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PubMed1977

The effect of cortisone on protein breakdown and synthesis in rat skeletal muscle.

The effect of cortisone administration on the rates of muscle protein breakdown and synthesis has been studied in the rat extensor digitorum longus muscle. Cortisone acetate (100 mg/kg body weight/day) was administered intraperitoneally for 1--3 days. Muscle wieght and protein content were significantly reduced by cortisone administration. Rates of protein breakdown were measured by tyrosine release from the isolated muscle into the intracellular pool and medium during a 2-h incubation with cycloheximide to block protein synthesis. Rates of protein synthesis were assayed by [14C]tyrosine incorporation into protein of the isolated muscle during a 2-h incubation. Cortisone administration inhibited significantly the rate of protein synthesis after 1--3 days treatment and also reduced significantly the rate of protein breakdown per muscle after 3 days treatment. The synthesis of myofibrillar and soluble proteins was affected to the same extent. These results strongly suggest that the effect of cortisone administration on muscle protein is mainly through its inhibition of protein synthesis rather than through an acceleration of protein breakdown.

Animals↗
PubMed2005

Diurnal patterns of salivary cortisol and cortisone output in chronic fatigue syndrome.

BACKGROUND: The aim of the present study was to obtain a naturalistic measure of diurnal hypothalamic-pituitary-adrenal (HPA) axis output in CFS patients unaffected by medication or comorbid psychiatric disorder likely to influence the axis. METHOD: Cortisol and cortisone levels were measured in saliva samples collected from 0600 h to 2100 h at 3-h intervals in CFS patients and healthy controls. RESULTS: Mean cortisol and cortisone concentrations were significantly lower in patients than controls across the whole day, as were levels at each individual time point except 2100 h. Cosinor analysis showed a significant diurnal rhythm of cortisol and cortisone that was not phase-shifted in CFS compared to controls. However, there was a lower rhythm-adjusted mean and a lower amplitude in CFS patients. The cortisol/cortisone ratio showed no diurnal rhythm and did not differ between CFS subjects and controls. LIMITATIONS: The sample size was relatively small, and drawn from specialist referral patients who had been ill for some time; generalisation of these results to other populations is therefore unwarranted. CONCLUSION: The main findings of this study are to provide further evidence for reduced basal HPA axis function in at least some patients with CFS and to show for the first time that salivary cortisone is also reduced in CFS and has a diurnal rhythm similar to that of cortisol. We have also demonstrated that the cortisol/cortisone ratio remains unchanged in CFS, suggesting that increased conversion of cortisol to cortisone cannot account for the observed lowering of salivary cortisol.

Adult↗
PubMed2000

Morning and afternoon serum levels of cortisone and cortisol in asthmatic patients.

While the diurnal change of serum cortisol in asthmatics has been suggested to influence the occurrence of attacks, this relation remains controversial. Serum concentrations of cortisol, cortisone, and cortisol precursors were measured in the morning and in the afternoon in asthmatic patients by reversed-phase high-performance liquid chromatography. Cortisol and cortisone were detected but their precursors were not. In remission or during attacks, the serum cortisone level in the morning was significantly lower than that in the afternoon, and the serum cortisol level in the morning did not significantly exceed that in the afternoon, which differs from the normal diurnal patterns. In patients with severe asthma in remission, the diurnal pattern of serum cortisone and cortisol was opposite to that seen in normal controls. During the attack, the serum cortisol level showed a lesser increase in the afternoon than in the morning. In patients with persistent asthmatic attacks, the serum cortisone level in the afternoon showed a significant increase as compared with that in remission while their serum cortisol level in the afternoon was equal to that in remission. The diurnal pattern and the duration of asthmatic attacks might be taken into consideration for steroid treatment of asthma.

Adolescent↗
PubMed1978

Low-dose cortisone for male infertility.

