scholarly journals Roles of energy status, KATP channels and channel arrest in fish brain K+ gradient dissipation during anoxia

1995 ◽  
Vol 198 (12) ◽  
pp. 2575-2580 ◽  
Author(s):  
D Johansson ◽  
G Nilsson
Keyword(s):  
Rainbow Trout ◽  
Crucian Carp ◽  
Energy Charge ◽  
Ion Homeostasis ◽  
Katp Channels ◽  
Iodoacetic Acid ◽  
Energy Status ◽  
Efflux Rate ◽  
Channel Arrest ◽  
K Permeability

The crucian carp (Carassius carassius L.) is one of the most anoxia-tolerant vertebrates known, being able to maintain ion homeostasis in its brain for many hours of anoxia. This study aims to clarify the importance of glycolysis during anoxia and also to investigate whether the extreme tolerance to anoxia could be due to down-regulation of K+ permeability ('channel arrest') and/or activation of ATP-sensitive K+ (KATP) channels. The latter was also tested in rainbow trout (Oncorhynchus mykiss). The results suggest that, during anoxia, the crucian carp brain is completely dependent on glycolysis, since blocking glycolysis with iodoacetic acid (IAA) rapidly caused an increase in [K+]o that coincided with a drastic drop in ATP level and energy charge. Testing the channel arrest hypothesis by measuring the K+ efflux rate after Na+/K+-ATPase had been blocked by ouabain revealed no change in K+ permeability in crucian carp brain in response to anoxia. Furthermore, superfusing the brain of anoxic crucian carp with the KATP channel blocker glibenclamide did not alter the efflux rate of K+ after glycolysis had been inhibited with IAA. Glibenclamide had no effect on K+ efflux rate in rainbow trout brain during anoxia.

Brain sensitivity to anoxia in fish as reflected by changes in extracellular K+ activity

1993 ◽  
Vol 264 (2) ◽  
pp. R250-R253 ◽  
Author(s):  
G. E. Nilsson ◽  
M. Perez-Pinzon ◽  
K. Dimberg ◽  
S. Winberg
Keyword(s):  
Blood Pressure ◽  
Rainbow Trout ◽  
Crucian Carp ◽  
Ion Homeostasis ◽  
Initial Increase ◽  
Freshwater Turtles ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Brain Failure ◽  
Crucian Carp Carassius Carassius ◽  
K Activity

Most vertebrates have a very limited tolerance to anoxia. The only exceptions to this rule are found among ectothermic species, notably crucian carp (Carassius carassius) and freshwater turtles. It has been assumed that the brains of these species are less sensitive to anoxia than ectothermic brains in general. However, it has not been possible to exclude that anoxia-intolerant species like rainbow trout (Oncorhynchus mykiss) die from heart failure rather than brain failure during anoxia, and that the average ectothermic brain is actually rather insensitive to anoxia. By simultaneously measuring the effect of anoxia on brain extracellular K+ activity ([K+]o), blood pressure, and heart rate in rainbow trout, we show that the rainbow trout brain rapidly loses ion homeostasis during anoxia, despite an initial increase in blood pressure. The rainbow trout brain showed a sudden transient increase in [K+]o (suggesting a rapid depolarization) after approximately 30 min of anoxia at 10 degrees C. At the same time the blood pressure was still close to the normoxic value. In a comparative experiment, crucian carp was found to maintain a low brain [K+]o for at least 6 h of anoxia. Thus the results suggest that the rainbow trout brain is anoxia-intolerant in itself, and that its ability to maintain ion gradients during anoxia is very much lower than that of crucian carp. If temperature differences are taken into account, the anoxia sensitivity of the rainbow trout brain is comparable to that of mammals.

