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At least 19 recordsLinked to original sources
PubMed1985

Effect of "flow anoxia" and "non flow anoxia" on the NAD/NADH redox state of the intact brain cortex of the cat.

In the present study, we compared the nicotinamide adenine dinucleotide (NAD) reducing potencies of "flow anoxia" and "non flow anoxia" in the cat brain cortex. In animals anaesthetized with alpha D-glucochloralose "flow anoxia" and "non flow anoxia" were produced by ventilating for 2 and 25 min, respectively, with nitrogen gas. Following "non flow anoxia" the brain cortices of dead animals were superfused with oxygen saturated artificial cerebrospinal fluid (mock CSF), and subsequently with CSF containing various concentrations (10(-3 -10 -1) M) of potassium cyanide. NADH (reduced NAD) fluorescence of the brain cortex was measured through a cranial window with a microscope fluororeflectometer. Ventilating the animals for 2 and 25 min with nitrogen gas increased cortical NADH fluorescence (NAD reduction) by 43.5 +/- 2.8% and 135.3 +/- 6.1%, respectively. Oxygen saturated CSF superfusion of the ischemic brain cortex restored the cortical NAD/NADH redox state to the preanoxic level (oxidation of NADH). 10(-1) M cyanide, applied after superfusion of the brain cortex with oxygen saturated CSF resulted in comparable NAD reduction to that produced by "non flow anoxia". On the basis of these findings it is suggested that "non flow anoxia" leads to much greater cortical NAD reduction than "flow anoxia", because oxygen tension in the cortex may not fall to zero mm Hg during nitrogen anoxia lasting for 2 min. Besides this, a more pronounced substrate mobilization and acidosis may also contribute to the greater NAD reducing potency of "now flow anoxia".(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effect of anoxia and pharmacological anoxia on whole-cell NMDA receptor currents in cortical neurons from the western painted turtle.

The mammalian brain undergoes rapid cell death during anoxia that is characterized by uncontrolled Ca(2+) entry via N-methyl-D-aspartate receptors (NMDARs). In contrast, the western painted turtle is extremely anoxia tolerant and maintains close-to-normal [Ca(2+)](i) during periods of anoxia lasting from days to months. A plausible mechanism of anoxic survival in turtle neurons is the regulation of NMDARs to prevent excitotoxic Ca(2+) injury. However, studies using metabolic inhibitors such as cyanide (NaCN) as a convenient method to induce anoxia may not represent a true anoxic stress. This study was undertaken to determine whether turtle cortical neuron whole-cell NMDAR currents respond similarly to true anoxia with N(2) and to NaCN-induced anoxia. Whole-cell NMDAR currents were measured during a control N(2)-induced anoxic transition and a control NaCN-induced transition. During anoxia with N(2) normalized, NMDAR currents decreased to 35.3%+/-10.8% of control values. Two different NMDAR current responses were observed during NaCN-induced anoxia: one resulted in a 172%+/-51% increase in NMDAR currents, and the other was a decrease to 48%+/-14% of control. When responses were correlated to the two major neuronal subtypes under study, we found that stellate neurons responded to NaCN treatment with a decrease in NMDAR current, while pyramidal neurons exhibited both increases and decreases. Our results show that whole-cell NMDAR currents respond differently to NaCN-induced anoxia than to the more physiologically relevant anoxia with N(2).

Animals↗
PubMed2000

Impact of post-anoxia stress on membrane lipids of anoxia-pretreated potato cells. A re-appraisal.