Thirty-eight males with idiopathic infertility were randomly treated with low-dose thyroid and low-dose cortisone. Pregnancy followed treatment with cortisone in 7 of 33 courses and followed treatment with thyroid in 4 of 30 courses (P = 0.5, not significant [NS]). The mean pretreatment count in all patients was 12.3 million/ml. The mean post-treatment count with thyroid was 11.2 million/ml as compared with 13 million/ml for cortisone treatment (P = 0.4, NS). Pretreatment motility was 45% as compared with 44% following thyroid treatment and 43% following cortisone treatment (P = 0.7, NS). The pregnancy rate seemed to correlate with pretreatment counts rather than with the type of treatment. The efficacy of low-dose cortisone for idiopathic fertility would seem to be in question.

Cell Count↗
PubMed1970

Effect of cortisone on the developmental pattern of the neutral and the acid beta-galactosidase of the small intestine of the rat.

1. The developmental pattern and effect of cortisone on acid beta-galactosidase and neutral beta-galactosidase were studied in postnatal rats by a recently proposed method for their independent determination. 2. After birth the acid beta-galactosidase activity increases in the ileum, whereas it decreases slightly in the jejunum. On day 16 after birth the activity in the ileum decreases and in 20-day-old rats activity in both parts of the intestine decreases to adult values. In suckling animals the activity in the ileum exceeds the jejunal activity severalfold and in adult animals the activity in the jejunum is slightly higher than that in the ileum. 3. Neutral beta-galactosidase activity is high after birth and decreases in both jejunum and ileum after day 20 after birth. In 12-20-day-old rats activity in both parts is essentially the same, but in adult animals jejunal activity exceeds ileal activity four-to five-fold. 4. Cortisone (0.5, 2.0 or 5.0mg/100g body wt. daily for 4 days) does not influence the activity of either enzyme in 60-day-old rats. Acid beta-galactosidase activity is decreased after cortisone treatment in 8-, 12-, 16-and 18-day-old rats, with sensitivity to cortisone increasing with the approach of weaning. No effect of cortisone on acid beta-galactosidase is seen in 8-day-old rats. Neutral beta-galactosidase activity is increased in the ileum of 8-, 12-, 16- and 18-day old rats, but only in the jejunum of 8-and 12-day-old rats.

Age Factors↗
PubMed1996

Urinary free cortisone and the assessment of 11 beta-hydroxysteroid dehydrogenase activity in man.

OBJECTIVE: Two isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyse the interconversion of cortisol to hormonally inactive cortisone; defects in the 11 beta-HSD2 isoform result in hypertension. The kidney, expressing high levels of 11 beta-HSD2, is the principal source of cortisone in man. We have validated the measurement of urinary free cortisone (UFE) excretion in normals and in patients with disorders of the pitultary-adrenal axis in an attempt to more accurately measure the activity of 11 beta-HSD2 in vivo. SUBJECTS: Forty-one normal adults, 12 normal children < 12 years of age, 15 patients with Cushing's syndrome, 12 with hypopitultarism on replacement hydrocortisone, 12 with the syndrome of apparent mineralocorticoid excess (AME) and 7 volunteers consuming liquorice. MEASUREMENTS: A complete 24-hour urine collection was analysed by gas chromatography/mass spectrometry for "A-ring' reduced cortisol and cortisone metabolites, i.e. tetrahydrocortisols (THF and allo-THF) and tetrahydrocortisone (THE). In addition, urinary free cortisol (UFF) and urinary free cortisone were quantified using deuterium-labelled internal standards. RESULTS: In normal adults and children, UFE excretion exceeded that of UFF (UFF 30.4 +/- 2.4 micrograms/24h (mean +/- SE), UFE 54.6 +/- 4.1 micrograms/24h, adults) (for conversion to nmol/24h multiply E by 2.78 and F by 2.76 respectively). Thus the normal UFF/UFE ratio was 0.54 +/- 0.05 in contrast to the (THF + allo-THF)/THE ratio of 1.21 +/- 0.06. UFE excretion was normal in hypopituitary patients on replacement hydrocortisone. Although UFE was elevated in all forms of Cushing's syndrome, the UFF/UFE ratio was grossly elevated in patients with the ectopic ACTH syndrome (14.0 +/- 6.7, n = 6). UFE was below the lower limit of the assay (< 1 microgram/24h) in most patients with the so-called type 1 variant of AME and significantly reduced in 4 patients described as having the type 2 variant of AME (10.5 +/- 3.5 micrograms/h, P < 0.05) and in 7 volunteers consuming liquorice (26.8 +/- 10.0 micrograms/24h, P < 0.01). In ectopic ACTH syndrome, AME, and liquorice ingestion the UFF/UFE ratio was more deranged than the (THF + allo-THF)/THE ratio. CONCLUSION: In normals the discrepant THF + allo-THF/ THE and UFF/UFE ratio suggests that much more of the UFE is derived from the kidney. Reduction in UFE excretion is seen following liquorice ingestion and in both variants of AME, though it is more profound in AME1. The high UFF/UFE ratio in the mineralocorticoid excess state seen in the ectopic ACTH syndrome is compatible with substrate-saturation of renal 11 beta-HSD2. The measurement of UFE and the UFF/UFE ratio is a significant advance in the analysis of human 11 beta-HSD activity in vivo; in particular, the UFF/UFE ratio appears to be a more sensitive index than the (THF + allo-THF)/THE ratio of renal 11 beta-HSD2 activity.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1999

