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PubMed2006

[Local changes in the rabbit brain cortex redox potential accompanying the formation of a conditioned defensive reflex].

The brain E is determined by ratio in rate of processes occuring in two energy compartments--in glycolysis (the more ancient one in evolution) in which glucose is splitted whithout oxygen utilization, and in oxidative metabolism which is younger in evolution than glycolysis and more effective than glycolysis. In the present investigation, the brain cortex E changes were recorded with implanted platinum electrodes. CDR was established by combination of light and electric shock applied to the left ear. It has been found that the combinations started to be accompanied by the E shift after the first 5-20 combinations. The E shifts were widely generalized over the cortex, and both increasing and decreasing E were well expressed within 50-200 combinations. As the number of combination increased, the increases in E were gradually replaced by the decreases in E. This dynamic in the balance of the major sources of the brain energy supply during the formation of CDR demonstrates, in our opinion, that subcellular structures or complexes of cells which appeared at the same stages of evolution as the compartment of oxidative metabolism make a significant contribution to the CDR acquisition when memory traces are created, while brain function during realization of well consolidated CDR are supported mainly by glycolysis.

Animals↗
PubMed2006

[Changes in the rabbit brain cortex redox potential accompaning episodes of ECoG-arousal during slow-wave sleep].

Local cortex E variations are well expressive indices of rate and peculiarities of energy metabolism. The brain E is determined by the ratio of processes occurring in two energy compartments in glycolysis, in whish glucose is split without oxygen utilization and in oxidative metabolism. In the present investigation, the brain cortex E changes were recorded with implanted platinum electrodes during slow wave sleep. Under such conditions, the E lowering detects acceleration in glycolytic compartment, whereas the E local rising shows acceleration in oxidative metabolism in the tissue surrounding the electrode. Earlier in rats, we have found that E significantly lowered in metabolic active cortical sites during episodes of SWS, and supposed that acceleration of glycolysis increased. Slow oscillations (a 20-40-sec prolongation of the amplitude up to several dozens millivolts) appeared at the same time. We considered these E slow oscillations to reflect changes in the rate in compartment of glycolysis. In this research, we have found the E slow oscillations to be created by regular episodes of ECoG-arousal which were accompanied by E decreases, i. e. by acceleration in glycolysis. We think the data presented show existence of functional system supporting a low level of arousal. As in any complex system with feed back connections, this system works in oscillatory regime.

Animals↗
PubMed1991

Increase in eukaryotic initiation factor 2B activity following fertilization reflects changes in redox potential.

One of the factors involved in the postfertilization activation of protein synthesis in the sea urchin, Strongylocentrotus purpuratus, is the activation of eIF-2B, the initiation factor responsible for guanine nucleotide exchange on eIF-2. Cell-free translation systems from unfertilized eggs are stimulated by added eIF-2B, although this dependency is rapidly lost in translation systems prepared at various times following fertilization. Cell-free translation systems prepared from unfertilized eggs show significantly lower eIF-2B activities than those prepared from 2-h embryos. However, the provision of an NADPH regeneration system significantly stimulates eIF-2B activity in egg extracts and, in addition, stimulates both binding of initiator tRNA to the small ribosomal subunit and protein synthetic activity. These data suggest that the activation of eIF-2B following fertilization reflects the fertilization-induced increase in NADPH levels.

Animals↗
PubMed1990

[Changes in redox potentials in serum samples as affected by adenosine triphosphate].

Irradiated serum samples show characteristic alterations of their redoxpotential. This reaction is in close correlation to metabolic alterations, that for instance occur with tumor growth or severe inflammatory diseases. The role of ATP as universal biochemical energy transmitter led us to study the influence of ATP on redoxpotential in serum. In result the sole addition of ATP to serum in vitro gave a clear alteration of the redoxpotentials. In healthy persons a shifting of redoxpotentials was seen to high positive values. On the other hand ATP has slight influence on sera of tumor patients.

Adenosine Triphosphate↗
PubMed1987

Glucagon-stimulated calcium efflux in the isolated perfused rat liver is dependent on cellular redox potential.