The importance of lipid peroxidation and its contributing pathways (via reactive oxygen species and lipoxygenase) during post-anoxia was evaluated with respect to the biphasic behavior of membrane lipids under anoxia (A. Rawyler, D. Pavelic, C. Gianinazzi, J. Oberson, R. Brändle [1999] Plant Physiol 120: 293-300), using potato (Solanum tuberosum cv Bintje) cell cultures. When anoxic cells in the pre-lytic phase were re-oxygenated for 2 h, superoxide anion was not detectable, the hydrogen peroxide (H(2)O(2)) level remained small and similar to that of controls, and cell viability was preserved. Lipids were intact and no lipid hydroperoxides were detected. However, small amounts of lipid hydroperoxides accumulated upon feeding anoxic cells with H(2)O(2) and incubation for an additional 2 h under anoxia. When cells that entered the lytic phase of anoxia were re-oxygenated for 2 h, the H(2)O(2) and superoxide anion levels were essentially unchanged. However, cell respiration decreased, reflecting the extensive lipid hydrolysis that had already started under anoxia and continued during post-anoxia. Simultaneous with the massive release of free polyunsaturated fatty acids, small amounts of lipid hydroperoxides were formed, reaching 1% to 2% of total fatty acids. Catalase and superoxide dismutase activities were not greatly affected, whereas the amount and activity of lipoxygenase tended to increase during anoxia. Lipid peroxidation in potato cells is therefore low during post-anoxia. It is mainly due to lipoxygenase, whereas the contribution of reactive oxygen species is negligible. But above all, it is a late event that occurs only when irreversible damage is already caused by the anoxia-triggered lipid hydrolysis.

Cell Hypoxia↗
PubMed1994

Prior episode of anoxia attenuates vasorelaxation in response to subsequent episode of anoxia.

To examine the effect of a prior episode of anoxia on subsequent anoxia-mediated vasorelaxation, norepinephrine-precontracted endothelium-intact rat aortic rings were first exposed to anoxia (95% N2-5% CO2 for 5, 15, or 30 min) then to normoxia (95% O2-5% CO2 for 15 min). These rings were exposed again to anoxia for 30 min. First exposure of rings to anoxia for 30 min resulted in 77 +/- 4% decrease in tone (vasorelaxation), whereas second exposure resulted in only 10 +/- 4% relaxation (n = 11, P < 0.001 vs. relaxation during first exposure). First exposure of rings to anoxia for 5 or 15 min also diminished relaxation to 59 +/- 3 and 19 +/- 8%, respectively, on second exposure to anoxia (both P < 0.01 vs. relaxation during 1st anoxia). Attenuation of vasorelaxation by prior episode of anoxia was not affected by treatment of rings with indomethacin (10(-5) M), the Ca2+ channel blocker felodipine (10(-6) M), the superoxide anion scavenger superoxide dismutase (100 micrograms/ml), or adenosine A1 and A2 blockers (each 10(-6) M). To examine the role of intact functional endothelium in attenuation of vasorelaxation during second anoxic exposure, rings were deendothelialized and treated with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 10(-4) M) or the guanylate cyclase inhibitor methylene blue (MB; 2 x 10(-5) M). In all deendothelialized rings, vasorelaxation during second anoxic exposure was similar to that during first anoxic exposure (100 +/- 0 vs. 98 +/- 3%, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1997

Effects of energy limitation on Ca2+ and K+ homeostasis in anoxia-tolerant and anoxia-intolerant hepatocytes.

To gain more insight into the mechanistic basis of anoxia tolerance and intolerance, a comparative study was conducted on calcium homeostasis in goldfish and trout hepatocytes subjected to different forms of energy limitation. Using the fluorescent Ca2+ indicator fura 2, we observed that both chemical anoxia and true anoxia led to an increase of the concentration of cytosolic free calcium (Ca2+i) in the anoxia-sensitive hepatocytes of rainbow trout, whereas Ca2+i was maintained at control levels in the anoxia-tolerant hepatocytes of goldfish. Various lines of evidence suggest an intracellular origin of the Ca2+ increase observed in trout cells. Cyclosporin A, a specific inhibitor of the mitochondrial permeability transition pore in mammalian cells, was ineffective in preventing the Ca2+ increase, whereas a high dose of fructose depressed the Ca2+ surge by approximately 50%. The latter effect was not accompanied by improvement of the energetic state of the cells. A comparison of chemical anoxia with true (physiological) anoxia revealed that both treatments affected energy metabolism to a similar degree in trout hepatocytes, whereas the decrease of ATP seen in goldfish hepatocytes during chemical anoxia was absent during true anoxia. Elevation of Ca2+i with the calcium ionophore A-23187 led to a decoupling of unidirectional K+ fluxes in both normoxic and anoxic trout cells, whereas in goldfish hepatocytes the coupling of K+ fluxes was not affected by the rise of Ca2+i.