An in vivo study of the cortisol-cortisone shuttle in subcutaneous abdominal adipose tissue.

OBJECTIVE: Previous in vitro studies have demonstrated significant 11-beta hydroxysteroid dehydrogenase (11 beta-HSD) oxo-reductase activity in visceral, but not subcutaneous adipose stromal cells. We have conducted an in vivo study of the cortisol-cortisone shuttle in subcutaneous abdominal adipose tissue. DESIGN: We measured arteriovenous (A-V) differences in serum cortisol and cortisone across subcutaneous abdominal adipose tissue and forearm muscle in a heterogeneous group of subjects. PATIENTS: We studied 34 subjects (male:female = 12:22), age median (interquartile range) 45 (19-65) years, body mass index 32.7 (20.4-77.1) kg m-2, total body fat 34.4 (5.6-119.1) kg. MEASUREMENTS: Serum cortisol and cortisone were measured in serum samples from a radial artery, superficial epigastric vein and deep forearm vein. Abdominal adipose and forearm blood flow rates were measured by 133Xenon washout and plethysmography, respectively. RESULTS: For cortisone, there was significant (P < 0.001) clearance by adipose tissue, with an A-V difference of 4 (1-7) nmol/l. For cortisol there was a trend for arterial concentrations (203 (142-292) nmol/l) to be lower than venous (225 (152-263) nmol/l), but this was not significant. The adipose tissue cortisone clearance rate correlated with total body fat (r = 0.35, P = 0.05). CONCLUSIONS: We have demonstrated 11 beta-HSD oxo-reductase activity in subcutaneous abdominal adipose tissue, which may be increased in obesity.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1970

Sedimentation properties of rat liver mitochondria. Effects of cortisone treatment.

A prediction of the velocity of sedimentation of rat liver mitochondria in sucrose gradients is made on the basis of recent measurements of the size of isolated mitochondria suspended in sucrose medium and the model proposed by Bentzel and Solomon to describe the osmotic behavior of mitochondria. The experimentally observed velocity is extremely close to the predicted value and confirms by a different approach the estimate of mitochondrial volume made by Baudhuin and Berthet on the basis of electron microscopic measurements. Because cortisone treatment of rats is known to result in a marked increase in mitochondrial size as observed under the electron microscope, mitochondria were co-isolated from livers of control and cortisone-treated animals, and the sedimentation behavior of the mixtures was examined by sucrose density gradient centrifugation. Mitochondria from cortisone-treated animals were found to sediment 1.4 times as rapidly as those from control animals, indicating that their increased size cannot entirely be due to an increased imbibition of fluid from the surrounding sucrose medium, and that the change in size must at least in part be due to a change in content of nondiffusible mitochondrial components. Although the increase in sedimentation velocity of mitochondria from cortisone-treated animals is striking, it is less than that predicted solely on the basis of their size relative to that of control mitochondria. It is concluded that the increases in mitochondrial size and content of nondiffusible components produced by cortisone treatment are accompanied by alterations in mitochondrial composition as well.

