THE EFFECT OF NEUTRAL SALTS ON PARTICLE PREPARATIONS FROM RAT LIVER: II. EFFECTS OF NEUTRAL SALTS ON TRICARBOXYLIC ACID CYCLE REACTIONS

1965 ◽  
Vol 43 (3) ◽  
pp. 359-372 ◽  
Author(s):  
E. R. Tustanoff ◽  
H. B. Stewart
Keyword(s):  
Rat Liver ◽  
Acid Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Neutral Salt ◽  
Acid Cycle ◽  
Pyruvate Oxidation ◽  
Highly Sensitive ◽  
Osmotic Activity

In a previous paper it was shown that neutral salt or sucrose, probably as a consequence of osmotic activity, interferes with the utilization of pyruvate by washed particle preparations from rat liver. In the present paper the effects of neutral salt on reaction sequences in the tricarboxylic acid cycle have been investigated. α-Oxoglutarate utilization is inhibited by salt in a fashion that closely resembles the osmolar inhibition of pyruvate oxidation. Citrate, but not cis-aconitate or isocitrate, utilization is inhibited by salt concentrations somewhat greater than those required for inhibition of α-oxo acid metabolism. Succinate, fumarate, and malate utilization are not highly sensitive to salt inhibition, and anaerobic utilization of citrate in the presence of 1,10-phenanthroline does not appear to be affected by salt.

scholarly journals The redistribution of carbon label by the reactions involved in glycolysis, gluconeogenesis and the tricarboxylic acid cycle in rat liver

1968 ◽  
Vol 110 (2) ◽  
pp. 313-335 ◽  
Author(s):  
D. F. Heath
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Rat Liver ◽  
Tricarboxylic Acid Cycle ◽  
Specific Radioactivity ◽  
Tricarboxylic Acid ◽  
State Theory ◽  
Variable Rate ◽  
Acid Cycle ◽  
Constant Rate

A scheme is presented that shows how the reactions involved in gluconeogenesis, glycolysis and the tricarboxylic acid cycle are linked in rat liver. Equations are developed that show how label is redistributed in aspartate, glutamate and phosphopyruvate when it is introduced as specifically labelled pyruvate or glucose either at a constant rate (steady-state theory) or at a variable rate (non-steady-state theory). For steady-state theory the fractions of label introduced as specifically labelled pyruvate that are incorporated into glucose and carbon dioxide are also given, and for both theories the specific radioactivities of aspartate and glutamate relative to the specific radioactivity of the substrate. The theories allow for entry of label into the tricarboxylic acid cycle via both oxaloacetate and acetyl-CoA, for 14CO2 fixation and for loss of label from the tricarboxylic acid cycle in glutamate, but not for losses in citrate. They also allow for incomplete symmetrization of label in oxaloacetate due to incomplete equilibration with fumarate both in the extramitochondrial part of the cell and in the mitochondrion on entry of oxaloacetate into the tricarboxylic acid cycle. In the latter case failure both of oxaloacetate to equilibrate with malate and of malate to equilibrate with fumarate are considered.

Cutaneous Burn Injury Alters Relative Tricarboxylic Acid Cycle Fluxes in Rat Liver

1999 ◽  
Vol 20 (4) ◽  
pp. 292-302 ◽  
Author(s):  
David M. Yarmush ◽  
Annette D. MacDonald ◽  
Brent D. Foy ◽  
Francois Berthiaume ◽  
Ronald G. Tompkins ◽  
...  
Keyword(s):  
Rat Liver ◽  
Burn Injury ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Cycle

scholarly journals Enhanced Post-Stationary-Phase Survival of a Clinical Thymidine-Dependent Small-Colony Variant of Staphylococcus aureus Results from Lack of a Functional Tricarboxylic Acid Cycle

2007 ◽  
Vol 189 (7) ◽  
pp. 2936-2940 ◽  
Author(s):  
Indranil Chatterjee ◽  
Mathias Herrmann ◽  
Richard A. Proctor ◽  
Georg Peters ◽  
Barbara C. Kahl
Keyword(s):  
Staphylococcus Aureus ◽  
Acetic Acid ◽  
Acid Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Altered Expression ◽  
Acid Cycle ◽  
Small Colony Variant ◽  
Stationary Phase Survival ◽  
Small Colony

ABSTRACT The mechanisms underlying the persistence of the Staphylococcus aureus small-colony variant (SCV) are not fully elucidated. In this study, clinical thymidine-dependent SCVs displayed altered expression of citB, clpC, and arcA genes, reduced acetate catabolization, and enhanced survival. These results implicate the importance of changes in tricarboxylic acid cycle and acetic acid metabolism in SCV survival and persistence.

scholarly journals Metabolic Activity Related to the Potassium Pump in the Midgut of Bombyx Mori Larvae

