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At least 19 recordsLinked to original sources
PubMed1986

Gangliosides as markers of cortisone-sensitive and cortisone-resistant rabbit thymocytes: characterization of thymus-specific gangliosides and preferential changes of particular gangliosides in the thymus of cortisone-treated rabbits.

Neutral glycosphingolipids and gangliosides in rabbit thymus, spleen, bone marrow, and erythrocyte ghosts were analyzed by conventional chemical and enzymatic procedures and negative ion fast atom bombardment mass spectrometry (FABMS). Thymus gangliosides showed a characteristic composition. Major gangliosides comprising 75% of the total thymus gangliosides were sialosyl lacto-N-neo-tetraosyl- and sialosyl lacto-N-nor-hexaosylceramides containing NeuGc and palmitic acid. These major thymus gangliosides were not detected in spleen, bone marrow, or erythrocytes, whereas GD1a, which was not present in the thymus even in a trace amount, was present in spleen and bone marrow. In addition, the major gangliosides in rabbit thymus were preferentially reduced when an animal was given an intraperitoneal injection of cortisone acetate, as found on analysis 48 h later. The decrease was accompanied by a concomitant increase in NeuAc-containing GM3 with longer chain fatty acids.

Animals↗
PubMed1990

Differences between concentrations of salivary cortisol and cortisone and of free cortisol and cortisone in plasma during pregnancy and postpartum.

We measured cortisol and cortisone in plasma--both total and free--and in saliva during the course of pregnancy and postpartum. Antepartum and postpartum concentrations and morning and afternoon concentrations of both steroids were compared. The mean concentrations of cortisol and cortisone increased towards term and were significantly greater at the end of pregnancy than postpartum, except for free cortisol in plasma in the afternoon. The daily rhythm of both steroids was maintained throughout pregnancy and postpartum. The correlations between salivary and plasma free concentrations of cortisol and cortisone as well as of the sum of cortisol + cortisone were highly significant. The mean concentrations of cortisone in saliva accurately reflected both total and free concentrations in plasma. For cortisol, however, the change of the concentrations in saliva, was somewhat different from that in plasma. Moreover, the mass ratio of plasma free cortisol to salivary cortisol was about 2, whereas for cortisone the ratio was only about 0.5, probably owing to the conversion of cortisol to cortisone by 11 beta-hydroxysteroid dehydrogenase in the salivary gland. Furthermore, the passage of cortisol and cortisone from plasma to saliva should not be regarded as simple diffusion, because in the first half of pregnancy the sum of the concentrations of cortisol + cortisone in saliva significantly exceeded the sum of their free concentrations in plasma.

Adult↗
PubMedDate not supplied

Evaluation of cortisone-heparin and cortisone-maltose tetrapalmitate therapies against rodent tumors. I. Biological studies.

The antitumor activity of either cortisone-heparin or cortisone-maltose tetrapalmitate combination or both was tested against two animal tumor models. The first model was orthotopically implanted bladder tumor established in syngeneic Fisher 344 rats. Shrinkage and growth arrest of the tumors were induced by cortisone and amplified by its combination with either heparin or maltose tetrapalmitate (MTP). The second model was trocar implanted C3HBA mammary tumor piece s.c. in syngeneic LPS and MTP responder C3H/HeN and non responder C3H/HeJ mice. The tumor was sensitive to growth inhibition by cortisone-MTP in the C3H/HeN but not by cortisone alone or cortisone-heparin. Tumor implanted in C3H/HeJ was much less sensitive to cortisone-MTP. Cortisone could be replaced by 17-alpha-hydroxyprogesterone, but not by cortexolone.

Animals↗
PubMed1952

The effect of cortisone on the Shwartzman reaction; the production of lesions resembling the dermal and generalized Shwartzman reactions by a single injection of bacterial toxin in cortisone-treated rabbits.

