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At least 19 recordsLinked to original sources

PubMed1979

Effects of levodopa and dopamine on plasma 11-hydroxycorticosteroid concentrations in mice.

The effects of levodopa on the plasma concentration of 11-hydroxycorticosteroids and glucose were examined in mice. In fasted, nialamide treated mice, but not in fed mice, levodopa produced a significant decrease in the plasma concentration of 11-hydroxycorticosteroids. This was accompanied by a significant and marked decrease in the plasma glucose concentration. These effects of levodopa could be mimicked by relatively small doses of dopamine injected intracerebroventricularly but not intravenously. The integrity of the hypothalamic-pituitary adrenal axis in nialamide-treated mice was suggested by the elevation in plasma 11-hydroxycorticosteroids produced by fasting or by insulin induced hypoglycaemia. These results indicate that in the mouse, as in other species, levodopa can inhibit stress provoked increases in the secretion of 11-hydroxycorticosteroids.

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PubMed1977

Effect of sodium sulfate on the hydrolysis of 17-hydroxycorticosteroid- and p-nitrophenyl-glucuronides with beta-glucuronidase preparations from bovine liver.

Previous papers dealt with the discovery that hydrolysis of 17-hydroxycorticosteroid glucuronides in urine with beta-glucuronidase preparations from bovine liver is increased by adding sodium sulfate to the incubation medium. Here, we conclude that sodium sulfate not only increases the activity of bovine liver beta-glucuronidase on 17-hydroxycorticosteroid glucuronides and p-nitrophenyl glucuronides, but also removes the inhibitory activity of substances of high molecular weight in urine and, moreover, inhibits urine putrefaction during the hydrolysis. The net effect is an increased yield of urinary 17-hydroxycorticosteroids. In the incubation with sodium sulfate (Na2SO4, final concentration 80 g/liter, 500 Fishman units of beta-glucuronidase per milliliter of urine, pH 5.0, 48 degrees C, 18 h) the analytical recovery of 17-hydroxycorticosteroid glucuronides added to 12 urine samples proved to be 98 +/- 1.8% (95-100).

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PubMed1992

Urinary free cortisol versus 17-hydroxycorticosteroids: a comparative study of their diagnostic value in Cushing's syndrome.

We evaluated the usefulness of the basal urinary 24-h excretion rates of free cortisol versus 17-hydroxycorticosteroids in the diagnosis of Cushing's syndrome. On an outpatient basis, both urinary free cortisol and 17-hydroxycorticosteroids levels were determined in 48 patients with Cushing's syndrome, as well as in 95 obese and 94 healthy control persons of normal weight. Determination of the urinary free cortisol content allowed a clear-cut distinction between the patients with hypercortisolism and the controls, resulting in a sensitivity of 100% and specificity of 98% for the diagnosis of Cushing's syndrome. The diagnostic accuracy of urinary free cortisol was distinctly superior to that of 17-hydroxycorticosteroids, which showed a wide overlap of values between the groups, with a sensitivity of 73% and a specificity of 94%. In conclusion, the measurement of basal urinary free cortisol provided an excellent diagnostic sensitivity and specificity in the assessment of adrenocortical function. This simple and accurate test thus seems to be particularly useful in the outpatient evaluation of patients with suspected Cushing's syndrome.

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PubMed1975

Determination of 17-hydroxycorticosteroids in human urine.

A study was undertaken to develop a method that could be used an an indication of the absorption of steroids. It was demonstrated that 17-hydroxycorticosteroids in urine could be quantitatively determined via absorptivity values obtained through the use of standard hydrocortisone-alcohol solutions or standard solutions of hydrocortisone in urine utilizing the blue tetrazolium assay method. This method is dependent upon the hydrolysis of conjugated urinary steroids by beef liver glucuronidase. The resultant concentration of 17-hydroxycorticosteroids is determined colorimetrically using blue tetrazolium.

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PubMed1975

The relationship of 17-hydroxycorticosteroid to acute necrotizing ulcerative gingivitis.

Eleven patients presenting with acute necrotizing ulcerative gingivitis (ANUG) collected 24-hour urine samples during and after the course of their ANUG. The Porter-Silber technique was used to determine the 17-hydroxycorticosteroid concent of the urine, a physiological measure of stress. All of the patients had significantly higher levels of 17-hydroxycorticosteroid during the course of their ANUG than after it had resolved.

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PubMed1976

Interference of bencyclan with 11-hydroxycorticosteroids determinations.

