Metabolic and Tissue Solute Changes Associated With Changes in the Freezing Tolerance of the Bivalve Mollusc Modiolus Demissus

1977 ◽  
Vol 69 (1) ◽  
pp. 1-12
Author(s):  
DENNIS J. MURPHY
Keyword(s):  
Oxygen Consumption ◽  
Low Temperature ◽  
Freezing Tolerance ◽  
Anaerobic Metabolism ◽  
Arrhenius Plot ◽  
Physiological Mechanism ◽  
Temperature Acclimation ◽  
Anaerobic Conditions ◽  
Rate Of Oxygen Consumption ◽  
Dependent Mechanism

1. A physiological mechanism responsible for increasing the freezing tolerance of the bivalve Modiolus demissus (Dillwyn) following low-temperature acclimation was demonstrated. 2. The rates of oxygen consumption of M. demissus acclimated to temperatures between 0 and 24 °C were presented as an Arrhenius plot. A change in slope occurred at 10 °C, suggesting that temperature alone was not responsible for the increased decline in the rate of oxygen consumption below 10 °C. 3. Low-temperature acclimation had no effect on blood Na+ or K+ concentrations but did reduce the concentration of blood Mg2+ and, in addition, resulted in the accumulation of end-products characteristic of anaerobic metabolism - tissue alanine and proline, and blood Ca2+. Furthermore, maintenance of M. demissus under anaerobic conditions increased freezing tolerance. 4. Taken together, these data indicate that the increased freezing tolerance of M. demissus acclimated to low temperatures involves a conversion to anaerobic metabolism. 5. The increase in blood Ca2+ following low-temperature acclimation was associated with the increased freezing tolerance. Finally, Mg2+ simulated the effect of Ca2+ on freezing tolerance, but was only 20% as effective. 6. These results suggest that a Ca2+-dependent mechanism responsible for increasing the freezing tolerance of M. demissus exists, and that the increase in blood Ca2+ is due to a conversion to anaerobic metabolism.

A Calcium-Dependent Mechanism Responsible for Increasing the Freezing Tolerance of the Bivalve Mollusc Modiolus Demissus

1977 ◽  
Vol 69 (1) ◽  
pp. 13-21
Author(s):  
DENNIS J. MURPHY
Keyword(s):  
Low Temperature ◽  
Freezing Tolerance ◽  
Time Course ◽  
Cell Membranes ◽  
Contractile Response ◽  
Temperature Acclimation ◽  
Freezing Injury ◽  
Total Change ◽  
Calcium Dependent ◽  
Dependent Mechanism

1. A time course of the changes in blood Ca2+ and freezing tolerance of Modiolus demissus (Dillwyn) demonstrated that increases in freezing tolerance parallel increases in blood Ca2+. The increases in freezing tolerance occurred rapidly, suggesting that Ca2+ affects freezing tolerance directly by its presence in the blood. 2. The presence of La3+ reduced the freezing tolerance of isolated foot muscle. Thus, Ca2+ appears to increase freezing tolerance directly by binding to cell membranes. 3. The loss of the contractile response of freeze-thawed foot muscle to Ach, KCl and caffeine and the continued response to CaCl2 suggested that cell membranes are the primary sites of freezing injury. 4. The increase in blood Ca2+ following low-temperature acclimation accounted for only 40% of the total change in freezing tolerance. Therefore, other mechanisms responsible for increasing the freezing tolerance of M. demissus following low temperature acclimation also exist.

scholarly journals Recovery heat in muscular contraction without lactic acid formation

1931 ◽  
Vol 108 (757) ◽  
pp. 279-301 ◽  
Keyword(s):  
Acetic Acid ◽  
Oxygen Consumption ◽  
Lactic Acid ◽  
Muscular Contraction ◽  
Acid Formation ◽  
Anaerobic Conditions ◽  
Spontaneous Breakdown ◽  
Rate Of Oxygen Consumption ◽  
Resting Muscle

In a comparison of muscles poisoned with mono-iodo-acetic acid (IAA) in the presence and in the absence of oxygen respectively, Lundsgaard (1930) found:- (1) That the spontaneous breakdown of phosphagen in poisoned resting muscle is much more rapid under anaerobic conditions. (2) That the onset of the characteristic contracture produced by IAA is accompanied always by an increase in the rate of oxygen consumption.