Adenosine Triphosphate↗
PubMed2001

Complete suppression of protein synthesis during anoxia with no post-anoxia protein synthesis debt in the red-eared slider turtle Trachemys scripta elegans.

Two previous studies of the effects of anoxia on protein synthesis in anoxia-tolerant turtles (Trachemys scripta elegans, Chrysemys picta bellii) have generated opposing results. Using the flooding-dose method, we measured the rate of protein synthesis following injection and incorporation of a large dose of radiolabelled phenylalanine to resolve the question of whether anoxia results in a downregulation of protein synthesis. After 1 h of anoxia, levels of protein-incorporated radiolabel indicated that protein synthesis rates in the intestine, heart, liver, brain, muscle and lungs were not significantly different from those of normoxic controls. However, from 1 to 6 h of anoxia, quantities of protein-incorporated radiolabel did not increase, suggesting that protein synthesis had ceased or had decreased below a measurable level. There was also no significant post-anoxia increase in protein synthesis rates above normoxic control levels during 3 h of recovery from anoxia. RNA-to-protein ratios did not change significantly in any tissue except the heart, in which RNA levels decreased below normoxic control levels after 6 h of anoxia. Except in the heart, downregulation of protein synthesis during anoxia does not appear to be mediated by changes in tissue RNA concentration.

Animals↗
PubMed1996

Membrane-metabolic coupling and ion homeostasis in anoxia-tolerant and anoxia-intolerant hepatocytes.

The relationship between membrane function and energy metabolism was studied in rainbow trout hepatocytes, an anoxia-intolerant cell system, and compared with the situation in hepatocytes from the goldfish, a typical anoxia-tolerant species. In trout hepatocytes, under normoxia and under chemical anoxia, inhibition of ATP consumption by the Na+ pump induced a decrease in ATP production of the same magnitude. In response to chemical anoxia, total ATP production was reduced to 15% and Na+ pump activity to 22% of the control rate under normoxia. Measurement of the cellular ATP content under these conditions revealed that, despite the reduction in Na+ pump activity, the cells became rapidly depleted of ATP, with the time course of this process resembling that observed in the anoxic rat hepatocyte. This is in contrast to the responses of goldfish hepatocytes, where, during chemical anoxia, 1) inhibition of the Na+ pump did not lead to a corresponding reduction in ATP production and 2) ATP levels, after a transient decrease, stabilized at a new steady state. To investigate the consequences of chemical anoxia on ion homeostasis, efflux and uptake rates of K+ were determined simultaneously. In the trout cells, chemical anoxia led to a decoupling of influx and efflux rates, the latter exceeding the former three- to eightfold. In contrast, goldfish hepatocytes were able to preserve ion homeostasis by a concerted decrease in Rb+ uptake and K+ efflux, so that the net flux of K+ was always close to zero. In neither species did chemical anoxia induce a change in pump density. Other potential control mechanisms are briefly discussed.

Adenosine Triphosphate↗
PubMed1991

Midazolam improves electrophysiologic recovery after anoxia and reduces the changes in ATP levels and calcium influx during anoxia in the rat hippocampal slice.

