH(4)(+). Anoxia in eutrophic lakes favouring the CH(4) production, is the major contributor to the atmospheric consequences of water eutrophication.
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PMID:Effect of ammonium and oxygen on methane and nitrous oxide fluxes across sediment-water interface in a eutrophic lake. 1285 80

Various evidence indicate that schizophrenia is a neurodevelopmental disorder. Epidemiological observations point to oxygen deficiencies during delivery as one of the early risk factors for developing schizophrenia. The aim of the present study was to examine the effect of postnatal anoxia in rats. Anoxia was experimentally induced by placing 9-day-old rat pups for 6 min in a chamber saturated with 100% nitrogen (N(2)). Exposure to anoxia on postnatal day (PND) 9 resulted in significantly reduced subcortical dopamine metabolism and turnover, as measured by striatal 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) concentrations. Furthermore, in the anoxic group only, striatal HVA concentrations were negatively correlated to prefrontal cortical N-acetylaspartate (NAA) levels. Similar findings of distorted prefrontal-subcortical interactions have recently been reported in schizophrenic patients. There was no effect of postnatal anoxia on either baseline or d-amphetamine-induced deficit in the prepulse inhibition (PPI) paradigm in adulthood. Accordingly, although oxygen deficiency early in life has been discussed as vulnerability factor in developing schizophrenia, exposure to postnatal anoxia in the rat does not show clear-cut phenomenological similarities with the disorder.
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PMID:Effects of postnatal anoxia on striatal dopamine metabolism and prepulse inhibition in rats. 1509 22

Excised root systems of tomato plants (early fruiting stage, 2nd flush) were subjected to a gradual transition from normoxia to anoxia by seating the hydroponic root medium while aeration was stopped. Oxygen level in the medium and respiration rate decreased and reached very low values after 12 h of treatment, indicating that the tissues were anoxic thereafter. Nitrate loss from the nutrient solution was strongly stimulated by anoxia (after 26 h) concomitantly with a release of nitrite starting only after 16 h of treatment. This effect was not observed in the absence of roots or in the presence of tungstate, but occurred with whole plants or with sterile in vitro cultured root tissues. These results indicate that biochemical processes in the root involve nitrate reductase. NR activity assayed in tomato roots increased during anoxia. This phenomenon appeared in intact plants and in root tissues of detopped plants. The stimulating effect of oxygen deprivation on nitrate uptake was specific; anoxia simultaneously entailed a release of orthophosphate, sulfate, and potassium by the roots. Anoxia enhanced nitrate reduction by root tissues, and nitrite ions were released into xylem sap and into medium culture. In terms of the overall balance, the amount of nitrite recovered represented only half of the amount of nitrate utilized. Nitrite reduction into nitric oxide and perhaps into nitrogen gas could account for this discrepancy. These results appear to be the first report of an increase in nitrate uptake by plant roots under anoxia of tomato at the early fruiting stage, and the rates of nitrite release in nutrient medium by the asphyxiated roots are the fastest yet reported.
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PMID:Nitrate uptake and nitrite release by tomato roots in response to anoxia. 1531 75

The effect of anoxia and the respiratory chain inhibitors azide and cyanide on the polyphosphate content of Phycomyces was studied by in vivo (31)P NMR spectroscopy. Anoxia was manifested by a decrease of core polyphosphates (PP(i)) and increase of intracellular inorganic phosphate (P(i)) signal. Normalized changes in PP(i)/P(i) ratio between control and nitrogen-purged mycelia suggest that the sensitivity to anoxia differs with growth phases. Azide acts in the same way as anoxia, by decreasing the PP(i)/P(i) ratio, while cyanide causes an increase of the PP(i)/P(i) ratio.
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PMID:The effect of anoxia on PolyP content of Phycomyces blakesleeanus mycelium studied by 31P NMR spectroscopy. 1615 82

Anoxia in the first week of life can induce neuronal death in vulnerable brain regions usually associated with an impairment of cognitive function that can be detected later in life. We set-up a model of subneurotoxic anoxia based on repeated exposures to 100% nitrogen during the first 7 days of post-natal life. This mild post-natal exposure to anoxia specifically modified the behaviour of the male adult rats, which showed an attention deficit and an increase in anxiety, without any impairment in spatial learning and any detectable brain damage (magnetic resonance imaging and histological analysis). Post-anoxic rats showed a reduction in the expression of group-I metabotropic glutamate receptors (i.e. mGlu1 and mGlu5 receptors) in the hippocampus and cerebral cortex, whereas expression of the mGlu 2/3 receptors, the NR1 subunit of NMDA receptors, and the GluR1 subunit of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors was unchanged. mGlu1 and mGlu5 receptor signalling was also impaired in postanoxic rats, as revealed by a reduced efficacy of the agonist (1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) to stimulate polyphosphoinositide hydrolysis in hippocampal slices. We conclude that rats subjected to subneurotoxic doses of anoxia during the early post-natal life develop behavioural symptoms that are frequently encountered in the inattentive subtype of the attention deficit hyperactivity disorder, and that group-I mGlu receptors may be involved in the pathophysiology of these symptoms.
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PMID:Sub-neurotoxic neonatal anoxia induces subtle behavioural changes and specific abnormalities in brain group-I metabotropic glutamate receptors in rats. 1618 18

