The effects of imidazole-4-acetic acid on cerebral carbohydrate metaboifsm

1982 ◽  
Vol 60 (12) ◽  
pp. 1610-1617
Author(s):  
M. Bovell ◽  
T. Chung ◽  
V. MacMillan ◽  
R. Shankaran
Keyword(s):  
Acetic Acid ◽  
Citric Acid ◽  
Cerebral Hemisphere ◽  
Citric Acid Cycle ◽  
High Energy ◽  
High Energy Phosphate ◽  
Acid Cycle ◽  
Glycolytic Intermediates ◽  
Tissue Contents ◽  
Eeg Pattern

The effects of intravenous administration of 50–400 mg/kg imidazole-4-acetic acid (IMA) on the carbohydrate metabolism of the rat brain were assessed by measurement of the cerebral hemisphere contents of energy phosphates and glycolytic – citric acid cycle metabolites. IMA (100–400 mg/kg) produced a spectrum of electroencephalographic (EEG) change ranging from desynchronization to electrical suppression which was associated with unchanged tissue contents of ATP, ADP, and AMP, increasing levels of phosphocreatine, glucose, and aspartate, and decreasing levels of pyruvate, lactate, α-ketoglutaratc, and malate. The changes in glycolytic intermediates were present within 5 min of injecting IMA (200 mg/kg) and the pattern suggested a suppression of glycolysis. The EEG stage of electrical suppression with episodic spiking (400 mg/kg) was associated with a 30% reduction of cortical high-energy phosphate use. The lowest dose of IMA (50 mg/kg) resulted in episodic EEG desynchronization which was associated with no significant changes of the measured metabolites. The results indicate that IMA is associated with metabolite changes that are compatible with a state of cerebral depression and that the desynchronous EEG pattern is without a biochemical con-elate of increased neuronal activity.

scholarly journals A Specialized Citric Acid Cycle Requiring Succinyl-Coenzyme A (CoA):Acetate CoA-Transferase (AarC) Confers Acetic Acid Resistance on the Acidophile Acetobacter aceti

2008 ◽  
Vol 190 (14) ◽  
pp. 4933-4940 ◽  
Author(s):  
Elwood A. Mullins ◽  
Julie A. Francois ◽  
T. Joseph Kappock
Keyword(s):  
Acetic Acid ◽  
Citric Acid ◽  
Citric Acid Cycle ◽  
Coenzyme A ◽  
Acid Resistance ◽  
Acetic Acid Bacteria ◽  
Acetobacter Aceti ◽  
Acid Cycle ◽  
Coa Transferase ◽  
Acetic Acid Resistance

ABSTRACT Microbes tailor macromolecules and metabolism to overcome specific environmental challenges. Acetic acid bacteria perform the aerobic oxidation of ethanol to acetic acid and are generally resistant to high levels of these two membrane-permeable poisons. The citric acid cycle (CAC) is linked to acetic acid resistance in Acetobacter aceti by several observations, among them the oxidation of acetate to CO2 by highly resistant acetic acid bacteria and the previously unexplained role of A. aceti citrate synthase (AarA) in acetic acid resistance at a low pH. Here we assign specific biochemical roles to the other components of the A. aceti strain 1023 aarABC region. AarC is succinyl-coenzyme A (CoA):acetate CoA-transferase, which replaces succinyl-CoA synthetase in a variant CAC. This new bypass appears to reduce metabolic demand for free CoA, reliance upon nucleotide pools, and the likely effect of variable cytoplasmic pH upon CAC flux. The putative aarB gene is reassigned to SixA, a known activator of CAC flux. Carbon overflow pathways are triggered in many bacteria during metabolic limitation, which typically leads to the production and diffusive loss of acetate. Since acetate overflow is not feasible for A. aceti, a CO2 loss strategy that allows acetic acid removal without substrate-level (de)phosphorylation may instead be employed. All three aar genes, therefore, support flux through a complete but unorthodox CAC that is needed to lower cytoplasmic acetate levels.

Lactate Reverses Insulin-Induced Hypoglycemic Stupor in Suckling—Weanling Mice: Biochemical Correlates in Blood, Liver, and Brain

1983 ◽  
Vol 3 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Jean Holowach Thurston ◽  
Richard E. Hauhart ◽  
James A. Schiro
Keyword(s):  
Amino Acids ◽  
Citric Acid ◽  
Energy Metabolism ◽  
Citric Acid Cycle ◽  
Plasma Lactate ◽  
Brain Glucose ◽  
Acid Cycle ◽  
Glucose Levels ◽  
Glycolytic Intermediates ◽  
Lactate Levels

The recovery of weanling mice from insulin-induced hypoglycemic stupor–coma after injection of sodium -l(+)-lactate (18 mmol/kg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmol/kg). Stimulated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy metabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Ten minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmol/L; plasma glucose levels were unchanged, but the β-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyruvate (37%), citrate (12%), and malate (19%); the increase in α-ketoglutarate (32%) was not significant. Lactate injection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO−3] and pH (examined by injection of 15 mmol/kg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral glycolytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and α-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glutamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypoglycemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic intermediates). Near normal levels of the Krebs citric acid cycle intermediates suggest that changes in these metabolites, amino acids, or derived substrates relate to the dramatic recovery of hypoglycemic mice after lactate injection.

EFFECT OF SERUM GONADOTROPHIN ON DEHYDROGENASES OF THE CITRIC ACID CYCLE IN THE OVARY OF THE RAT

1963 ◽  
Vol 42 (4) ◽  
pp. 480-484 ◽  
Author(s):  
B. Eckstein ◽  
R. Landsberg
Keyword(s):  
Citric Acid ◽  
Citric Acid Cycle ◽  
Age Groups ◽  
Succinic Dehydrogenase ◽  
Immature Rat ◽  
Acid Cycle ◽  
Immature Rats ◽  
Rat Ovary

ABSTRACT The succinic, malic and isocitric dehydrogenases in the ovary of immature and mature, normal and serum gonadotrophin injected rats were examined. The Qo2 of these enzymes were markedly enhanced in the gonadotrophin injected rats of both age groups, except in the case of succinic dehydrogenase in the ovary of the immature rats, where a slight non-significant decrease was noted. It is concluded that in the mature rat ovary, gonadotrophin administration stimulates the activity of all the examined dehydrogenases of the citric acid cycle, whereas in the immature rat ovary, at least the isocitric- and malic dehydrogenases are thus stimulated.

scholarly journals CHROMATOGRAPHIC DETERMINATION OF THE ACIDS OF THE CITRIC ACID CYCLE IN TISSUES

1951 ◽  
Vol 193 (1) ◽  
pp. 277-283 ◽  
Author(s):  
CharlesE. Frohman ◽  
JamesM. Orten ◽  
ArthurH. Smith
Keyword(s):  
Citric Acid ◽  
Citric Acid Cycle ◽  
Chromatographic Determination ◽  
Acid Cycle
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