Since blockers of excitatory transmission have been shown to reduce anoxic and ischemic neuronal damage, augmentation of inhibitory transmission by agents such as midazolam might have a similar protective effect. Rat hippocampal slices were maintained in vitro and used to determine whether and by what mechanism midazolam improves recovery of evoked responses after anoxia. The Schaffer collateral pathway in the slice was stimulated electrically, and an extracellular potential, the evoked population spike, was recorded from the CA1 pyramidal cells, which are postsynaptic. The slices were made anoxic by substituting artificial cerebrospinal fluid aerated with 95% nitrogen-5% carbon dioxide for fluid aerated with 95% oxygen-5% carbon dioxide. Percentage recovery was expressed as the amplitude of the evoked population spike 60 min after anoxia divided by its preanoxic amplitude. Protection in this model is defined as a significant (P less than 0.05) improvement in percentage recovery compared to the recovery of untreated slices. There was no recovery of the response recorded from CA1 pyramidal cells after 5 min of anoxia (4 +/- 2%) (mean +/- standard error of the mean [SEM]). Slices were treated with midazolam 10 min before, during, and 10 min after anoxia. Midazolam (1 microM) did not enhance recovery after anoxia when dissolved either in water (3 +/- 3%) or in dimethyl sulfoxide (DMSO) (1 +/- 1%). A higher concentration of midazolam (100 microM) did enhance recovery when dissolved in DMSO (27 +/- 7%) but not when dissolved in water (5 +/- 2%). To test whether prolonged pretreatment with midazolam dissolved in water would enhance recovery, slices were treated for 30 min prior to anoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1993

Response of protein synthesis to anoxia and recovery in anoxia-tolerant hepatocytes.

Hepatocytes from the western painted turtle (Chrysemys picta bellii) display a profound metabolic suppression under anoxia. Fractional rates of protein synthesis fell by 92% during 12 h anoxia at 25 degrees C and were indistinguishable from the rate obtained with cycloheximide. Normoxic recovery saw protein synthesis increase to 160% of control values and return to normal after 2 h. The GTP-to-GDP ratio, implicated in the control of translation, fell threefold during anoxia. Purine nucleotide phosphate profiles suggest that this change occurs through increasing concentrations of ADP and GDP, with concentrations of ATP and GTP and total purines remaining constant. The normoxic cost for protein synthesis was calculated at 47.6 +/- 6.8 mmol ATP/g protein. Normoxic protein synthesis accounted for 36% of overall ATP turnover rates, close to the extent of O2 consumption inhibitable by cycloheximide (28%). Under anoxia, the proportion of ATP turnover utilized by protein synthesis did not change significantly. ATP turnover rates for urea synthesis reflected a similar pattern, falling 72% under anoxia. These results reflect the cell's ability to suppress protein synthesis under anoxia in a manner that is coordinated with the reduction in total metabolic rate.

Adaptation, Physiological↗
PubMed1989

[Anoxia-reoxygenation injury in isolated rat myocytes is modulated by cell sodium during the anoxia period].

Using the model of anoxia-reoxygenation injury in isolated rat myocytes, we observed that incubation of myocytes with ouabain, inhibitor of Na+-K+ ATPase, during anoxia period significantly increased the cell sodium content. These myocytes demonstrated severe injury and intracellular calcium overload during reoxygenation period. The sodium content of myocytes at the end of anoxia period was positively correlated with the overload of intracellular calcium at reoxygenation (r = 0.882, P less than 0.01). Mn2+, an inhibitor of Na+-Ca2+ exchange, significantly attenuated the anoxia-reoxygenation injury when given during reoxygenation period. Mn2+ also inhibited the cell injury caused by incubation of myocytes with Na+-free medium. These results suggest that anoxia-reoxygenation injury of rat myocytes is modulated by cell sodium during the anoxia period, and the Na+-Ca2+ exchange mechanism plays an important role in influx of extracellular calcium during reoxygenation period.

Animals↗
PubMed1995

High levels of ascorbic acid, not glutathione, in the CNS of anoxia-tolerant reptiles contrasted with levels in anoxia-intolerant species.

