Induction Of Anoxia Research Articles

Cyanobacterial Abundance and Microcystin Profiles in Two Southern British Lakes: The Importance of Abiotic and Biotic Interactions.

Freshwater cyanobacteria blooms represent a risk to ecological and human health through induction of anoxia and release of potent toxins; both conditions require water management to mitigate risks. Many cyanobacteria taxa may produce microcystins, a group of toxic cyclic heptapeptides. Understanding the relationships between the abiotic drivers of microcystins and their occurrence would assist in the implementation of targeted, cost-effective solutions to maintain safe drinking and recreational waters. Cyanobacteria and microcystins were measured by flow cytometry and liquid chromatography coupled to tandem mass spectrometry in two interconnected reservoirs varying in age and management regimes, in southern Britain over a 12-month period. Microcystins were detected in both reservoirs, with significantly higher concentrations in the southern lake (maximum concentration >7 µg L−1). Elevated microcystin concentrations were not positively correlated with numbers of cyanobacterial cells, but multiple linear regression analysis suggested temperature and dissolved oxygen explained a significant amount of the variability in microcystin across both reservoirs. The presence of a managed fishery in one lake was associated with decreased microcystin levels, suggestive of top down control on cyanobacterial populations. This study supports the need to develop inclusive, multifactor holistic water management strategies to control cyanobacterial risks in freshwater bodies.

Phosphorus mobility under short-term anoxic conditions in two shallow eutrophic coastal systems (Curonian and Sacca di Goro lagoons)

The effects of short-term anoxia on phosphorus mobility were investigated in estuarine sediments collected from two eutrophic European lagoons. Study areas differ with regard to climate and salinity: the boreal Curonian Lagoon (Lithuania) is oligohaline while the Mediterranean Sacca di Goro (Italy) is mesohaline. In each lagoon two sites were chosen representing areas impacted by river plume discharge and areas impacted by high organic matter deposition. Benthic fluxes of dissolved oxygen, inorganic phosphorus (DIP), iron (Fe2+) and manganese (Mn2+) were measured by dark intact core incubations in oxic and anoxic conditions. The latter were induced by incubation prolonged by up to 40 h depending on oxygen consumption rates. Solid phase P pools and pore water profiles of DIP, Fe2+, Mn2+ and sulfides were also measured before and after the induction of anoxia. Although incubation temperature and organic matter content were similar in plume and organic impacted areas of the two estuaries, higher benthic oxygen consumption rates were observed in Sacca di Goro, suggesting higher reactivity of the organic pool. Short-term anoxia had a significant effect on benthic fluxes of DIP (sulfide and Fe2+) only at the organic-rich and saline site of Sacca di Goro while internal buffers prevented inorganic P regeneration at the remaining sites. However, the analysis of pore water and solid phase pools revealed large variations during the transition and provided insights on the mechanisms controlling P dynamics. Both stations influenced by river plume deposition had high total inorganic P content (but most of it was refractory) and high reactive Mn pools, continuously regenerated by ventilation and irrigation of sediments by macrofauna. In these sites, oxygen depletion resulted in large accumulation of reduced Mn in the pore water but high fluxes of Mn2+ were also measured in the oxic part of the incubation suggesting the relevance of this respiration process. Thus Mn reduction preserved oxidized Fe pool and ultimately prevent P mobilization. Our results suggest that fluxes of DIP across the sediment–water interface are controlled by an array of different and site-specific mechanisms. These biogeochemical buffers are effective and contrast massive P release to the water column in highly productive systems as coastal lagoons, where episodes of transient oxygen shortage are frequent.

Reduced contribution from Na+/H+ exchange to acid extrusion during anoxia in adult rat hippocampal CA1 neurons.