In the absence of any exogenous substrates, glucagon (1 X 10(-9) M) stimulated 45Ca2+ efflux from perfused livers derived from fed rats but not in livers of 24-h-fasted animals. In livers of 24-h-fasted animals perfused under conditions which would decrease cellular NAD(P)H/NAD(P)+ ratio (pyruvate (2.0 mM) or acetoacetate (10.0 mM], glucagon (1 X 10(-9) M) did not stimulate 45Ca2+ efflux. Similarly, in livers of 24-h-fasted animals perfused with substrates which increase cellular NAD(P)H content (lactate (2.0 mM) or beta-hydroxybutyrate (10.0 mM], glucagon (1 X 10(-9) M) did not increase 45Ca2+ efflux. Glucagon (1 X 10(-9) M) elicited an increase in 45Ca2+ efflux from livers of 24-h-fasted animals, only when the livers were perfused with [lactate]/[pyruvate] and [beta-hydroxybutyrate]/[acetoacetate] ratios similar to those reported for livers of fed rats. Stimulation of 45Ca2+ efflux elicited by either 8-CPT-cAMP, a cAMP analog, or high glucagon concentrations (1 X 10(-8) M) was not affected whether livers were perfused with pyruvate (2.0 mM) or lactate (2.0 mM). Administration of isobutylmethylxanthine (50 microM) alone, or glucagon (1 X 10(-9) M) in the presence of isobutylmethylxanthine (50 microM) stimulated 45Ca2+ efflux from livers of 24-h-fasted animals perfused with pyruvate (2.0 mM) but not from livers perfused with lactate (2.0 mM). The ability of glucagon (1 X 10(-9) M) to elevate tissue cAMP levels was also regulated by the oxidation-reduction state of the livers. The data indicate that glucagon-stimulated 45Ca2+ efflux from perfused livers is mediated via cAMP and is dependent on the oxidation-reduction state of the livers.

1-Methyl-3-isobutylxanthine↗
PubMed1987

The redox potential, rH and pH values in the gastrointestinal tract of small ruminants.

Oxidation-reduction potentials (Eh), pH and rH in the gastrointestinal tract were measured in six goats and two sheep fed on ground barley and hay, with or without the addition of urea. Each ration was supplied for three weeks. The animals were slaughtered after morning feeding, the contents of relevant parts of the gastrointestinal tract were sampled, pH and Eh values were measured and rH values calculated. The range of the oxidation-reduction potential was rather extensive, from -300 to +186 mV. The variability of rH values was smaller, being between 4.6 and 12.9, except for three values. The following linear relationship holds for findings of Eh and pH: Eh (mV) = 292-69.9 pH with a correlation coefficient of r = 0.84. In those parts of the gastrointestinal tract, where the fermentation process occurs (the rumen, caecum and colon), the Eh and rH values are lower than those in the abomasum and duodenum. Urea addition has no effect on the oxidation-reduction equilibrium.

Animal Feed↗
PubMed1985

The interaction between the cytosolic pyridine nucleotide redox potential and gluconeogenesis from lactate/pyruvate in isolated rat hepatocytes. Implications for investigations of hormone action.

By using very low concentrations of cells to minimize alterations in substrate concentrations, we demonstrated that the lactate/pyruvate ratio of the incubation medium, which determines the cytosolic NADH/NAD+ ratio, affects gluconeogenic flux in suspensions of isolated hepatocytes from fasted rats. At a fixed extracellular pyruvate concentration of 1 mM and with the lactate/pyruvate ratio varied from 0.6 to 10 and to 50, glucose production rates increased from 2.5 to 5.5 and then decreased to 1.8 nmol/mg of cell protein/min. This finding paralleled the observation of Sugano et al. (Sugano, T., Shiota, M., Tanaka, T., Miyamae, Y., Shimada, M., and Oshino, N. (1980) J. Biochem. (Tokyo) 87, 153-166) who noted a similar biphasic response in the perfused liver system when lactate was held constant and pyruvate varied. The biphasic relationship can be explained by the influence of the NADH/NAD+ ratio on the near-equilibrium reactions catalyzed by glyceraldehyde-3-phosphate dehydrogenase and malate dehydrogenase in the hepatocyte cytosol. By shifting the equilibrium of the glyceraldehyde-3-phosphate dehydrogenase reaction, a rise in the NADH/NAD+ ratio decreases the concentration of 3-phosphoglycerate which, because of the linkage of 3-phosphoglycerate to phosphoenolpyruvate through two near-equilibrium reactions, reduces the concentration of phosphoenolpyruvate and therefore causes a decline in flux through pyruvate kinase. This decrease in pyruvate kinase flux results in an enhanced gluconeogenic flux. At higher NADH/NAD+ ratios, however, the oxalacetate concentration drops to such an extent that the consequent decreased flux through phosphoenolpyruvate carboxykinase exceeds the decline in flux through pyruvate kinase, producing a decrease in gluconeogenic flux. The lactate/pyruvate ratio was found to influence the actions of three hormones thought to stimulate gluconeogenesis by different mechanisms. Except for an inhibition by glucagon seen at the lowest lactate/pyruvate ratio tested, the stimulations by this hormone were relatively insensitive to lactate/pyruvate ratios, while angiotensin II produced greater stimulations of gluconeogenesis as the lactate/pyruvate ratio was increased. Dexamethasone, added in vitro, stimulated gluconeogenesis significantly only at very low and very high lactate/pyruvate ratios.

Angiotensin II↗