Ascorbic acid and glutathione (GSH) are antioxidants and free radical scavengers that provide the first line of defense against oxidative damage in the CNS. Using HPLC with electrochemical detection, we determined tissue contents of these antioxidants in brain and spinal cord in species with varying abilities to tolerate anoxia, including anoxia-tolerant pond and box turtles, moderately tolerant garter snakes, anoxia-intolerant clawed frogs (Xenopus laevis), and intolerant Long-Evans hooded rats. These data were compared with ascorbate and GSH levels in selected regions of guinea pig CNS, human cortex, and values from the literature. Ascorbate levels in turtles were typically 100% higher than those in rat. Cortex, olfactory bulb, and dorsal ventricular ridge had the highest content in turtle, 5-6 mumol g-1 of tissue wet weight, which was twice that in rat cortex (2.82 +/- 0.05 mumol g-1) and threefold greater than in guinea pig cortex (1.71 +/- 0.03 mumol g-1). Regionally distinct levels (2-4 mumol g-1) were found in turtle cerebellum, optic lobe, brainstem, and spinal cord, with a decreasing anterior-to-posterior gradient. Ascorbate was lowest in white matter (optic nerve) in each species. Snake cortex and brainstem had significantly higher ascorbate levels than in rat or guinea pig, although other regions had comparable or lower levels. Frog ascorbate was generally in an intermediate range between that in rat and guinea pig. In contrast to ascorbate, GSH levels in anoxia-tolerant turtles, 2-3 mumol g-1 of tissue wet weight, were similar to those in mammalian or amphibian brain, with no consistent pattern associated with anoxia tolerance. GSH levels in pond turtle CNS were significantly higher (by 10-20%) than in rat for several regions but were generally lower than in guinea pig or frog. GSH in box turtle and snake CNS were the same or lower than in rat or guinea pig. The distribution GSH in the CNS also had a decreasing anterior-to-posterior gradient but with less variability than ascorbate: levels were similar in optic nerve, brainstem, and spinal cord. The paradoxically high levels of ascorbate in turtle brain, which has a lower rate of oxidative metabolism than mammalian, suggest that ascorbate is an essential cerebral antioxidant. High levels may have evolved to protect cells from oxidative damage when aerobic metabolism resumes after a hypoxic dive.

Adaptation, Physiological↗
PubMed1994

Effect of anoxia on isolated turtle tissues: is the response to anoxia mediated by protein kinase second messengers?

Organ slices from the turtle Trachemys scripta elegans were incubated under aerobic and anoxic conditions to examine the effect of protein kinase (PrK) second messengers in potentiating the biochemical responses to anoxia exposure. Incubating liver slices from aerobic animals under anoxic conditions produced biochemical changes exactly similar to those observed in vivo: phosphofructokinase (PFK) was more sensitive to citrate inhibition and the percentage of glycogen phosphorylase (GP) in the active a form increased. On the other hand, incubating brain and heart tissue slices under anoxic conditions produced no changes in PFK and GP kinetic constants. Addition of PrK second messengers (dibutyryl-cAMP or Ca2+ plus phorbol myristate acetate) to the incubated tissues did not promote anoxia-associated changes in aerobically incubated tissues nor did they prevent anoxia-associated changes in anaerobically incubated tissues. These results suggest that unidentified external hormonal signals mediate heart and brain responses to anoxia. It is also apparent that cAMP and Ca2+ plus phospholipid do not play a role in bringing about the anoxia-induced changes in PFK, GP and fructose 2,6-bisphosphate in liver of turtles.

Aerobiosis↗
PubMed1985

The effect of perinatal anoxia on amino acid metabolism in the developing brain. Part II: The effect of perinatal anoxia on the free amino acid patterns in CSF of infants and children.