The effect of anoxia on Na+/H+ exchange activity was examined in acutely isolated adult rat hippocampal CA1 neurons loaded with the H+-sensitive fluorophore, BCECF. Five-minute anoxia imposed under nominally HCO3-/CO2-free conditions induced a fall in pHi, the magnitude of which was smaller following prolonged exposure to medium in which N-methyl-D-glucamine (NMDG+) was employed as an extracellular Na+ (Na(+)(o)) substitute. Also consistent with the possibility that Na+/H+ exchange becomes inhibited soon after the induction of anoxia, rates of Na(+)(o)-dependent pHi recovery from internal acid loads imposed during anoxia were slowed, compared to rates of Na(+)(o)-dependent pHi recovery observed prior to anoxia. At the time at which rates of pHi recovery were reduced during anoxia, cellular adenosine triphosphate (ATP) levels had fallen to 35% of preanoxic levels, suggesting that ATP depletion might contribute to the observed inhibition of Na+/H+ exchange. In support, incubation of neurons with 2-deoxyglucose and antimycin A under normoxic conditions induced a fall in cellular ATP levels that was also associated with reduced Na(+)(o)-dependent rates of pHi recovery from imposed acid loads; conversely, pre-treatment with 10 mm creatine attenuated the effects of anoxia to reduce both ATP levels and Na(+)(o)-dependent rates of pHi recovery from internal acid loads. Taken together, the results are consistent with the possibility that functional Na+/H+ exchange activity in adult rat CA1 neurons declines soon after the onset of anoxia, possibly as a result of anoxia-induced falls in intracellular ATP.

Intracellular pH response to anoxia in acutely dissociated adult rat hippocampal CA1 neurons.

The effects of anoxia on intracellular pH (pH(i)) were examined in acutely isolated adult rat hippocampal CA1 neurons loaded with the H(+)-sensitive fluorophore, 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein. During perfusion with HCO/CO(2)- or HEPES-buffered media (pH 7.35) at 37 degrees C, 5- or 10-min anoxic insults were typified by an intracellular acidification on the induction of anoxia, a subsequent rise in pH(i) in the continued absence of O(2), and a further internal alkalinization on the return to normoxia. The steady-state pH(i) changes were not consequent on changes in [Ca(2+)](i) and, examined in the presence of HCO, were not significantly affected by (DIDS). In the absence of HCO, the magnitude of the postanoxic alkalinization was attenuated when external Na(+) was reduced by substitution with N-methyl-D-glucamine (NMDG(+)), but not Li(+), suggesting that increased Na(+)/H(+) exchange activity contributes to this phase of the pH(i) response. In contrast, 100-500 microM Zn(2+), a known blocker of H(+)-conductive pathways, reduced the magnitudes of the internal alkalinizations that occurred both during and following anoxia. The effects of NMDG(+)-substituted medium and Zn(2+) to reduce the increase in pH(i) that occurred after anoxia were additive. Consistent with the steady-state pH(i) changes, rates of pH(i) recovery from internal acid loads imposed immediately after anoxia were increased, and the application of Zn(2+) and/or perfusion with NMDG(+)-substituted medium slowed pH(i) recovery. Reducing extracellular pH from 7.35 to 6.60, or reducing ambient temperature from 37 degrees C to room temperature, also attenuated the increases in steady-state pH(i) observed during and after anoxia and reduced rates of pH(i) recovery from acid loads imposed in the immediate postanoxic period. Finally, inhibition of the cAMP/protein kinase A second-messenger system reduced the magnitude of the rise in pH(i) after anoxia in a manner that was dependent on external Na(+); conversely, activation of the system with isoproterenol increased the postanoxic alkalinization, an effect that was attenuated by pretreatment with propranolol, Rp-cAMPS, or when NMDG(+) (but not Li(+)) was employed as an external Na(+) substitute. The results suggest that a Zn(2+)-sensitive acid efflux mechanism, possibly a H(+)-conductive pathway activated by membrane depolarization, contributes to the internal alkalinization observed during anoxia in adult rat CA1 neurons. The rise in pH(i) after anoxia reflects acid extrusion via the H(+)-conductive pathway and also Na(+)/H(+) exchange, activation of the latter being mediated, at least in part, through a cAMP-dependent signaling pathway.

The Role of Myoglobin in Retarding Oxygen Depletion in Anoxic Heart

The present study explores the role of myoglobin (Mb) in retarding the development of anoxia in the perfused working rat heart. We examine this phenomenon by analyzing the behavior and the kinetics of Mb oxygenation and cytochrome aa3 (cytaa3) redoxation. Absorbance changes, measured at wavelength pairs specific to Mb and cytaa3, show parallelism between the Mb oxygenation status and the redox states of cytaa3. Induction of anoxia leads to early and accelerated Mb deoxygenation whereas cytaa3 reduction marks a slight delay and its rate is twice slower than that of Mb. Then, when Mb is desatured above 50%, the cytaa3 reduction becomes accelerated. With the reoxygenated perfusion following the anoxia, the rate of Mb reoxygenation is twice faster than that of the cytaa3 reoxidation. When the oxygen-binding function of Mb, in situ in the heart, is abolished by treatment with sodium nitrite (NaNO2), the redox kinetics of cytaa3 show significant perturbations. Induction of anoxia leads to a precocious and accelerated reduction of cytaa3, compared to the same anoxic heart before the treatment. At reoxygenation, the reoxidation rate of cytaa3 decreases significantly, compared to that before the treatment. Similarly, in the nitrite treated heart, the phosphocreatine (PCr) level decreases to 60 % of the control, whereas the inorganic phosphate (Pi) level increases to 300 %. ATP concentration, however, remains constant. We conclude from these results that Mb may support mitochondrial respiration at the critical levels of the myocardial O2 supply.