scholarly journals A Method for Estimating the Velocity at Which Anaerobic Metabolism Begins in Swimming Fish

Water ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1430
Author(s):  
Feifei He ◽  
Xiaogang Wang ◽  
Yun Li ◽  
Yiqun Hou ◽  
Qiubao Zou ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Swimming Speed ◽  
Crucian Carp ◽  
Anaerobic Metabolism ◽  
Swimming Performance ◽  
Beat Frequency ◽  
Critical Swimming Speed ◽  
Swimming Efficiency ◽  
Rate Of Oxygen Consumption ◽  
Tail Beat

Anaerobic metabolism begins before fish reach their critical swimming speed. Anaerobic metabolism affects the swimming ability of fish, which is not conducive to their upward tracking. The initiation of anaerobic metabolism therefore provides a better predictor of flow barriers than critical swimming speed. To estimate the anaerobic element of metabolism for swimming fish, the respiratory metabolism and swimming performance of adult crucian carp (Carassius auratus, mass = 260.10 ± 7.93, body length = 19.32 ± 0.24) were tested in a closed tank at 20 ± 1 °C. The swimming behavior and rate of oxygen consumption of these carp were recorded at various swimming speeds. Results indicate (1) The critical swimming speed of the crucian carp was 0.85 ± 0.032 m/s (4.40 ± 0.16 BL/s). (2) When a power function was fitted to the data, oxygen consumption, as a function of swimming speed, was determined to be AMR = 131.24 + 461.26Us1.27 (R2 = 0.948, p < 0.001) and the power value (1.27) of Us indicated high swimming efficiency. (3) Increased swimming speed led to increases in the tail beat frequency. (4) Swimming costs were calculated via rate of oxygen consumption and hydrodynamic modeling. Then, the drag coefficient of the crucian carp during swimming was calibrated (0.126–0.140), and the velocity at which anaerobic metabolism was initiated was estimated (0.52 m/s), via the new method described herein. This study adds to our understanding of the metabolic patterns of fish at different swimming speeds.

Effect of Anticonvulsants on the Uptake of 5-Methyltetrahydrofolic Acid by the Choroid Plexus in Rabbits

1977 ◽  
Vol 53 (1) ◽  
pp. 75-80
Author(s):  
H. Taguchi ◽  
Z. Abdul-Cader ◽  
J. Perry ◽  
E. H. Reynolds ◽  
I. Chanarin
Keyword(s):  
Folic Acid ◽  
Low Temperature ◽  
Choroid Plexus ◽  
Incubation Medium ◽  
Pernicious Anaemia ◽  
Inhibitory Effect ◽  
Anaerobic Conditions ◽  
Acid Therapy ◽  
Pteroylglutamic Acid

1. The isolated choroid plexus of the rabbit takes up 5-methyltetrahydrofolate from the incubation medium. 2. Other folate analogues (pteroylglutamic acid, methotrexate, 5-formyltetrahydrofolate = folinic acid) inhibited the uptake of 5-methyltetrahydrofolate. 3. The uptake of 5-methyltetrahydrofolate was inhibited by low temperature, anaerobic conditions and dinitrophenol. 4. The anticonvulsant drugs, diphenylhydantoin and phenobarbital, had no effect on 5-methyltetrahydrofolate uptake. 5. The inhibitory effect of pteroylglutamic acid on the uptake of 5-methyltetrahydrofolate by the choroid plexus may explain the effect of long-term folic acid therapy in aggravating vitamin B12 neuropathy in pernicious anaemia.

Proximal tubule dysfunction in cystine-loaded tubules: effect of phosphate and metabolic substrates

1996 ◽  
Vol 271 (3) ◽  
pp. F717-F722
Author(s):  
G. Bajaj ◽  
M. Baum
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Tricarboxylic Acid Cycle ◽  
Dimethyl Ester ◽  
Proximal Tubules ◽  
Intracellular Atp ◽  
Metabolic Substrates ◽  
Rate Of Oxygen Consumption ◽  
Intracellular Phosphate

