Stimulation of the protonmotive force and pyruvate uptake in mitochondria after dexamethasone treatment of rats

1985 ◽  
Vol 13 (4) ◽  
pp. 744-745
Author(s):  
ALAN D. MARTIN ◽  
MICHAEL A. TITHERADGE
Keyword(s):  
Protonmotive Force ◽  
Dexamethasone Treatment ◽  
Stimulation Of

Effects of dexamethasone and metopirone on ovulation in the goldfish, Carassius auratus

1977 ◽  
Vol 55 (8) ◽  
pp. 1342-1350 ◽  
Author(s):  
S. Pandey ◽  
T. J. Lam ◽  
Y. Nagahama ◽  
W. S. Hoar
Keyword(s):  
Carassius Auratus ◽  
Histological Analysis ◽  
Nuclear Size ◽  
Dexamethasone Treatment ◽  
Gonadotropin Secretion ◽  
Histological Evidence ◽  
Induced Ovulation ◽  
Goldfish Carassius Auratus ◽  
Treated Fish ◽  
Stimulation Of

At 12 ± 1 °C, a temperature at which goldfish will not ovulate, metopirone induced ovulation in gravid fish. Histological analysis revealed marked stimulation of the pituitary–interrenal axis but did not reveal any change in stainability (granulation) or nuclear size of gonadotrops. It is suggested that metopirone induced ovulation in goldfish by stimulating secretion of 11-deoxycortisol and (or) 11-deoxycorticosterone. Other possibilities are discussed.When the ambient temperature was gradually raised to 20 ± 1 °C, dexamethasone treatment blocked the ovulatory response consistently seen in the saline-injected controls. However, fish injected with human chorionic gonadotropin in addition to dexamethasone ovulated like the saline-injected controls. No change in stainability (granulation) was seen in gonadotrops of dexamethasone-treated fish (20 ± 1 °C) compared to saline-injected and uninjected controls held at 12 ± 1 °C, but marked degranulation was observed in saline-injected fish warmed to 20 ± 1 °C. There appeared to be a reduction of gonadotrope nuclear size in some dexamethasone-treated fish. It is suggested that dexamethasone inhibited ovulation in goldfish by suppressing gonadotropin secretion. Action by way of suppression of corticosteriodogenesis, for which there is good histological evidence, is also discussed, as well as the possibility of direct ovarian action.

scholarly journals Regulation of oxidative phosphorylation in different muscles and various experimental conditions

2003 ◽  
Vol 375 (3) ◽  
pp. 799-804 ◽  
Author(s):  
Bernard KORZENIEWSKI
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Phosphorylation ◽  
Muscle Contraction ◽  
Mitochondrial Protein ◽  
Experimental Studies ◽  
Kinetic Properties ◽  
Protonmotive Force ◽  
Experimental Conditions ◽  
Parallel Activation ◽  
Stimulation Of

It has been shown previously that direct stimulation of oxidative-phosphorylation complexes in parallel with the stimulation of ATP usage is able to explain the stability of intermediate metabolite (ATP/ADP, phosphocreatine/creatine, NADH/NAD+, protonmotive force) concentrations accompanied by a large increase in oxygen consumption and ATP turnover during transition from rest to intensive exercise in skeletal muscle. It has been also postulated that intensification of parallel activation in the ATP supply–demand system is one of the mechanisms of training-induced adaptation of oxidative phosphorylation in skeletal muscle. In the present paper, it is demonstrated, using the computer model of oxidative phosphorylation in intact skeletal muscle developed previously, that the direct activation of oxidative phosphorylation during muscle contraction can account for the following kinetic properties of oxidative phosphorylation in skeletal muscle encountered in different experimental studies: (i) increase in the respiration rate per mg of mitochondrial protein at a given ADP concentration as a result of muscle training and decrease in this parameter in hypothyroidism; (ii) asymmetry (different half-transition time, t1/2) in phosphocreatine concentration time course between on-transient (rest→work transition) and off-transient (recovery after exercise); (iii) overshoot in phosphocreatine concentration during recovery after exercise; (iv) variability in the kinetic properties of oxidative phosphorylation in different kinds of muscle under different experimental conditions. No other postulated mechanism is able to explain all these phenomena at the same time and therefore the present paper strongly supports the idea of the parallel activation of ATP usage and different oxidative-phosphorylation complexes during muscle contraction.

scholarly journals Effect of treatment of rats with dexamethasone in vivo on gluconeogenesis and metabolite compartmentation in subsequently isolated hepatocytes

1984 ◽  
Vol 219 (1) ◽  
pp. 117-123 ◽  
Author(s):  
E H Allan ◽  
M A Titheradge
Keyword(s):  
Pyruvate Carboxylase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Intact Cell ◽  
Isolated Hepatocytes ◽  
Dexamethasone Treatment ◽  
Acetyl Coa ◽  
General Activation ◽  
Effect Of Treatment ◽  
Stimulation Of