1985 ◽  
Vol 116 (1) ◽  
pp. 69-78
Author(s):  
P. PARENTI ◽  
B. GIORDANA ◽  
V. F. SACCHI ◽  
G. M. HANOZET ◽  
A. GUERRITORE
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Glutamic Acid ◽  
Amino Acid Metabolism ◽  
Acid Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Electrical Potential ◽  
Tricarboxylic Acid ◽  
Electrical Potential Difference ◽  
Acid Cycle

The transepithelial electrical potential difference across the isolated midgut of Bombyx mori larvae is dependent on the presence of potassium and is unaffected by the addition of hexoses to perfusion media, whereas it is enhanced by alanine, aspartic acid, glutamic acid and the corresponding 2- oxoacids, glutamine and malate. The midgut enzyme profile indicates that the substrates for the tricarboxylic acid cycle are supplied mainly by amino acid metabolism via transaminases. Accordingly, aminoxyacetate drastically reduces the intestinal transepithelial electrical potential difference stimulated by amino acids. Measurement of the free amino acid concentration in the lumen content, intestinal cells and haemolymph shows that glutamic acid, asparagine and glutamine are accumulated in the cell, whilst the haemolymph is enriched with basic amino acids and with glycine, alanine, serine and tyrosine, the major components of the silk fibroin. Therefore, amino acid metabolism directly related to the tricarboxylic acid cycle seems to be the primary source of energy for the potassium pump activity in B. mori midgut.

scholarly journals Gene expression analysis in mitochondria from chagasic mice: alterations in specific metabolic pathways

2004 ◽  
Vol 381 (3) ◽  
pp. 743-752 ◽  
Author(s):  
Nisha GARG ◽  
Arpad GERSTNER ◽  
Vandanajay BHATIA ◽  
James DeFORD ◽  
John PAPACONSTANTINOU
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Mitochondrial Function ◽  
Pyruvate Dehydrogenase ◽  
Acid Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Pyruvate Dehydrogenase Complex ◽  
Tricarboxylic Acid ◽  
Acid Cycle ◽  
Dehydrogenase Complex

Cardiac hypertrophy and remodelling in chagasic disease might be associated with mitochondrial dysfunction. In the present study, we characterized the cardiac metabolic responses to Trypanosoma cruzi infection and progressive disease severity using a custom-designed mitoarray (mitochondrial function-related gene array). Mitoarrays consisting of known, well-characterized mitochondrial function-related cDNAs were hybridized with 32P-labelled cDNA probes generated from the myocardium of mice during immediate early, acute and chronic phases of infection and disease development. The mitoarray successfully identified novel aspects of the T. cruzi-induced alterations in the expression of the genes related to mitochondrial function and biogenesis that were further confirmed by real-time reverse transcriptase–PCRs. Of note is the up-regulation of transcripts essential for fatty acid metabolism associated with repression of the mRNAs for pyruvate dehydrogenase complex in infected hearts. We observed no statistically significant changes in mRNAs for the enzymes of tricarboxylic acid cycle. These results suggest that fatty acid metabolism compensates the pyruvate dehydrogenase complex deficiencies for the supply of acetyl-CoA for a tricarboxylic acid cycle, and chagasic hearts may not be limited in reduced energy (NADH and FADH2). The observation of a decrease in mRNA level for several subunits of the respiratory chain complexes by mitoarray as well as global genome analysis suggests a limitation in mitochondrial oxidative phosphorylation-mediated ATP-generation capacity as the probable basis for cardiac homoeostasis in chagasic disease.

scholarly journals The stimulation of tricarboxylic acid-cycle flux by α-adrenergic agonists in perfused rat liver

1986 ◽  
Vol 233 (2) ◽  
pp. 321-324 ◽  
Author(s):  
W M Taylor ◽  
E van de Pol ◽  
F L Bygrave
Keyword(s):  
Rat Liver ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Acid Cycle ◽  
Total Tissue ◽  
Stimulation Of

Output of 14CO2 from 1-14C-labelled glutamate, 2-oxoglutarate or octanoate and from 4-methyl-2-oxo[2-14C]pentanoate was increased by more than 100% after infusion of phenylephrine into perfused livers of fed rats. Infusion of ethanol or sorbitol raised 3-hydroxybutyrate/acetoacetate ratios and decreased the output of 14CO2. Increases in 14CO2 output induced by phenylephrine were observed in the presence or absence of ethanol or sorbitol and were accompanied by elevated 3-hydroxybutyrate/acetoacetate ratios under all conditions examined. Phenylephrine had no effect on total tissue ATP/ADP ratios in livers from fed or starved rats. The data suggest that phenylephrine-induced increases in tricarboxylic acid-cycle flux do not arise from lowered matrix NADH/NAD+ or ATP/ADP ratios.

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