Newborn animals are more resistant to anoxia than older animals, partly due to an increased tolerance of the immature heart to anoxia. Newborn animals also have a more robust preterminal gasp. We investigated the relationship between gasping and cardiac function in immature and maturing rats exposed to anoxia. Immature postnatal day 7 (PND7) rats (n = 13) and maturing PND17 rats (n = 13) were exposed to 100% nitrogen (anoxia) for 10 min. Echocardiography was used to calculate cardiac contractility (CC) by left ventricular shortening fraction and cardiac output (CO) from Doppler velocity recordings of pulmonary artery blood flow. In a separate group of PND7 rats, CC and CO were recorded after the paralytic agent pancuronium was used to prevent gasping. Anoxia decreased CC and CO in PND7 and PND17 rats, followed by a partial and transient recovery. Gasping preceded recovery of CO and was required to sustain CO. Gasping in PND7 rats lasted longer (541 s versus 351 s, p < 0.01) and resulted in a greater recovery of CC and CO. Anoxia-induced gasping and the associated recovery of cardiac function were abolished by paralysis. Thus, anoxia-induced gasping transiently improves cardiac function, and more robust gasping in immature rats is associated with increased cardiac anoxic tolerance.
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PMID:Preterminal gasping during hypoxic cardiac arrest increases cardiac function in immature rats. 1686 99

Microbial denitrification plays a key role in determining the availability of soil nitrogen (N) to plants. However, factors influencing the structure and function of denitrifier communities in the rhizosphere remain unclear. Waterlogging can result in root anoxia and increased denitrification, leading to significant N loss from soil and potential nitrous oxide (N(2)O) emissions. This study investigated denitrifier gene abundance, community structure and activity in the rhizosphere of wheat in response to anoxia and N limitation. Denitrifier community structure in the rhizosphere differed from that in bulk soil, and denitrifier gene copy numbers (nirS, nirK, nosZ) and potential denitrification activity were greater in the rhizosphere. Anoxia and N limitation, and in particular a combination of both, reduced the magnitude of this effect on gene abundance (in particular nirS) and activity, with N limitation having greater impact than waterlogging in rhizosphere soil, in contrast to bulk soil where the impact of waterlogging was greater. Increased N supply to anoxic plants improved plant health and increased rhizosphere soil pH, which resulted in enhanced reduction of N(2)O. Both anoxia and N limitation significantly influenced the structure and function of denitrifier communities in the rhizosphere, with reduced root-derived carbon postulated to play an important role.
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PMID:Effect of nitrogen and waterlogging on denitrifier gene abundance, community structure and activity in the rhizosphere of wheat. 2300 39

Albino Wistar rats of both sexes were given a conditioned taste aversion training (CTA). Saccharin was used as the conditional stimulus (CS) and apomorphine-induced illness as the unconditional stimulus (US) on day 4. Amnestic treatment with electroconvulsive shock (ECS) or nitrogen anoxia were given to the rats at various points within the 180-min long CS-US interval as well as after the US. They were reexposed to the CS on days 5 and 6 in order to evaluate CTA and its extinction respectively. Apomorphine injection alone produced significant CTA as long as the CS-US interval was less than 120 min but not beyond it. Saline injections, with or without amnestic treatments, produced only an adaptation to and preference for saccharin. ECS could prevent CTA when delivered within 85 min before or 110 min after the US. Anoxia was effective at a much shorter range of time than ECS. The results are discussed in the perspectives of neophobia, saccharin aversion, amnestic agents and the character as well as gradients of amnesia produced.
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PMID:Amnesic effects of electroshock and anoxia on conditioned taste aversion learning in rats. 2489 36

The transient receptor potential (trp) gene superfamily encodes TRP proteins that act as multimodal sensor cation channels for a wide variety of stimuli from outside and inside the cell. Upon chemical or physical stimulation of cells, TRP channels transduce electrical and/or Ca(2+) signals via their cation channel activities. These functional features of TRP channels allow the body to react and adapt to different forms of environmental changes. Indeed, members of one class of TRP channels have emerged as sensors of reactive oxygen species (ROS), reactive nitrogen species (RNS), reactive carbonyl species (RCS), and gaseous messenger molecules including molecular oxygen (O2), hydrogen sulfide (H2S), and carbon dioxide (CO2). Hydrogen peroxide (H2O2), an ROS, triggers the production of ADP-ribose, which binds and activates TRPM2. In addition to TRPM2, TRPC5, TRPV1, and TRPA1 are also activated by H2O2 via modification of cysteine (Cys) free sulfhydryl groups. Nitric oxide (NO), a vasoactive gaseous molecule, regulates TRP channels directly via Cys S-nitrosylation or indirectly via cyclic GMP (cGMP)/protein kinase G (PKG)-dependent phosphorylation. Anoxia induced by O2-glucose deprivation and severe hypoxia activates TRPM7 and TRPC6, respectively, whereas TRPA1 serves as a sensor of mild hypoxia and hyperoxia in vagal and sensory neurons. TRPA1 also detects other gaseous molecules, such as hydrogen sulfide (H2S) and carbon dioxide (CO2). In this review, we highlight our current knowledge of TRP channels as chemosensors for ROS, RNS, RCS, and gaseous molecules and discuss their functional impacts on physiological and pathological events.
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PMID:TRPs as chemosensors (ROS, RNS, RCS, gasotransmitters). 2496 69


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