Animals↗
PubMed1955

Studies on the antipyretic action of cortisone in pyrogen-induced fever.

The mode of action of cortisone as an antipyretic has been studied in rabbits challenged with intravenous injections of bacterial pyrogens. The fever induced by pyromen or dextran was found to be markedly suppressed when cortisone was administered in liberal amounts (25 mg. twice daily) for 3 days prior to the challenge. Although the cortisone effectively blocked the febrile response to both pyrogens, it failed to influence the transient but marked leucopenia which characteristically precedes the onset of fever. The antipyretic action of the drug also was shown to bear no relation to the activity of the serum factor recently demonstrated by Farr, Grant, and others to be involved in the production of pyrogen-induced fever. In preliminary experiments with typhoid vaccine as the inciting pyrogen, the presence of serum factor activity in normal blood and its absence in the blood of pyrogen-tolerant rabbits was confirmed. Subsequently the blood of rabbits treated with antipyretically effective doses of cortisone was shown to contain just as much serum factor activity as that of normal rabbits. In addition, previous incubation of the pyrogen with serum factor failed to influence the antipyretic effect of the drug. It is concluded from these findings that in suppressing pyrogen fever, cortisone acts neither upon the leucopenic reaction nor upon the fever-accelerating factor of the serum. By exclusion it would appear that the drug must influence some later stage of the fever-producing process. The mechanisms involved in the later stages of the response to exogenous pyrogen remain undefined, and the need for determining whether they are related to the prefebrile leucopenia is emphasized.

Animals↗
PubMed1957

The influence of cortisone on experimental viral infection. V. Inhibition of influenza virus synthesis.

Cortisone is a highly potent inhibitor of influenza virus synthesis in the chick embryo, inducing manifest inhibition in doses of 0.1 to 1.0 microg/egg. Inhibition of viral synthesis is only temporarily manifest. As infection continues, the negation by cortisone of the self-limiting effects of viral autointerference obscures the coincident cortisone effect on synthesis. The inhibitory effect of cortisone may be induced late in the course of viral multiplication, after conclusion of the latent period. It is proposed that inhibition of viral synthesis with cortisone is a corollary of the steroid's inhibitory effects on growth and protein synthesis of the infected host. The role of adrenal corticoids in the regulation of infection with obligate intracellular parasites deserves continued investigation.

Animals↗
PubMed1959

Effects of bacterial endotoxin on metabolism. I. Carbohydrate depletion and the protective role of cortisone.

Mice of different strains were protected against the lethal effect of bacterial endotoxin by concurrent injections of cortisone. Either inadequate amounts of cortisone or excessive quantities of endotoxin voided the protection. Analyses of blood sugar, liver glycogen, muscle glycogen, and total body carbohydrate in the skinned eviscerated carcass were carried out on different strains of mice given endotoxin and/or cortisone. Poisoned animals were virtually depleted of all carbohydrate while mice given cortisone alone had concentrations of carbohydrate from three to four times that of normal mice. Mice given a lethal amount of endotoxin and a protective dose of cortisone had two to three times as much carbohydrate as animals injected with the same amount of endotoxin alone but significantly less than that found in normal mice. Dibenzyline failed to alter the lethal effect of endotoxin and to reduce the carbohydrate loss that accompanied endotoxin administration. Endotoxin, at the dosage level employed, lowered the temperature of mice 2 degrees -3 degrees C. during the first hour or two postinjection and the temperature remained essentially unaltered during the next 4 to 5 hours. Loss in body carbohydrate in endotoxin-poisoned mice cannot be explained, therefore, as the result of an elevated metabolic rate accompanying hyperthermia. Endotoxin prevented the conversion of injected glucose into liver glycogen but not into muscle glycogen. Mouse liver mitochondria, in the presence of endotoxin, released from ATP approximately the same amount of inorganic phosphate as that released in the presence of dinitrophenol.

