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.

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 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.

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.

A stable long-term hepatocyte culture system for studies of physiologic processes: cytokine stimulation of the acute phase response in rat and human hepatocytes

1992 ◽  
Vol 8 (3) ◽  
pp. 219-225 ◽  
Author(s):  
Augustinus Bader ◽  
Inne H. Borel Rinkes ◽  
Ellen I. Closs ◽  
Colleen M. Ryan ◽  
Mehmet Toner ◽  
...  
Keyword(s):  
Acute Phase ◽  
Acute Phase Response ◽  
Culture System ◽  
Human Hepatocytes ◽  
Phase Response ◽  
Hepatocyte Culture ◽  
Cytokine Stimulation ◽  
Stimulation Of
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