Interactions Between Glycine Decarboxylase, the Tricarboxylic Acid Cycle and the Respiratory Chain in Pea Leaf Mitochondria

1985 ◽  
Vol 12 (2) ◽  
pp. 119 ◽  
Author(s):  
DA Day ◽  
M Neuberger ◽  
R Douce
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Glycine Decarboxylase ◽  
Succinate Oxidation ◽  
Acid Cycle ◽  
Oxidation Reduction ◽  
The Matrix ◽  
Steady State Levels ◽  
High Matrix ◽  
Respiratory Complex I

In pea leaf and potato mitochondria, external NADH oxidation was inhibited by concurrent oxidation of endogenous NADH and succinate. Succinate oxidation was also inhibited by concurrent oxidation of external NADH, but oxidation of endogenous NADH was not. NAD+-depletion studies suggested that glycine decarboxylase and other NAD-linked enzymes competed for available NAD+ within the matrix. However, at both high and low NAD+ levels, only the tricarboxylic acid cycle enzymes and malic enzyme were inhibited during concurrent oxidation with glycine. Measurements of the oxidation-reduction state of matrix NADH suggested that most of the mitochondria in the preparations contained both glycine decarboxylase and the tricarboxylic acid cycle enzymes and that steady-state levels of NADH were maximal with glycine alone as substrate. That is, there was no evidence for two populations of mitochondria being present. Nonetheless, malate stimulated state 4 and rotenone-inhibited O2 uptake in the presence of glycine. We conclude from these results that the priority glycine has as a substrate for leaf mitochondria is due to a priority that electrons from respiratory complex I have over those from complex II and the external NADH dehydrogenase, and the ability of glycine decarboxylase to compete favourably with tricarboxylic acid cycle enzymes for NAD+ in the matrix. Glycine may inhibit oxidation of other NAD-linked substrates by maintaining high matrix NADH/ NAD+ ratios. However, malate plus pyruvate appear to have access to some electron transport that is not accessible to glycine, at least under ADP-limiting conditions.

Tricarboxylic acid cycle activity in perfused rat lungs after O2 exposure

1992 ◽  
Vol 262 (4) ◽  
pp. L495-L501 ◽  
Author(s):  
D. J. Bassett ◽  
S. S. Reichenbaugh
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Enzyme Inactivation ◽  
Pyridine Nucleotides ◽  
Acid Cycle ◽  
Metabolic Conditions ◽  
Steady State Levels ◽  
14Co2 Production ◽  
Tricarboxylic Acid Cycle Intermediates

O2-induced impairment of mitochondrial energy generation was examined in intact lungs isolated from rats after 18-30 h exposure to either air or 100% O2 in vivo. Mitochondrial metabolic rates were determined by separate measurements of 14CO2 production from [1-14C]pyruvate and [U-14C]palmitate, perfused under normal and stimulated metabolic conditions brought about by perfusion with the uncoupler of oxidative phosphorylation, 2,4-dinitrophenol (DNP). In the absence of DNP, O2 exposure did not significantly alter 14CO2 productions from either substrate. DNP increased lung pyruvate and palmitate catabolism to CO2 twofold in air-exposed lungs but did not alter 14CO2 production in lungs isolated from O2-exposed rats. These data demonstrated an O2-induced impairment of maximal mitochondrial metabolism of both pyruvate and palmitate that could not be explained by alterations in tissue free coenzyme A or by loss of pyridine nucleotides. However, comparisons of the steady-state levels of tricarboxylic acid cycle intermediates between O2- and air-exposed lungs did identify isocitrate dehydrogenase as a possible site of O2-induced enzyme inactivation.

Studies in the respiratory and carbohydrate metabolism of plant tissues. VII. Experimental studies with potato tubers of an inhibition of the respiration and of a ‘block’ in the tricarboxylic acid cycle induced by ‘oxygen poisoning’

1955 ◽  
Vol 143 (913) ◽  
pp. 523-549 ◽  
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Experimental Studies ◽  
General Term ◽  
Tricarboxylic Acid ◽  
Pure Oxygen ◽  
Prolonged Treatment ◽  
Potato Tubers ◽  
Acid Cycle ◽  
Oxidation Reduction ◽  
Oxygen Poisoning