Animals↗
PubMed1953

The mechanism of action of cortisone in experimental hypersensitivity. II. Hypersensitivity of the serum sickness type.

Cortisone markedly suppressed the cardiovascular and renal lesions of serum sickness type hypersensitivity which ordinarily develop following the intravenous injection of bovine albumin. The inhibitory effect of cortisone on the allergic granulomatous lesions of the spleen was less striking; the lesions were less extensive, but the percentage of animals affected was unchanged. Cortisone in the dosage employed had no effect on the elimination of antigen following its intravenous administration or on the appearance of circulating antibody. These findings indicate that inhibition of the lesions of serum sickness by cortisone does not depend on the suppression of antibody production. Therefore, it is inferred that cortisone somehow protects the animal from the damaging effects of antigen-antibody union.

Animals↗
PubMed1953

The effect of tuberculin and cortisone singly and in combination on explanted tissues of guinea pigs, mice and rabbits.

Tuberculin (P.P.D.) and cortisone acetate, singly and in combination, were added to explanted splenic tissue derived from guinea pigs, mice, and rabbits, and buffy coats obtained from rabbits. These tissues came from normal animals or from animals which had been infected with the tubercle bacillus or immunized with killed tubercle bacilli. 5 microg./ml. of tuberculin or 0.5 microg./ml. of cortisone was the largest concentration of the respective reagents which was tolerated by cultured cells from normal animals. From the results with all tissues studied it would appear that P.P.D. selectively damaged only the growing cells of splenic tissues from sensitive guinea pigs and to a lesser degree the migrating cells of buffy coats obtained from sensitive rabbits. Cortisone appeared to have increased toxicity for only explanted splenic cells from tuberculin-sensitive guinea pigs. The specific effect of P.P.D. on tissues from tuberculin-sensitive animals was not modified by cortisone under the conditions of these experiments. Thus these data furnished no evidence that cortisone had any direct effect on the response of the sensitive cells to P.P.D.

Allergens↗
PubMed1954

Effects of cortisone on regenerating rat liver.

The effects of continuous administration of cortisone on the metabolism of regenerating rat liver have been studied. Whereas the restoration of the weight of the liver after partial hepatectomy was not markedly affected by cortisone, the multiplication of cells was reduced to a significant degree after the first 2 days of regeneration. Liver restoration in terms of nucleic acids was similarly inhibited by cortisone. The results are consistent with the interpretation that the inhibition of cell multiplication in this system is dependent on and keeps pace with the inhibition of nucleic acid synthesis by this drug. At almost any time after hepatectomy, the nucleic acid content of the liver cells was the same in treated and in untreated animals. In ancillary studies, it was shown that cortisone caused the cells of regenerating liver to be increased in size and weight through the increased infiltration of lipids. Changes in water, protein, and carbohydrate content of the liver cells did not contribute to this increase in the weight of the cells. Since all animals were treated with cortisone for 5 days before hepatectomy, data were also obtained on the effect of this agent on the resting liver. This course of treatment brought about a significant decrease in the number of cells per unit wet weight and in the water content of the livers. The nucleic acid content of the cells at hepatectomy, on the other hand, was unchanged.

Animals↗
PubMed1976

Genetics of cortisone-induced cleft palate in the mouse-embryonic and maternal effects.