1. Cortisone, in a dose of 25 mg. daily and with a pretreatment period of 3 days, in rabbits weighing 1 to 1.5 kilos, did not inhibit the dermal Shwartzman reaction produced by meningococcal or S. marcescens toxin. 2. In cortisone-treated rabbits, a single intradermal injection of toxin produced a primary reaction of hemorrhage and necrosis in the skin at the injected site. This lesion resembled the Shwartzman reaction in its gross and histological appearance. 3. Like the Shwartzman reaction, the primary hemorrhagic reaction in cortisone-treated rabbits was prevented by nitrogen mustard, and the preventive effect of nitrogen mustard was partly eliminated when the femoral marrow was protected against the latter agent. 4. A single intravenous injection of meningococcal or S. marcescens toxin, in cortisone-treated rabbits, was followed by bilateral cortical necrosis of the kidneys in the majority of instances. The renal lesions, as well as hemorrhages in the lungs, spleen, liver, and gastrointestinal tract, resembled the lesions of the generalized Shwartzman reaction. Histologically, the glomerular capillaries in both types appeared to be occluded by homogeneous, eosinophilic material which showed a strongly positive Schiff reaction. 5. The renal lesion following a single injection of toxin in cortisone-treated animals, and that following two intravenous injections in the generalized Shwartzman reaction, were both completely prevented by nitrogen mustard. This effect of nitrogen mustard was inhibited when the femoral marrow was protected against the latter agent. 6. The injection of S. marcescens toxin into the skin of normal rabbits did not cause systemic symptoms, nor was it possible to provoke the generalized Shwartzman reaction by this route. In cortisone-treated rabbits, a similar intradermal injection was regularly followed by the development of bilateral cortical necrosis of the kidneys, indicating that absorption of toxin from the skin occurred in these animals. 7. Possible mechanisms to account for the observations are discussed. The authors are obliged to Professor James R. Dawson for many helpful suggestions during the course of this investigation.

Animals↗
PubMedDate not supplied

Evaluation of cortisone-heparin and cortisone-maltose tetrapalmitate therapies against rodent tumors. II. Pathological studies.

Pathological studies were undertaken in three tumor-host models which were subjected to cortisone based treatments. The first model was Fisher 344 rats with established orthotopically implanted syngeneic bladder tumor. Cortisone-herapin and cortisone-maltose tetrapalmitate (MTP) treatments induced focal areas of tumor necrosis and necrobiosis, whereas cortisone alone caused necrobiosis. The second model was C3HBA mammary tumor fragments implanted subcutaneously in syngeneic MTP responder C3H/HeN and MTP non-responder C3H/HeJ female mice. Only cortisone-MTP treatment led to an absence of capillary extension from surrounding blood vessels into the scant tumor stroma. The third model, ethyl carbamate induced primary lung cancer in AJ mice, was tested only with cortisone-herapin combination. The treatment caused central zones of necrosis.

Animals↗
PubMed1991

A possible defect in the inter-conversion between cortisone and cortisol in prepubertal patients with congenital adrenal hyperplasia receiving cortisone acetate therapy.

Oral administration of cortisone acetate is widely used to treat prepubertal patients with congenital adrenal hyperplasia (CAH). However, efficient 'first pass' hepatic conversion of the biologically inactive cortisone (E) to cortisol (F) by the 11-reductase component of the 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) system is required for suppression of the hypothalamic-pituitary-adrenal (HPA) axis. 11-beta-HSD activity can be assessed by measurement of urinary tetrahydroderivatives of E (tetrahydrocortisone, THE) and F (tetrahydrocortisol, THF), formed in separate hepatic compartments by reduction of the A ring. Inadequate HPA axis suppression is frequently encountered in peripubertal CAH patients receiving cortisone acetate therapy. In this paper, we describe THE and THF concentration in 24 h urine samples collected every 3-6 months from 14 prepubertal patients with simple virilizing CAH. The patients had been receiving cortisone acetate and 9 alpha-fluorohydrocortisone since diagnosis and were investigated for 2-4 years during which there was marked intra- and inter-individual variation in the level of suppression. Good and poor control of HPA axis suppression were defined on the basis of a profile of early morning serum 17-hydroxyprogesterone, androstenedione, plasma renin activity and 24 h urinary excretion of pregnanetriol, pregnanetriolone and 5 beta, 17 alpha-hydroxypregnanolone. Serum steroids were measured by RIA and urinary metabolites quantitated as methyloxime-trimethylsilylimidazole derivatives by gas chromatography and GC-mass spectrometry. There were no significant differences in the THE/THF ratio between male (n = 9) and female (n = 5) patients during either good or poor therapeutic control. The data were therefore analyzed without consideration of patient sex. Urinary THE/THF (mean +/- SD) was significantly higher in patients during periods of poor control (6.56 +/- 2.51, P less than 0.001) compared with periods of good control (3.73 +/- 0.96) in the same patients. THE/THF levels were also significantly (P less than 0.001) higher in CAH patients, irrespective of the level of control, than those for the normal subjects (1.79 +/- 0.20). Furthermore, THE excretion was significantly higher during periods of poor control compared with good control at all doses of cortisone acetate administered (10-50 mg/day). There were no significant differences in THF excretion. THE levels also rose significantly (P less than 0.001) in response to increasing total dose during periods of poor control. The increase in THF excretion was slight and significant only at doses greater than 40 mg/day compared with doses less than 15 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1980

Pharmacokinetic interpretation of plasma cortisol and cortisone concentrations following a signle oral administration of cortisone acetate to human subjects.