Prolonged treatment of potato tubers at 1° C with an atmosphere of pure oxygen eventually induces a marked inhibition of the rate of CO 2 output; there is also an accumulation of pyruvate and of 'citrate’ and a decrease in the contents of α -ketoglutarate and of malate as compared with potatoes held in air. These changes in the acids appear to be in accord with the development during sojourn in pure oxygen of a ‘block’ in the tricarboxylic acid cycle between ‘citrate’ and α -ketoglutarate. The indications in previous work (Barron, Link, Klein & Michel 1950; Barker & Mapson 1953 b ) that the tricarboxylic acid cycle may operate in potato tubers under certain metabolic conditions are thus supported. The treatment with pure oxygen also results in a progressive shift to the more oxidized state in the ascorbic acid and glutathione oxidation-reduction systems; finally, the potato tissue develops a brown discoloration presumably due to polyphenolase action. The change in the balance of the two oxidation-reduction systems towards oxidation may be caused, in part, by a reduced rate of regeneration of coenzyme II because of the ‘block’ in the tricarboxylic acid cycle. The paper also contains the results of preliminary experiments on the reversibility of the above changes. The data add to the knowledge of the varied metabolic phenomena which have been observed in many different types of living tissue, both plant and animal, and which are conveniently classified under the general term ‘oxygen poisoning’ (Stadie, Riggs & Haugaard 1944).

scholarly journals ELECTRON MICROSCOPE HISTOCHEMICAL EVIDENCE FOR A PARTIAL OR TOTAL BLOCK OF THE TRICARBOXYLIC ACID CYCLE IN THE MITOCHONDRIA OF PRESYNAPTIC AXON TERMINALS

1971 ◽  
Vol 51 (1) ◽  
pp. 216-222 ◽  
Author(s):  
Ferenc Hajós ◽  
Sándor Kerpel-Fronius
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Energy Coupling ◽  
Tricarboxylic Acid ◽  
Synaptic Function ◽  
Coupling Mechanism ◽  
Succinate Oxidation ◽  
Acid Cycle ◽  
Axon Terminals ◽  
Massive Accumulation

Respiration-linked, massive accumulation of Sr2+ is used to reveal the coupled oxidation of pyruvate, α-oxoglutarate, succinate, and malate by in situ mitochondria. All of these substrates were actively oxidized in the dendritic and perikaryal mitochondria, but no α-oxoglutarate or succinate utilization could be demonstrated in the mitochondria of the presynaptic axon terminals. A block at an early step of α-oxoglutarate and succinate oxidation is proposed to account for the negative histochemical results, since the positive reaction with pyruvate and malate proves that these mitochondria possess an intact respiratory chain and energy-coupling mechanism essential for Sr2+ accumulation. This indicates that the mitochondria in the axon terminals would be able to generate energy for synaptic function with at least some of the respiratory substrates. With regard to the block in the tricarboxylic acid cycle, the oxaloacetate necessary for citrate formation is suggested to be provided by fixation of CO2 into some of the pyruvate.

scholarly journals The reduction of diamide by rat liver mitochondria and the role of glutathione

1978 ◽  
Vol 176 (3) ◽  
pp. 649-664 ◽  
Author(s):  
P C Jocelyn
Keyword(s):  
Reduced Glutathione ◽  
Tricarboxylic Acid Cycle ◽  
High Energy ◽  
Tricarboxylic Acid ◽  
Rat Liver Mitochondria ◽  
Acid Cycle ◽  
Respiratory Inhibitors ◽  
Glutathione Concentration ◽  
The Matrix ◽  
Mitochondrial Glutathione