To clarify the effects of perinatal anoxia on the subsequent amino acid metabolism in the brain of children, free amino acid levels in the cerebrospinal fluid (CSF) were determined in 15 children diagnosed as having cerebral palsy and/or mental retardation with perinatal anoxia, and 58 control children without anoxia, aged from 4 days to 12 yrs. There was no significant difference in total amino acid levels between anoxic children and the controls. In the controls, the Gln level in CSF was high, Arg, Asp and Glu levels in CSF were almost the same during infancy and childhood, and the levels of Orn, Lys, His, Tau, Thr, Ser, Asn, Gly, Ala, Val, Met, Ile, Leu, Tyr and Phe in CSF decreased with age until pre-school age. In the newborns and infants among the anoxic children, the levels of most free amino acids in CSF were relatively high compared with those of the controls and, except Glu and Gln, decreased with age during infancy. The Orn, His, Gly, Tyr and Phe levels in CSF of anoxic children were lower than those of the controls in older infants. These results suggest that perinatal anoxia affected free amino acid patterns in CSF of newborns and infants and that the subsequent disturbance of amino acid metabolism in their brains remained after birth.

Amino Acids↗
PubMed2001

Regulation of intracellular pH in anoxia-tolerant and anoxia-intolerant teleost hepatocytes.

Mechanisms of intracellular pH (pHi) regulation were investigated in anoxia-tolerant hepatocytes from goldfish Carassius auratus, and compared to the situation in the anoxia-intolerant hepatocytes from trout Oncorhynchus mykiss. Under normoxic conditions, the pHi of goldfish hepatocytes was regulated by a Na(+)/H(+) exchanger and a Na(+)-independent Cl(-)/HCO(3)(-) exchanger, the latter being activated only after acidification of the cells. Mechanisms of acid secretion appear to be fuelled, at least in part, by lactate formation under fully aerobic conditions, as inhibition of glycolysis caused a drastic reduction of steady state proton release. In trout hepatocytes both a Na(+)/H(+) exchanger and a Cl(-)/HCO(3)(-) exchanger were found to be tonically active, as described previously. During chemical anoxia a constant pHi was maintained in goldfish hepatocytes, whereas it was reversibly reduced by 0.3 units in the trout cells. Under these conditions a reversible increase in the rate of acid secretion was induced in the cells from both species. In the goldfish cells this was based on a SITS-sensitive transporter, possibly involving export of lactate, with no contribution from Na(+)/H(+) exchange. By contrast, in hepatocytes from trout, CN-induced acid secretion was dominated by the activity of the Na(+)/H(+) exchanger. Brief exposure to extracellular acidosis had no dramatic effects on the energetics of hepatocytes from either species.

Adenosine Triphosphate↗
PubMed1985

The effect of perinatal anoxia on amino acid metabolism in the developing brain. Part I: The effect of experimental anoxia on the free amino acid patterns in the brain of neonatal rats.

The effect of perinatal anoxia on the subsequent amino acid pattern in the brain during a period of 2 wks after birth was investigated using neonatal rats. Sixty-nine neonatal albino rats of the Wistar strain were divided into 3 groups: the 1st control group (n = 36), the 2nd anoxic group (n = 30) and the 3rd anoxic-ischemic group (n = 3). In the 1st and 2nd groups, 6 rats out of each group were sacrificed on the each of the following days respectively, the 1st, 3rd, 5th, 7th, 10th and 15th days of life for amino acid assays of brain. In the 3rd group, 3 rats were sacrificed 2 days after ligation of the carotid artery on one side, and free amino acid levels in both cerebral hemispheres were separately measured. In the controls, the levels of GABA, Asp and Glu in the brain increased, those of Tau and Gly decreased and those of PE, Thr, Ser, Gln, Ala and Leu did not change during the experimental period. The total free amino acid level in the brain of the controls remained almost completely unchanged during this period. After anoxic exposure the levels of GABA, Tau, PE, Asp, Thr, Glu, Gln and Ala, and the total free amino acid level in the brain decreased until the 7th day of life and thereafter rapidly increased. The Gly level continuously decreased and the Ser and Leu levels did not change during the experiment. The GABA and Gly levels after anoxia decreased and were still low on the 15th day of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMedDate not supplied

Importance of glycolysis for the energetics of anoxia-tolerant and anoxia-intolerant teleost hepatocytes.