The pharmacokinetic and biopharmaceutic profiles of a single dose of oral cortisone acetate were developed for 23 healthy normal adult volunteers using cortisone and cortisol plasma concentration data. Cortisone acetate was rapidly absorbed and converted to the therapeutic moiety cortisol. There was a linear increase in plasma concentrations and, therefore, areas under plasma concentration-time curves with increasing doses of 5, 10, and 25 mg. Twenty-five-mg doses given as 1 x 25 mg or 5 x 5 mg were found to be bioequivalent. The increased efficacy of oral over intramuscular cortisone acetate can be attributed to the increased conversion to cortisol as a result of first-pass metabolism following oral dosing.

Administration, Oral↗
PubMed2005

A concise method for the preparation of deuterium-labeled cortisone: synthesis of [6,7-2H]cortisone.

A method is described for the synthesis of isotopically labeled cortisone from commercially available cortisone acetate through a Delta(4,6)-dieneone. Direct deuteration of the dienone acetate with various catalysts in different solvent systems failed to give an isolable product. Initial hydrolysis of the side-chain ester of the Delta(4,6)-dieneone and subsequent derivatization gave the key intermediate, 17alpha,20;20,21-bismethylenedioxy-pregna-4,6-diene-3,11-dione, which could be satisfactorily deuterated to the desired product. The availability of [6,7-(2)H]cortisone will provide a tool for the future study of the metabolism of cortisone in human tissues.

Cortisone↗
PubMed1957

The influence of cortisone on experimental viral infection. IV. Negation of interference as the mechanism by which cortisone induces increased virus yields.

The interference with viral synthesis which is induced by large quantities of non-infective influenza B virus is inhibited or negated with small quantities of cortisone and other C-21 steroids. The specificity of this effect is attested by the inactivity of 11-alpha hydroxy epimers of highly active compounds. Maximal activity in negation of interference is associated with the presence of oxygen at the C-11 position of the steroid molecule. In view of the demonstration that negation of interference can occur, it is concluded that the phenomenon of multiplicity reactivation of non-infective virus is not primarily influenced by cortisone. Rather, it is suggested that the reactivation phenomenon is unmasked by cortisone through its inhibiting effect on the autointerference intrinsic in multiplicity infection. If it is accepted that influenza virus infections in ovo are self-limited in part by viral autointerference, present evidence is consistent with the view that negation of this autointerference is the mechanism by which cortisone induces definitively increased yields of virus.

Cortisone↗
PubMed1993

Assay of human plasma cortisone by liquid chromatography: normal plasma concentrations (between 8 and 10 a.m.) of cortisone and corticosterone.

A high-performance liquid chromatographic method using ultraviolet detection to quantitate human plasma concentrations of cortisone simultaneously with cortisol and corticosterone is described. The method is based on the use of an octadecyl silica column (100 mm x 2 mm I.D., 3 microns), an ultraviolet absorbance detector (242 nm) with a 10 mm path length flow-cell, and a mobile phase composed of water-tetrahydrofuran-acetonitrile (82:10:8, v/v) containing 5 ml/l triethylamine and citric acid to adjust the pH of the buffer to 6.5. Flumethasone is used as the internal standard. The detection limit of the method for the three steroids is 300 ng/l using a 1-ml sample. The average inter-assay coefficient of variation for cortisone is 3.3% and the average recovery is 100.8%. Possible interferences from common drugs and endogenous and exogenous steroids in the method have been studied. Plasma concentrations (drawn from 8 to 10 a.m.) of cortisone and corticosterone for 43 normal volunteers have been determined.

Chromatography, High Pressure Liquid↗
PubMed1978

The excretion of free cortisol, cortisone, cortisol sulfate and cortisone sulfate in peripheral vascular disease, diabetes mellitus and hyperthyroidism.