Diamide is reduced by mitochondria utilizing endogenous substrates with Vmax. 20nmol/min per mg of protein and Km 75micrometer. The reaction is inhibited by: (a) thiol-blocking reagents (N-ethylmaleimide, p-hydroxymercuribenzoate, mersalyl and 2,6-dichlorophenol-indophenol);(b) respiratory inhibitors (arsenicals, malonate and antimycin, but not cyanide or oligomycin; inhibition by antimycin is reversed by ATP); (c) uncouplers (carbonyl cyanide p-trifluoromethoxyphenylhydrazone, 2,4-dinitrophenol and valinomycin with K+; inhibition by the first of these uncouplers is not reversed by cyanide); (d) reagents affecting energy conservation (Ca2+, increasing pH, phosphate; phosphate inhibition is augmented by catalytic ADP or ATP and augmentation is abolished by respiratory inhibitors). Concentrations of mitochondrial glutathione are high when diamide reduction is uninhibited, but low after adding one of the above inhibitors such that the reduction rate is roughly proportional to the glutathione concentration. Endogenous ATP concentrations are lower in the presence of diamide than without, but the difference is abolished by respiratory inhibitors. With oligomycin added, however, ATP concentrations are higher in the presence of diamide and this positive increment is decreased by antimycin, N-ethylmaleimide and malonate. In the presence of diamide and an uncoupler, the mitochondrial glutathione content does not fall if various reducible substrates are present, although the inhibition of diamide reduction is not relieved. Some of these substrates prevent the fall in reduced glutathione concentration found with diamide and phosphate. They also relieve the inhibition of diamide reduction and the relief is sensitive to butylmalonate. The inhibition of diamide reduction by N-ethylmaleimide, mersalyl or p-hydroxymercuribenzoate is not relieved by reducible substrates, but the latter mitigate the fall in the concentration of glutathione. Inhibitors of carriers of tricarboxylic acid-cycle intermediates also inhibit reduction of diamide. The reduced glutathione concentration remains high when they are added singly, but falls when two of them are combined. It is proposed that diamide may enter the matrix as a protonated adduct formed with the thiol groups of mitochondrial carriers and then be reduced in the matrix by glutathione, which is regenerated via NADH, energy-dependent transhydrogenase and NADP+-specific glutathione reductase. Some of the high-energy equivalents required for the transhydrogeneration may be generated by the substrate phosphorylation step of the tricarboxylic acid cycle.

scholarly journals Effects of sevoflurane anesthesia and abdominal surgery on the systemic metabolome: a prospective observational study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yiyong Wei ◽  
Donghang Zhang ◽  
Jin Liu ◽  
Mengchan Ou ◽  
Peng Liang ◽  
...  
Keyword(s):  
Abdominal Surgery ◽  
General Anesthesia ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Metabolic Changes ◽  
Sevoflurane Anesthesia ◽  
Glutamate Metabolism ◽  
Acid Cycle ◽  
Link Type ◽  
The Mean

Abstract Background Metabolic status can be impacted by general anesthesia and surgery. However, the exact effects of general anesthesia and surgery on systemic metabolome remain unclear, which might contribute to postoperative outcomes. Methods Five hundred patients who underwent abdominal surgery were included. General anesthesia was mainly maintained with sevoflurane. The end-tidal sevoflurane concentration (ETsevo) was adjusted to maintain BIS (Bispectral index) value between 40 and 60. The mean ETsevo from 20 min after endotracheal intubation to 2 h after the beginning of surgery was calculated for each patient. The patients were further divided into low ETsevo group (mean − SD) and high ETsevo group (mean + SD) to investigate the possible metabolic changes relevant to the amount of sevoflurane exposure. Results The mean ETsevo of the 500 patients was 1.60% ± 0.34%. Patients with low ETsevo (n = 55) and high ETsevo (n = 59) were selected for metabolomic analysis (1.06% ± 0.13% vs. 2.17% ± 0.16%, P < 0.001). Sevoflurane and abdominal surgery disturbed the tricarboxylic acid cycle as identified by increased citrate and cis-aconitate levels and impacted glycometabolism as identified by increased sucrose and D-glucose levels in these 114 patients. Glutamate metabolism was also impacted by sevoflurane and abdominal surgery in all the patients. In the patients with high ETsevo, levels of L-glutamine, pyroglutamic acid, sphinganine and L-selenocysteine after sevoflurane anesthesia and abdominal surgery were significantly higher than those of the patients with low ETsevo, suggesting that these metabolic changes might be relevant to the amount of sevoflurane exposure. Conclusions Sevoflurane anesthesia and abdominal surgery can impact principal metabolic pathways in clinical patients including tricarboxylic acid cycle, glycometabolism and glutamate metabolism. This study may provide a resource data for future studies about metabolism relevant to general anaesthesia and surgeries. Trial registration www.chictr.org.cn. identifier: ChiCTR1800014327.

scholarly journals Triheptanoin partially restores levels of tricarboxylic acid cycle intermediates in the mouse pilocarpine model of epilepsy

2013 ◽  
Vol 129 (1) ◽  
pp. 107-119 ◽  
Author(s):  
Mussie G. Hadera ◽  
Olav B. Smeland ◽  
Tanya S. McDonald ◽  
Kah Ni Tan ◽  
Ursula Sonnewald ◽  
...  
Keyword(s):  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Cycle ◽  
Pilocarpine Model ◽  
Tricarboxylic Acid Cycle Intermediates
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