Energy status of the rat lung after exposure to elevated PO2

1978 ◽  
Vol 45 (1) ◽  
pp. 56-59 ◽  
Author(s):  
A. B. Fisher
Keyword(s):  
Bovine Serum Albumin ◽  
Bovine Serum ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Rat Lung ◽  
Energy Status ◽  
Hyperoxic Exposure ◽  
Isolated Lung ◽  
Lactate And Pyruvate

To study hyperoxic effects on adenine nucleotide content and lactate and pyruvate production by lungs, rats were exposed to oxygen at 1 ATA for 18, 24, or 48 h or to 4 ATA for 1 h. Subsequently, lungs were removed from rats, placed in an isolated-lung apparatus, ventilated with 5% CO2 in O2, and perfused with Krebs-Ringer bicarbonate medium containing 5.5 mM glucose and 4% bovine serum albumin. Uptake of serotonin from the perfusate was depressed 28% in rats exposed to hyperbaric oxygen compared with unexposed controls. Concentrations of adenine nucleotides, the ATP/ADP ratio, and the “energy charge” were similar in control and oxygen-exposed rats. The production of lactate and the ratio of lactate to pyruvate production were significantly higher in rats exposed to oxygen for 48 h compared with other exposure regimens. Comparison of these results with those previously reported for serotonin uptake in lungs after hyperoxic exposure indicates that serotonin clearance is depressed prior to alteration of the energy status of the rat lung.

scholarly journals Switching of metabolic programs in response to light availability is an essential function of the cyanobacterial circadian clock

2017 ◽  
Author(s):  
Anna M. Puszynska ◽  
Erin K. O’Shea
Keyword(s):  
Transcription Factor ◽  
Carbon Metabolism ◽  
Energy Charge ◽  
Light Availability ◽  
Light Conditions ◽  
Energy Status ◽  
Carbon Utilization ◽  
Genome Wide ◽  
Essential Function ◽  
Circadian Transcription

AbstractThe transcription factor RpaA is the master regulator of circadian transcription in cyanobacteria, driving genome-wide oscillations in mRNA abundance. Deletion ofrpaAhas no effect on viability in constant light conditions, but renders cells inviable in cycling conditions when light and dark periods alternate. We investigated the mechanisms underlying this viability defect, and demonstrate that therpaA-strain cannot maintain appropriate energy status at night, does not accumulate carbon reserves during the day, and is defective in transcription of genes crucial for utilization of carbohydrate stores at night. Reconstruction of carbon utilization pathways combined with provision of an external carbon source restores energy charge and viability of therpaA-strain in light/dark cycling conditions. Our observations highlight how a circadian program controls and temporally coordinates essential pathways in carbon metabolism to maximize fitness of cells facing periodic energy limitations.

scholarly journals Metabolic Effects of Dietary Glycerol Supplementation in Muscle and Liver of European Seabass and Rainbow Trout by 1H NMR Metabolomics

Metabolites ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 202 ◽  
Author(s):  
Mariana Palma ◽  
Ludgero Tavares ◽  
João Rito ◽  
Luís Henriques ◽  
João Silva ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
1H Nmr ◽  
Energy Charge ◽  
Dicentrarchus Labrax ◽  
Metabolite Profile ◽  
Sustainable Growth ◽  
Metabolic Effects ◽  
Adenylate Energy Charge ◽  
Multivariate Statistical ◽  
European Seabass

The sustainable growth of fish aquaculture will require the procurement of non-marine feed sources. Glycerol is a potential feed supplement whose metabolism may spare the catabolism of dietary amino acids, thereby extending the use of the feed protein to other physiological functions such as growth. In the present study, the effects of dietary glycerol supplementation on the muscle and liver metabolomes of rainbow trout (Oncorhynchus mykiss) and European seabass (Dicentrarchus labrax) were evaluated. Fish juveniles were fed diets with 0%, 2.5%, and 5% glycerol. Muscle and liver aqueous fractions were extracted and 1H NMR spectra were acquired. Metabolite profiles derived from the 1H NMR signals were assessed using univariate and multivariate statistical analyses. The adenylate energy charge was determined in the muscle. For both species, the muscle metabolite profile showed more variability compared to that of the liver and was most perturbed by the 5.0% glycerol diet. For the liver metabolite profile, rainbow trout showed fewer differences compared to European seabass. No differences were observed in energy charge between experimental groups for either species. Thus, rainbow trout appeared to be less susceptible to tissue metabolite perturbations, compared to seabass, when the diet was supplemented with up to 5% glycerol.