The importance of glycolysis, as an ATP-producing and substrate-providing pathway, was studied in anoxia-tolerant (goldfish) and anoxia-intolerant (trout) hepatocytes. Inhibition of glycolysis with iodoacetic acid (IAA) left aerobic ATP production largely unaffected in hepatocytes from both species but caused a significant decrease of ATP contents in the goldfish cells. Ouabain-sensitive oxygen consumption (osVo2), an estimate of mitochondrial ATP production coupled to ATP consumption by the Na(+) pump, was significantly reduced in IAA-treated goldfish hepatocytes, whereas it was unaltered in trout hepatocytes. Partial reduction of mitochondrial respiration, achieved by titration with cyanide (CN), strongly stimulated glycolytic flux but did not affect ATP contents of hepatocytes from both species. Under these conditions, osVo2 became undetectable. Rb(+)-uptake rates, providing a direct estimate of Na(+)-pump activity, were in good agreement with estimates derived from osVo2 in IAA-treated cells, showing a decrease in goldfish and no change in trout. However, they indicated persistent Na(+)-pump activity despite the lack of osVo2 in CN-treated cells. Overall, these data indicate that in goldfish hepatocytes Na(+)-pump activity is more dependent on glycolytic ATP production as compared to trout hepatocytes. Protein synthesis of goldfish hepatocytes was inhibited in IAA- and CN-treated cells, possibly reflecting the hierarchical organization of energy metabolism. In trout hepatocytes, protein synthesis could be sustained at control levels, given that energetic substrate provision was not limited.

Acclimatization↗
PubMed1987

Stress response in Drosophila subobscura. II. Puff activity during anoxia and recovery from anoxia.

When individuals of Drosophila subobscura at 0 hr prepupa are submitted to anoxia (4 hr and 24 hr, respectively), their puffing pattern is very similar to that shown by individuals at the moment of development in which treatment began. The same expression of genes (the same puffing pattern and the same protein pattern) is induced in this species by recovery from anoxia as well as by heat shock treatment at 31 degrees C.

Animals↗
PubMed2000

Oxygen-dependent energetics of anoxia-tolerant and anoxia-intolerant hepatocytes.

The oxygen-dependence of cellular energetics was investigated in hepatocytes from goldfish Carassius auratus (anoxia-tolerant) and rainbow trout Oncorhynchus mykiss (anoxia-intolerant). In goldfish hepatocytes, an approximately 50 % reduction in the rate of oxygen consumption was observed in response to both acute and prolonged hypoxia, the latter treatment shifting the threshold for this reduction to a higher oxygen level. A concomitant increase in the rate of lactate production did not compensate for the decreased aerobic ATP supply, resulting in an overall metabolic depression of 26 % during acute hypoxia and of 42 % during prolonged hypoxia. Trout hepatocytes showed a similar suppression of cellular respiration after prolonged hypoxia but were unresponsive to acute hypoxia. Similarly, the rate of lactate production was unaltered during acute hypoxia but was increased during prolonged hypoxia, metabolic depression amounting to 7 % during acute hypoxia and 30 % during prolonged hypoxia. In both species, the affinity of hepatocytes for oxygen decreased during hypoxia, but this alteration was not sufficient in absolute terms to account for the observed decrease in aerobic ATP supply. Protein synthesis was suppressed in both cell types under hypoxia, whereas Na(+)/K(+)-ATPase activity decreased in trout but not in goldfish hepatocytes, emphasising the importance of membrane function in these cells during conditions of limited energy supply.

Adenosine Triphosphate↗