Effect of Anoxia on Spontaneous Discharges of the Cochlear Single Unit in Guinea Pigs

The present experiment examined the effect of anoxia on the spontaneous discharges of cochlear single units in guinea pigs; several additional animals were tested for the combined effect of anoxia and sodium salicylate. Following the induction of anoxia, initial increases in the number of spontaneous discharges were seen in 19 of the 34 cochlear single units tested. Neurons showing high frequencies during normal respiration tended toward increased rates of discharge during anoxia. In the 5 animals pretreated with sodium salicylate, remarkable increases in the spike rates were noted following the induction of anoxia.

31P-NMR spectroscopy: the metabolic profile of malignant hyperpyrexic porcine skeletal muscle.

31Phosphorus-NMR spectroscopy may have the potential to help in the noninvasive diagnosis of malignant hyperpyrexia (MH). Changes in the phosphate-metabolite profile of MH-susceptible (MHS) skeletal muscle occur more readily under conditions of anoxia than in control muscle. Induction of anoxia caused a rapid fall in intracellular phosphocreatine, an elevation of inorganic phosphate, and finally a diminution of ATP in MHS muscle. The onset of metabolic change was slower in control tissue. Increased oxygen consumption may occur in anoxic MHS muscle, which leads to accelerated glycolysis and a rapid fall in the intracellular high-energy phosphates. In MHS muscle an abnormality may exist in carbohydrate metabolism linked with poor resynthesis of the high-energy phosphates, which may be precipitated under anaerobic conditions. Accelerated muscle metabolism is also observed in the presence of 2 mM caffeine and 3% halothane in MHS muscle. Changes in the concentrations of metabolites could be mapped noninvasively under anoxic conditions using topical 31P-NMR.

耳鳴の電気生理学的研究 単一か牛神経自発放電のＡｎｏｘｉａによる変化

The present expeiments examined the influence of anoxia on spontaneous discharges of cochlear single units in guinea pigs; in several animals the combined effect of anoxia and sodium salicylate was observed. Anoxia was induced by stopping the respirator. Following the induction of anoxia, there was an initial increase in the number of spontaneous discharges in 19 of the 34 cochlear single units tested, after the amplitude of the discharges gradually decreased. The remaining 15 neurons displayed no increase during anoxia, although the same final disappearance of discharges was observed. Neurons showing high frequencies (over 100sp/sec) during normal respiration showed increase during anoxia. In 5 animals pretreated with sodium salicylate, a remarkable increase in the spike rates of spontaneous discharges were noted following the induction of anoxia.

Effect of Anoxia on Spontaneous Discharges of the Cochlear Single Unit in Guinea Pigs

The present experiment examined the effect of anoxia on the spontaneous discharges of cochlear single units in guinea pigs; several additional animals were tested for the combined effect of anoxia and sodium salicylate. Following the induction of anoxia, initial increases in the number of spontaneous discharges were seen in 19 of the 34 cochlear single units tested. Neurons showing high frequencies during normal respiration tended toward increased rates of discharge during anoxia. In the 5 animals pretreated with sodium salicylate, remarkable increases in the spike rates were noted following the induction of anoxia.

Influence of rat blood on radiation protection of mammalian cells by cysteamine and cystamine in vitro.

The protective effect of cystamine and cystamine on T-cells in normal growth-medium was studied in the presence of whole rate blood (WRB). The protective effectiveness of both agents was increased by the addition of WRB, but much less so on the activity of cystamine. In the presence of WRB a dose-reduction factor of 1-5 was obtained at the low concentration of 0-05 mM cysteamine. The increase in protection was not due to induction of anoxia or to a release of glutathione from the rat red cell. The increase in protection may be due to protector RS radicals reacting with rat red cells.