Hepatocytes prepared from rats treated with dexamethasone for 2 or 3h and maintained in the presence of 10 microM-dexamethasone in the preparation and incubation buffers showed significantly elevated rates of gluconeogenesis compared with those prepared from control animals. Dexamethasone treatment also increased the sensitivity of the cells to glucagon and the catecholamines. Analysis of the concentrations of metabolites in the gluconeogenic pathway indicated that dexamethasone decreased the intracellular concentration of pyruvate and increased those of phosphoenolpyruvate, acetyl-CoA and citrate, suggesting a stimulation of the reaction(s) converting pyruvate into phosphoenolpyruvate. This was substantiated by analysis of the pattern of metabolites found in the mitochondrial compartment after digitonin fractionation of the cells. Inclusion of 3-mercaptopicolinate in the incubation enhanced the effect of the hormone on the distribution of metabolites. Thus, in the absence of an effect of the steroid at the level of phosphoenolpyruvate carboxykinase or pyruvate kinase, dexamethasone treatment still increased the formation of malate, aspartate and citrate from pyruvate, indicating a stimulation in the intact cell of pyruvate carboxylase. It is suggested that the stimulation of pyruvate carboxylase is a result of a general activation of mitochondrial function, with an increase in the intramitochondrial concentrations of acetyl-CoA and ATP, a decrease in glutamate and an enhanced intramitochondrial [ATP]/[ADP] ratio.

scholarly journals Energy-conserving reactions in phosphorylating electron-transport particles from Nitrobacter winogradskyi. Activation of nitrite oxidation by the electrical component of the protonmotive force

1976 ◽  
Vol 156 (3) ◽  
pp. 481-491 ◽  
Author(s):  
J G Cobley
Keyword(s):  
Electron Transport ◽  
Reaction Medium ◽  
Respiratory Control ◽  
Nadh Oxidation ◽  
Protonmotive Force ◽  
Maximal Effect ◽  
Carbonyl Cyanide ◽  
Electrical Component ◽  
Stimulation Of ◽  
No2 Oxidation

1. In electron-transport particles (ET particles) prepared from Nitrobacter winogradskyi, the uncoupling agent carbonyl cyanide phenylhydrazone increased the rate of NADH oxidation but decreased the rate of oxidation of NO2-. Its effectiveness in stimulating NADH oxidation closely paralleled its effectiveness in inhibiting NO2- oxidation. 2. In the presence of ADP and phosphate the oxidation of NADH was stimulated, whereas the oxidation of NO2- was inhibited. In the presence of excess of Pi the concentration dependence with respect to ADP was the same for acceleration of NADH oxidation and inhibition of NO2- oxidation. 3. Oligomycin inhibited NADH oxidation and stimulated the oxidation of NO2-. The concentration of oligomycin required to produce half-maximal effect in both systems was the same. 4. The apparent Km for NO2- was not affected by ADP together with Pi, by uncoupling agent or by oligomycin. 5. With NADH as substrate, classical respiratory control was observed. With NO2- as substrate the respiratory-control ratio was less than unity. 6. A reversible uptake of H+ accompanied the oxidation of NO2- by ET particles. 7. In the presence of NH4Cl or cyclohexylamine hydrochloride, H+ uptake was abolished and increased rates of NO2- oxidation were observed. When valinomycin was present in the reaction medium, low concentrations of NH4Cl inhibited NO2- oxidation. 8. Pretreatment of ET particles with oligomycin enhanced the stimulation of NO2- oxidation induced by NH4Cl or by cyclohexylamine hydrochloride. Pretreatment with the uncoupler carbonyl cyanide phenylhydrazone prevented these stimulations. 9. In the presence of dianemycin together with K+, the uptake of H+ was abolished and the rate of NO2- oxidation was increased. In contrast, in the presence of valinomycin together with K+, the uptake of H+ was increased, and the rate of NO2- oxidation decreased. 10. Sodium tetraphenylboron was found to be an inhibitor of NO2- oxidation, but caused a stimulation of NADH oxidation which was dependent on the presence of NH4Cl or cyclohexylamine hydrochloride. 11. It is concluded that the enhanced rate of NO2- oxidation observed in the absence of energy-dissipating processes clearly relates to some state before the involvement of adenine nucleotides, and it is suggested that the oxidation of NO2- generates a protonmotive force, the electrical component of which controls the rate of NO2- oxidation.