Differences between mouse strains in frequency of embryonic, cortisone-induced cleft palate were examined. Probit analysis demonstrated a family of linear and parallel dose-response curves for different inbred and hybrid embryos. Since the differences between genotypes were not in the slopes of the response curves but rather in their location, it is proposed that the median effective dose (ED50) of cortisone required to induce cleft palate (or the tolerance) provides a more appropriate definition of the response trait and its difference that a frequency statement. The tolerance of C57BL/6J is dominant to that of A/J. A maternal effect of A/J relative to C57BL/6J dams caused a two-fold reduction in the embryonic tolerance of cortisone. Cortisone-induced cleft palate and mortality were separate response traits. In these and previous studies on cortisone- and other glucocorticoid-induced cleft palate in the mouse, the nature of the cleft-palate-response curve appeared to be the same for all glucocorticoids, and within-strain differences in tolerance could be used as measures of potency or bioassays for a particular effect of the glucocorticoids.

Animals↗
PubMed1988

The effects of cortisone on acetylcholinesterase (AChE) in the neonatal and aged thymus.

Acetylcholinesterase (AChE) histochemistry and biochemistry was used to characterize the distribution and species of this enzyme within the developing thymus gland of the mouse. The results indicate that AChE-positive nerves and related structures are involved in a steroid-induced mechanism for regulating thymocyte populations. Low doses of cortisone injected into mice produce an activation of quiescent cholinergic nerves and the appearance of several new molecular forms of AChE within areas of the thymus where thymocyte death is prevalent. The action of cortisone on AChE is age dependent. In neonates, AChE activity is extremely high in the cortex of the gland, and cortisone causes little or no increase in AChE activity. In mice three to six weeks old, cortisone exerts its most profound effect on the AChE activity within the thymus. In mice eight months old and older, the AChE activity of the normal thymus is restricted to nerves and nerve-related structures at the cortical-medullary boundaries, with little or no activity observed in the cortex. Injections of cortisone in these mice does not cause an increase in AChE activity in the cortex and only slightly enhances activity within the cortico-medullary boundaries.

Acetylcholinesterase↗
PubMed1976

Gastrointestinal candidiasis in rats treated with antibiotics, cortisone, and azathioprine.

Conventional albino rats treated with peroral chloramphenicol, gentamicin, and/or parenteral cortisone were challenged with Candida albicans Antibiotics and cortisone were equally effective in predisposing the animals to colonization by the fungus. All animals treated with both antibiotics and cortisone developed defined, focal, superficial invasion of the cornified squamous epithelium of the stomach next to its junction with the glandular mucosa, as well as focal superficial invasion of the esophagus. Equivalent yeast cell and mycelial inocula of C. albicans were equally effective in producing colonization and invasion of the gut. Dissemination of the fungus from the gut was not found even after the addition of azathioprine to the treatment regimen; however, such addition did predispose to more extensive and severe lesions of the esophagus and stomach. Approximately 25% of infected cortisone- and antibiotic-treated rats developed agglutinins against C. albicans by 22 to 23 days after challenge, whereas 15% developed precipitins. The antibiotic-cortisone-treated rat may be a useful and consistent experimental model in the study of gastrointestinal candidiasis.

Animals↗
PubMed1983

Reactivation of Chlamydia trachomatis lung infection in mice by cortisone.

To study the latency, chronicity, and recurrent nature of chlamydial infection, we attempted to reactivate Chlamydia trachomatis lung infection in mice by immunosuppressive therapy with cortisone. Mice were treated with subcutaneous injections of cortisone acetate (125 mg/kg) every other day, starting on day 14 after intranasal inoculation of C. trachomatis serotype B (TW-5). C. trachomatis was recovered from the lungs beginning day 6 after the start of cortisone treatment until the end of the observation period on day 12 of treatment. Overall, the reactivation was successful in 8 of 55 mice treated with cortisone, in contrast to 0 of 41 inoculated, untreated mice (P = 0.009) and 0 of 35 uninoculated, treated mice. Cortisone treatment affected the ability of peritoneal exudate cells to respond to migratory inhibition after exposure to purified whole organisms of C. trachomatis serotype B (TW-5) but had little effect on serum antibody titers, indicating a possible role for cellular immunity in resistance against C. trachomatis infection in the lung.

Animals↗