Role of ATP-sensitive K+ channels in ischemic preconditioning of skeletal muscle against infarction

1997 ◽  
Vol 273 (1) ◽  
pp. H44-H51 ◽  
Author(s):  
C. Y. Pang ◽  
P. Neligan ◽  
H. Xu ◽  
W. He ◽  
A. Zhong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Energy Charge ◽  
Katp Channels ◽  
High Energy ◽  
Intraarterial Infusion ◽  
Muscle Flaps ◽  
Charge Potential

We studied the role and mechanism of ATP-sensitive K+ (KATP) channels in ischemic preconditioning (IPC) of skeletal muscle against infarction in vivo. Surgically denervated, noncontractile latissimus dorsi muscle flaps in pentobarbitone-anesthetized pigs were assigned to nine groups: control; IPC (3 cycles of 10-min ischemia/reperfusion); preischemic lemakalim (LMK, 0.18 mg/muscle); postischemic LMK; sodium 5-hydroxydecanoate (5-HD, 27 mg/muscle) before IPC; glibenclamide (Glib 0.3 mg/kg iv) before IPC; 5-HD before preischemic LMK; 5-HD before ischemia; and Glib before ischemia. Except for Glib, all drugs were delivered to each muscle by 10-min local intraarterial infusion to avoid systemic effects. All muscle flaps underwent 4 h of global ischemia. Infarction was assessed at 48 h of reperfusion. In a separate study, muscle biopsies were taken before, during, and after ischemia for assay of high-energy phosphate and lactate contents and myeloperoxidase (MPO) activity. It was observed that muscle infarction in the IPC (24 +/- 2%) and preischemic LMK (21 +/- 2%) groups were smaller (P < 0.05) than that in the control (42 +/- 2%). The anti-infarction effect of IPC and LMK was blocked by 5-HD or Glib. IPC and preischemic LMK caused a higher (P < 0.05) muscle content of ATP and energy charge potential, a lower (P < 0.05) muscle content of lactate during ischemia, and a lower (P < 0.05) muscle MPO activity throughout 16 h of reperfusion compared with the control. These observations indicated for the first time that KATP channels are also involved in the anti-infarction effect of IPC in noncontractile skeletal muscle in vivo. Presently, the cause and importance of energy-sparing and neutrophil-inhibitory effects of IPC and LMK are not known.

Energy status of the rapidly paced canine myocardium in congestive heart failure

1992 ◽  
Vol 73 (6) ◽  
pp. 2363-2367 ◽  
Author(s):  
C. Montgomery ◽  
N. Hamilton ◽  
C. D. Ianuzzo
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Adenine Nucleotide ◽  
Adenine Nucleotides ◽  
Energy Charge ◽  
Lactate Concentration ◽  
Energy Status ◽  
Glycogen Depletion ◽  
Myocardial Layers ◽  
Adenine Nucleotide Pool

Rapid ventricular pacing (RVP) is used as an experimental model of congestive heart failure (CHF). The purpose of this study was to determine the energy status of the dog myocardium after the development of CHF via chronic RVP. The myocardium had a significantly lower (P < 0.05) energy charge (EC) during CHF (0.63 +/- 0.01) than in sham-operated controls (0.82 +/- 0.02). This was due to significant differences in concentrations in ATP (-48%), ADP (29%), and AMP (275%) in the RVP group. However, the total adenine nucleotide pool was not different between groups. Myocardial lactate concentration was also similar. Glycogen was significantly lower (P < 0.05) by 20% at peak CHF. The adenine nucleotides were similar among the different myocardial layers (endo-, mid-, and epicardium). The administration of enalapril (an inhibitor of angiotension-converting enzyme) to decrease vascular resistance had no effect on the myocardial energy status of CHF dogs. These findings suggest that the lower EC in CHF animals is not the result of subendocardial ischemia. Also, lower EC is not associated with endogenous glycogen depletion or increased lactate concentration. The energy status of the myocardium in RVP-induced CHF is unlike that seen in ischemia-induced heart failure. This suggests that CHF in RVP is not vascular in origin.