Glycolytic Control Mechanisms: II. KINETICS OF INTERMEDIATE CHANGES DURING THE AEROBIC-ANOXIC TRANSITION IN PERFUSED RAT HEART

Abstract The tissue levels of the glycolytic intermediates and adenine nucleotides were measured in perfused rat hearts supplied with 20 mm glucose during the transition from aerobiosis to carbon monoxide-induced anoxia. Facilitation of phosphofructokinase occurred as early as 20 sec after the induction of anoxia at 37°, as shown by an increase of fructose diphosphate and a fall of hexose monophosphate levels. Inorganic phosphate, creatine, adenosine monophosphate, and ADP levels increased simultaneously, while ATP and creatine-phosphate levels decreased. The increases of the nucleotides slightly preceded the rise of fructose diphosphate, and the largest percentage changes were in AMP and inorganic phosphate. These results are in accordance with the postulated activation of phosphofructokinase in vivo by AMP and phosphate. At 25°, the adenine nucleotide changes were much smaller, and an increase of phosphate accounted for the observed activation of phosphofructokinase. Maximum activation of phosphofructokinase occurred between 40 and 60 sec after the onset of anoxia. Overshoots in the levels of many glycolytic intermediates were observed during the transition from the aerobic to the anoxic steady states, indicating a complex sequence of interactions between the various control sites in the glycolytic pathway. Aerobic recovery after a brief period of anoxia was associated with an inhibition of phosphofructokinase, and a return of the levels of high energy phosphate intermediates to their preanoxic values.

The modification of tissue response to radiation injury.

A survey is made of protection by procedures carried out before irradiation; an attempt is made to examine the logical processes which lay behind the various experiments, rather than the experimental data itself. It is suggested that there has been a tendency for research workers in this field to be divided into separate schools. One began with the demonstration >50 yr ago, that the response of human skin to x rays could be diminished by the application of pressure by means of a vacuum cup, and culminated in the discovery in 1950 that induction of anoxia is an effective method of protecting rats against total-body irradiation. The second trend had its origin in the work of radiochemists in the 1930's that radiochemical reactions, which were brought about by the products of the radiolysis of water, could be modified by simple procedures such as dilution or addition of other solvents, and later discovery of similar effects in biological systems. The separation of these two trends has not been absolute, and other mechanisms of radioprotection have also been considered. The work of Bacq and the Liege School is considered in detail. The anoxia hypothesis is often referred to in the literature ofmore » chemical protection, but there appears to be confusion as to its exact nature and limits. Two mechanisms had been suggested which related chemical protection to anoxia: pharmacological effects in vivo, and simple chemical removal of oxygen in vitro. It has been postulated that some protective drugs produce partial anoxia in vivo to explain many of the observed results, and it has appeared reasonable to suggest that all drugs, including those of the sulfhydryl group, act via anoxia, at least as far as the protection of mammalian tissues is concerned. Careful examination of the arguments brought forward in support of the anoxia hypothesis (as applied to mammalian tissues) shows that they are not as conclusive as they once appeared to be. The reversal of cysteine protection by oxygen under pressure does not prove that cysteine causes anoxia; this result is also compatible with the theory that oxygen and the protective agent are competing for interaction with a damaged site. Even so, the anoxia theory has fared better than the radical scavenger theory in that the majority of pharmacologically active compounds probably act in this way in vivo, and it is wise to eliminate anoxia as a possible cause when a drug is given in such high doses as to cause death in unirradiated controls. Also, sulfhydryl compounds do remove oxygen from solution, and this removal probably provides the explanation of some results. Drugs of the cysteine-cysteamine group can cause anoxia in a mammal if given in high enough doses; thus, both the mechanisms relating sulfhydryl compounds and anoxia which were suggested do, in fact, operate, but it now appears that a third pathway, not related to anoxia, may be a vital one both in vivo and in vitro. In this third theory, the cysteinecysteamine group of agents act primarily by the formation of mixed disulfides with tissue proteins. This hypothesis is more limited than either of the two so far considered, in that it is restricted to this one class of protectors. Factors supporting this hypothesis are pointed out. It is concluded, with respect to the mechanism of action of chemical protectors in vivo, that the majority of the pharmacologically active drugs, such as the amines, act by bringing about a state of tissue hypoxia. The cysteinecysteamine- AET group, on the other hand, although they can cause anoxia in some systems, have a protective action which is not entirely attributable to anoxia, and which is most readily explained in terms of healing of damage in a target molecule. (BBB)« less