Pre- and postnatal stimulation of pulmonary surfactant protein D by dexamethasone treatment of rats

Life Sciences ◽  
1992 ◽  
Vol 50 (23) ◽  
pp. 1761-1767 ◽  
Author(s):  
Yoshinori Ogasawara ◽  
Yoshio Kuroki ◽  
Akihiro Tsuzuki ◽  
Shigeru Ueda ◽  
Hideo Misaki ◽  
...  
Keyword(s):  
Pulmonary Surfactant ◽  
Surfactant Protein ◽  
Surfactant Protein D ◽  
Dexamethasone Treatment ◽  
Pulmonary Surfactant Protein ◽  
Stimulation Of

EFFECTS OF ACTH AND DEXAMETHASONE ON THE ZONA GLOMERULOSA OF THE RAT ADRENAL CORTEX: AN ULTRASTRUCTURAL STEREOLOGIC STUDY

1977 ◽  
Vol 85 (3) ◽  
pp. 608-614 ◽  
Author(s):  
Gastone G. Nussdorfer ◽  
Giuseppina Mazzocchi ◽  
Claudia Robba ◽  
Anna S. Belloni ◽  
Piera Rebuffat
Keyword(s):  
Electron Microscopy ◽  
Golgi Apparatus ◽  
Adrenal Cortex ◽  
Chronic Treatment ◽  
Zona Glomerulosa ◽  
Dexamethasone Treatment ◽  
Morphometric Methods ◽  
Rat Adrenals ◽  
Stimulation Of

ABSTRACT The effects of a chronic treatment with ACTH and dexamethasone on the zona glomerulosa of intact rat adrenals were investigated by morphometric methods and electron microscopy. It was found that ACTH increases the volume of the zona glomerulosa, of the cells, nuclei, mitochondrial compartment as well as the surface of SER and mitochondrial cristae. Also noticeable was the hypertrophy of the Golgi apparatus. Opposite effects were obtained after dexamethasone treatment. These findings are interpreted as indicating that ACTH is involved in the maintenance and stimulation of the growth and steroidogenic capacity of the adrenal zona glomerulosa.

scholarly journals The stimulation of mitochondrial pyruvate carboxylation after dexamethasone treatment of rats

1984 ◽  
Vol 219 (1) ◽  
pp. 107-115 ◽  
Author(s):  
A D Martin ◽  
E H Allan ◽  
M A Titheradge
Keyword(s):  
Pyruvate Dehydrogenase ◽  
Active Form ◽  
Specific Inhibitor ◽  
Hormone Treatment ◽  
Dexamethasone Treatment ◽  
Pyruvate Metabolism ◽  
Glucocorticoid Treatment ◽  
Pyruvate Carboxylation ◽  
Liver Homogenates ◽  
Stimulation Of

Treatment of rats for 3 h with dexamethasone was shown to stimulate both pyruvate carboxylation and decarboxylation in the subsequently isolated mitochondria. The effect of hormone treatment on pyruvate carboxylation was also apparent in liver homogenates assayed within minutes of killing the animal and was independent of the temperature at which the assay was performed, suggesting that it was not an artifact of the mitochondrial preparation procedure. The stimulation of both aspects of pyruvate metabolism in the intact organelle was independent of the induction of either pyruvate carboxylase or pyruvate dehydrogenase. Similarly, there was no change in the percentage of pyruvate dehydrogenase in the active form, indicating that the effect of steroid treatment on pyruvate oxidation was not via changes in the degree of phosphorylation of the enzyme. Adrenalectomizing the animals for a period of 14 days before the experiment had no effect on either parameter. Glucocorticoid treatment of the animals increased the rate of pyruvate uptake into the mitochondria, as measured by the titration of pyruvate metabolism with alpha-cyano-4-hydroxycinnamate, a specific inhibitor of the pyruvate translocator. It also increased the intramitochondrial concentrations of acetyl-CoA and ATP and led to an elevated [ATP]/[ADP] ratio within the mitochondria. It is suggested that both enzymes of pyruvate metabolism exist in the mitochondria under considerable restraint and that glucocorticoids act to relieve this restraint by alterations in substrate supply and the intramitochondrial concentrations of effector molecules.

Effects of dexamethasone on the activity of histidine decarboxylase, ornithine decarboxylase, and DOPA decarboxylase in rat oxyntic mucosa

1991 ◽  
Vol 69 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Masataka Araki ◽  
Mitsuo Nakamura ◽  
Seiichi Takenoshita ◽  
Hirokazu Shoda ◽  
Yukio Nagamachi ◽  
...  
Keyword(s):  
Ornithine Decarboxylase ◽  
Histidine Decarboxylase ◽  
Serum Gastrin ◽  
Single Injection ◽  
Dopa Decarboxylase ◽  
Peptic Ulcers ◽  
Dexamethasone Treatment ◽  
Oxyntic Mucosa ◽  
Significant Change ◽  
Stimulation Of