Intracellular cystine loading by use of cystine dimethyl ester (CDME) results in a generalized inhibition in proximal tubule transport due, in part, to a decrease in intracellular ATP. The present study examined the importance of phosphate and metabolic substrates in the proximal tubule dysfunction produced by cystine loading. Proximal tubule intracellular phosphorus was 1.8 +/- 0.1 in control tubules and 1.1 +/- 0.1 nmol/mg protein in proximal tubules incubated in vitro with CDME P < 0.001). Infusion of sodium phosphate in rabbits and subsequent incubation of proximal tubules with a high-phosphate medium attenuated the decrease in proximal tubule respiration and prevented the decrease in intracellular ATP with cystine loading. Tricarboxylic acid cycle intermediates have been shown to preserve oxidative metabolism in phosphate-depleted proximal tubules. In proximal tubules incubated with either 1 mM valerate or butyrate, there was a 42 and 34% reduction (both P < 0.05) in the rate of oxygen consumption with cystine loading. However, tubules incubated with 1 mM succinate or citrate had only a 13 and 14% P = NS) reduction in the rate of oxygen consumption, respectively. These data are consistent with a limitation of intracellular phosphate in the pathogenesis of the proximal tubule dysfunction with cystine loading.

Viability and respiratory activity ofPseudomonas syringaecells starved in buffer

1995 ◽  
Vol 41 (4-5) ◽  
pp. 372-377 ◽  
Author(s):  
João P. S. Cabral
Keyword(s):  
Oxygen Consumption ◽  
Electron Transport ◽  
Pseudomonas Syringae ◽  
Respiratory Activity ◽  
Bacterial Cells ◽  
Intact Cells ◽  
Rate Of Oxygen Consumption ◽  
Metabolic Activities ◽  
Different Levels ◽  
Number Of Cells

Pseudomonas syringae cells starved in buffer released orcinol-reactive molecules and materials that absorbed ultraviolet light. The number of cells culturable in nutrient medium decreased more rapidly than the number of intact particles determined by microscopy. The results suggested that starvation resulted in the lysis of an increasing number of cells, and that a fraction of the intact particles were not culturable. Starvation also resulted in a decrease in the rate of oxygen consumption with acetate, glycerol, and succinate, but at different levels. Whereas the respiration of acetate and glycerol decreased concomitantly with culturability, the respiration of succinate decreased to levels similar to the concentration of intact cells, suggesting that all intact particles respired the succinate, but only the culturable cells respired the acetate and glycerol. The results suggest that measuring the activity of the electron-transport system can overestimate the viability of starved bacterial cells, and that complex metabolic activities such as the respiration of acetate and glycerol are probably better suited for the evaluation of this parameter.Key words: Pseudomonas syringae, starvation, culturability, viability, respiration.

scholarly journals EFFECTS OF AZIDE AND CHLORETONE ON THE SODIUM AND POTASSIUM CONTENTS AND THE RESPIRATION OF FROG SCIATIC NERVES

1958 ◽  
Vol 41 (5) ◽  
pp. 959-988 ◽  
Author(s):  
W. P. Hurlbut
Keyword(s):  
Oxygen Consumption ◽  
Respiratory Depression ◽  
Conduction Block ◽  
Slow Conduction ◽  
Ionic Distribution ◽  
Rate Of Oxygen Consumption ◽  
Sciatic Nerves ◽  
Time Courses ◽  
Sodium And Potassium

Azide (0.2 to 5.0 mM) and chloretone (2.0 to 15.0 mM) reversibly inhibited 20 to 90 per cent of the resting respiration of frog sciatic nerves, and caused a loss of potassium and a gain of sodium in this tissue. The changes in ionic contents that developed after 5 or 10 hours were roughly correlated with the degree of respiratory depression, but the time courses of these changes were different with the two reagents. In azide these changes appeared to begin immediately, while in chloretone, at concentrations between 3.0 and 5.0 mM, the ionic shifts developed after a delay of several hours. Fifteen millimolar chloretone produced immediate changes in ionic contents several times greater than those produced by anoxia. The changes in ionic distribution produced in 5 hours by anoxia, 5.0 mM azide, or 5.0 mM chloretone were at least partially reversible; those produced by 15.0 mM chloretone were irreversible. With the exception of 15.0 mM chloretone the ionic shifts produced by these reagents may be due primarily to the depression of the respiration, although there are indications that azide acts, in addition, by another pathway. Concentrations of azide or chloretone that depressed the resting rate of oxygen consumption more than 50 per cent produced a slow conduction block, while 15.0 mM chloretone blocked conduction within 15 minutes.

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