Changes in the adenylate energy charge ofNippostrorigylus brasiliensisandNematodirus battusduring the development of immunity to these nematodes in their hosts

Parasitology ◽  
1978 ◽  
Vol 76 (2) ◽  
pp. 211-220 ◽  
Author(s):  
A. J. Ballantyne ◽  
M. J. Sharpe ◽  
D. L. Lee
Keyword(s):  
Immune Response ◽  
Energy Charge ◽  
Nippostrongylus Brasiliensis ◽  
Adenylate Energy Charge ◽  
Energy Status ◽  
High Level

SummaryInfection of rats with 2000 infective juveniles ofNippostrongylus brasiliensisand of lambs with 60000 infective juveniles ofNematodirus battusresults in a well-marked immunity to these nematodes in their respective hosts. There is a fall in the adenylate energy charge value of these nematodes during the course of these infections, reaching values of 0·37 in males and 0·27 in females ofN. brasiliensis, and 0·31 in males and 0·23 in females ofN. battustowards the end of the infections. In hosts given relatively small numbers of infective juveniles, the values for the nematodes removed from the hosts late in the infection remain at a relatively high level. These results indicate that the immune response of the host may affect the energy status of these nematodes, and this could help to explain their subsequent expulsion from the immune host.

scholarly journals Some Kinetic and Metabolic Characteristics of Calcium-Induced Potassium Transport in Human Red Cells

1972 ◽  
Vol 60 (4) ◽  
pp. 406-429 ◽  
Author(s):  
Floyd M. Kregenow ◽  
Joseph F. Hoffman
Keyword(s):  
Flux Ratio ◽  
Iodoacetic Acid ◽  
Cell System ◽  
Na Transport ◽  
Metabolic Characteristics ◽  
Substrate Removal ◽  
Maximum Value ◽  
Metabolic Dependence ◽  
K Permeability ◽  
Human Red Cells

When fresh human erythrocytes or their ghosts are incubated with Ca + IAA (iodoacetic acid) + adenosine, K permeability increases; K permeability also increases when energy-depleted cells or their ghosts are incubated with Ca alone. Na transport decreases or remains unaltered in both situations. The Ca-induced increase in K permeability in the depleted cell system is qualitatively similar to that seen in the fresh cell system and furnishes a means for studying the metabolic dependence of calcium's action. Studies with the depleted system suggest that the normal refractiveness of the cell to calcium is provided by a metabolically dependent substrate. Removal of this substrate allows Ca to enter the cell and exert its effect. By using 47Ca, a maximum value was obtained (3–7 x 10-6 moles/liter of red blood cells) for the quantity of calcium that is taken up by the cell and responsible for the change in K permeability. Measurements of the unidirectional fluxes of K, obtained during the time Ca increases K permeability, appear to satisfy the flux ratio equation for passive diffusion through a membrane.

scholarly journals Switching of metabolic programs in response to light availability is an essential function of the cyanobacterial circadian output pathway

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Anna M Puszynska ◽  
Erin K O'Shea
Keyword(s):  
Transcription Factor ◽  
Carbon Metabolism ◽  
Energy Charge ◽  
Light Availability ◽  
Light Conditions ◽  
Energy Status ◽  
Carbon Utilization ◽  
Genome Wide ◽  
Essential Function ◽  
Circadian Transcription

The transcription factor RpaA is the master regulator of circadian transcription in cyanobacteria, driving genome-wide oscillations in mRNA abundance. Deletion of rpaA has no effect on viability in constant light conditions, but renders cells inviable in cycling conditions when light and dark periods alternate. We investigated the mechanisms underlying this viability defect, and demonstrate that the rpaA- strain cannot maintain appropriate energy status at night, does not accumulate carbon reserves during the day, and is defective in transcription of genes crucial for utilization of carbohydrate stores at night. Reconstruction of carbon utilization pathways combined with provision of an external carbon source restores energy charge and viability of the rpaA- strain in light/dark cycling conditions. Our observations highlight how a circadian output pathway controls and temporally coordinates essential pathways in carbon metabolism to maximize fitness of cells facing periodic energy limitations.

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