Since accelerated turnover of histamine in oxyntic mucosa may be an important factor in the pathogenesis of peptic ulcers, the effect of dexamethasone and other glucocorticoids on the activity of gastric histidine decarboxylase (HDC) was studied in the rat. The activity of HDC in rat oxyntic mucosa increased significantly after dexamethasone was injected s.c. to rats at doses larger than 0.4 mg/kg body weight. The maximum response of the HDC activity to dexamethasone (4 mg/kg) was observed 8 h after the treatment. The activity of ornithine decarboxylase (ODC) increased at 4 h, while that of DOPA decarboxylase showed no significant change throughout the 16-h period following a single injection of dexamethasone. The mucosal levels of histamine, putrescine, and spermidine rose significantly after the steroid treatment, while the spermine levels remained nearly constant. There was no sex difference in these responses to dexamethasone. Betamethasone showed nearly the same effects as dexamethasone on the decarboxylase activities and the mucosal levels of diamines. Serum gastrin levels showed no significant change for the first 4 h and then rose significantly 8 and 16 h after dexamethasone treatment. Pentagastrin (0.5 mg/kg) increased the HDC activity, while it showed no significant effect on either the mucosal ODC activity or levels of polyamines and histamine. These data suggest that dexamethasone influences the metabolism of histamine and polyamines in rat oxyntic mucosa both directly and via stimulation of gastrin release.Key words: dexamethasone, betamethasone, oxyntic mucosa, histidine decarboxylase, ornithine decarboxylase, DOPA decarboxylase.

scholarly journals Evidence for the stimulation of dolichol and mannolipid synthesis by glucocorticoids in HeLa cells

1981 ◽  
Vol 198 (1) ◽  
pp. 23-28 ◽  
Author(s):  
C K Ramachandran ◽  
C E Hignite ◽  
S L Gray ◽  
G Melnykovych
Keyword(s):  
Cell Surface ◽  
Hela Cell ◽  
Cell Cultures ◽  
Hela Cells ◽  
Surface Glycoprotein ◽  
Dexamethasone Treatment ◽  
Cell Surface Glycoprotein ◽  
Dolichyl Phosphate ◽  
Stimulation Of

The effects of addition of 1 microM-dexamethasone on the rate of transfer of mannose from GDP-mannose into mannolipid have been studied in HeLa cell cultures. Concurrent with an increase in incorporation of mannose into glycoproteins, the incorporation of mannose from GDP-mannose in vitro into mannolipid and dolichol-linked oligosaccharides was increased after dexamethasone treatment. Stimulation of mannolipid synthesis showed a correlation with the 11 beta, 17 alpha, 21-trihydroxy structure of C21 steroids. Dexamethasone treatment also resulted in an increased incorporation of acetate into dolichol and dolichyl phosphate. The results suggest that the effect of dexamethasone on the cell-surface glycoprotein accumulation is related to increased sugar-linked dolichol synthesis.

scholarly journals Effect of dexamethasone on the synthesis of dolichol-linked saccharides and glycoproteins in hepatocytes prepared from control and inflamed rats

1985 ◽  
Vol 227 (2) ◽  
pp. 675-682 ◽  
Author(s):  
M Sarkar ◽  
S Mookerjea
Keyword(s):  
Hepatocyte Culture ◽  
Oligosaccharide Synthesis ◽  
Dexamethasone Treatment ◽  
Assay Mixture ◽  
Cell Homogenate ◽  
Lipid Formation ◽  
Stimulation Of

Hepatocytes were prepared from control and inflamed rats. The incorporation of [14C]mannose into protein was increased in inflamed compared with control hepatocytes. The incorporation of [14C]mannose into protein was also increased when the hepatocytes were cultured in presence of dexamethasone (1 microM), either from control or inflamed rats. At the same time the incorporation of [14C]mannose into dolichol phosphate mannose and dolichol-linked oligosaccharide was increased due to inflammation. The presence of dexamethasone in the hepatocyte culture caused an increased formation of these two products; in particular its effect on oligosaccharide lipid formation was very pronounced. The ratios of activities of formation of [14C]mannose-labelled oligosaccharide lipid in inflamed over control hepatocytes gradually decrease when increasing amounts of exogenous dolichol phosphate was added in cell homogenate assay mixture. These results suggest that the increase of oligosaccharide lipid formation in inflammation could be due to a higher concentration of endogenous dolichol phosphate, as was shown for dolichol phosphate mannose formation in inflammation [Sarkar & Mookerjea (1984) Biochem. J. 219, 429-436]. In contrast, the ratio of activities of [14C]mannose-labelled oligosaccharide lipid between dexamethasone-treated and untreated hepatocytes shows only a slight increase when increasing concentrations of exogenous dolichol phosphate were added to the assays. This suggests that the stimulation of dolichol pyrophosphate oligosaccharide synthesis observed in dexamethasone treatment is probably due to the higher level of enzymes involved in oligosaccharide synthesis rather than higher level of endogenous dolichol phosphate in these cells.

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