In four groups of persons, 1/healthy individuals, 2/ patients with diabetes mellitus, 3/ patients with peripheral vascular disease, and 4/ patients with hyperthyroidism, the urinary excretion of free cortisol, cortisone, cortisol sulfate and cortisone sulfate was estimated. In groups 2 and 3 the excretion of all four substances was elevated. In hyperthyroidism a preponderance of free cortisone over cortisol was registered. The ratios of the followed substances suggest in patients with peripheral vascular disease a detoriation in the normal excretion of the followed corticoids, based on a preponderance of 11-OH-corticosteroids over their 11-oxo-derivatives. This observation could be implicated in the mild hyperglycemia or decreased glucose tolerance, that is often found in atherosclerotic disease.

Adult↗
PubMed1979

The effect of cortisone acetate on pulmonary lesions in a rabbit model of hypersensitivity pneumonitis (cortisone and hypersensitivity pneumonitis).

Rabbits were sensitized with Micropolyspora faeni by intratracheal inoculations and later challenged with the same antigen either with or without parenteral administration of cortisone acetate prior to challenge. Animals developed anti-M. faeni serum precipitins, M. faeni-induced alveolar macrophage migration inhibition, and positive 48-hr skin reactivity to M. faeni. Sensitized animals also demonstrated an augmented pulmonary histopathological response following respiratory challenge with M. faeni when compared to non-sensitized controls. Cortisone acetate abrogated this augmented pulmonary histopathological response following challenge with M. faeni. Cortisone acetate also abolished the positive alveolar macrophage migration inhibition found in sensitized animals.

Alveolitis, Extrinsic Allergic↗
PubMed1966

The influence of cortisone on experimental viral infection. 8. Suppression by cortisone of interferon formation in mice injected with Newcastle disease virus.

The administration, of 5.0 mg of cortisone 6 to 24 hr prior to the intravenous injection of mice with NDV was associated with a marked reduction in the interferon response as measured in serum and spleen. Reduced concentrations of interferon following cortisone pretreatment were demonstrable from 6 to 16 hr following injection of virus.

Animals↗
PubMed1999

Plasma cortisol concentrations following cortisone infusion in dogs before and after treatment with cortisone acetate.

OBJECTIVE: To evaluate effects of iatrogenic hyperadrenocorticism on plasma cortisol concentrations produced by an infusion of hydrocortisone in dogs. PROCEDURE: Plasma cortisol concentrations were measured regularly during a 6 h infusion of hydrocortisone sodium succinate at two dose rates. The infusions were performed before and after treatment for 30 d with oral cortisone acetate at 10 mg/kg/24 h, divided thrice daily. Adrenal activity during the experimental period was assessed by weekly ACTH stimulation tests. RESULTS: Both infusion rates produced lower plasma cortisol concentrations after treatment for 30 d with cortisone. CONCLUSION: Prior exposure to high concentrations of glucocorticoids may result in accelerated metabolism of glucocorticoids administered subsequently. This may necessitate increased dosages when using glucocorticoids to support inadequate adrenal function.

Administration, Oral↗
PubMed1986

Dual immunofluorescence studies of cortisone-induced thymic involution: evidence for a major cortical component to cortisone-resistant thymocytes.

Cortisone-resistant thymocytes (CRT) have been used as the experimental equivalent of medullary thymocytes for the past 15 yr. Studies with CRT have provided evidence that the medullary population is similar to mature T cells in phenotype and function and may therefore be the major source of thymus emigrants. However, we have recently demonstrated that CRT differ from medullary thymocytes in their expression of the homing receptor molecule recognized by the monoclonal antibody MEL-14. Thus, many CRT express high levels of the MEL-14-defined homing receptor, whereas medullary thymocytes are MEL-14- to MEL-14lo. In normal adult mice, only 1 to 3% of thymocytes are MEL-14hi; these cells are located exclusively in the cortex and many are phenotypically and functionally mature. In this study we have used dual immunofluorescence techniques to further characterize those thymocytes resistant to cortisone treatment. Aside from being of mature phenotype with respect to expression of peanut agglutinin binding sites and the cell surface molecules H-2K, Ly-1, Lyt-2, and L3T4, CRT can be divided into MEL-14lo and MEL-14hi subpopulations, suggesting that they may actually be derived from both the medullary and the MEL-14hi cortical thymocyte subsets.

Animals↗