Falsely high fluorimetric readings were obtained in plasma and urine 11-hydroxycorticosteroids (mostly cortisol) assays during the administration of bencyclan to hypertensive patients. No valid conclusion can be drawn from 11-hydroxycorticosteroids assays in bencyclan treated patients.

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PubMed1977

Improved hydrolysis of urinary 17-hydroxycorticosteroid glucuronides with beta-glucuronidase from Helix pomatia, on adding sodium sulfate.

Sodium sulfate increases the hydrolysis of urinary 17-hydroxycorticosteroid glucuronides with beta-glucuronidase preparations derived from Helix pomatia because it removes the inhibitory activity of urinary high-molecular-weight substances. For maximum hydrolysis of urinary 17-hydroxycorticosteroid glucuronides, the hydrolysis [5 ml of urine, 0.5 ml of 2 mol/liter acetate buffer (pH 5.0)] should be conducted in the presence of sodium sulfate (final concentration: 80 g/liter) with (a) 600 Fishman units of the enzyme per milliliter of urine (18 h at 52 degrees C) or (b) with 1500 units of the enzyme per milliliter of urine (3 h at 57 degrees C). Under conditions a, analytical recovery of steroid glucuronides added to 12 urine samples was 99 +/- 2.1% (96-102%). Values obtained for 20 urine samples with this method were 99 +/- 2.7% (93-104%) as great as those yielded by a method in which 600 units of the enzyme from bovine liver are used together with sodium sulfate (18 h at 48 degrees C).

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PubMedDate not supplied

Natrium, potassium, cholesterol and total free 11-hydroxycorticosteroids variations in thymectomized and thymic extract treated rats.

The authors investigated the effect of thymectomy and TP2 thymic polypeptide extract administration on total, esterified and free cholesterol in the plasma and the adrenals, as well as on plasma Na and K and plasma free total 11-hydroxycorticosteroids. The results showed that total, esterified and free cholesterol decrease in the adrenals by 23.20%, 28.57% and 17.70% maximum respectively, in the thymectomized rat and that under the influence of the TP2 extract the values increase by 14.81%, 15.38% and 12.67%, respectively. Plasma cholesterol did not change. Thymectomy caused an increase in the plasma 11-hydroxycorticosteroids value by 13.4% and administration of the TP2 extract lowered their value by 58.11%. The plasma Na and K values did not change.

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PubMed1987

Cefoxitin interferes with the "Clini-Skreen" column method for urinary 17-hydroxycorticosteroids.

Cefoxitin interferes with determination of urinary 17-hydroxycorticosteroids. The apparent concentration of hormone is increased from three- to 10-fold in samples from patients receiving cefoxitin when the Amberlite XAD-2 "Clini-Skreen" column is used. To determine the mechanism of interference, we reacted aqueous solutions of cefoxitin, cortisol, cortisone, and 11-deoxycortisol with phenylhydrazine; recorded the adsorption spectra; and determined the molar absorptivities and the equilibrium and rate constants. Also, we recorded the absorption spectra of phenylhydrazine with eight other cepha antibiotics and benzylpenicillin. Cortisol, cortisone, 11-deoxycortisol, and cefoxitin react with phenylhydrazine and absorb light with superimposable spectra and absorption maxima of 410 nm. The other antibiotics react with phenylhydrazine but absorbance maxima of the products vary, none being at 410 nm. Cortisol, cortisone, and 11-deoxycortisol react with phenylhydrazine 35-fold faster, have equilibrium constants ninefold greater, and have molar absorptivities 1.6 times that of cefoxitin. Thus, cefoxitin interferes with determination of urinary 17-hydroxycorticosteroids by forming a chromophore with the same absorbance maximum and with a molar absorptivity similar to cortisol, but much more slowly.

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PubMedDate not supplied

[Mediation of the lithium increase in rat liver tryptophan pyrrolase activity by 11-hydroxycorticosteroids].

After a single intraperitoneal administration lithium carbonate (50 and 100 mg per kg of body weight) caused an increase in the tryptophane pyrrolase activity in rat liver tissue by 50-80% within 5 hrs and did not affect the enzyme within 1, 3 and 20 hrs. Content of lithium was quite unaltered in rat blood serum after administration of lithium carbonate at a dose of 50 mg/kg; it slightly exceeded the therapeutic level at a dose of 100 mg/kg. Addition of the lithium preparation (7-10(-3)-7-10(-5) M) to liver homogenates did not change the tryptophane pyrrolase activity in vitro. The same doses of lithium (50 and 100 mg/kg) caused a 2.5-fold increase in content of 11-hydrocorticosteroids in rat blood plasma; the effect was prevented by previous administration of dexamethasone. In experiments with adrenalectomized rats lithium did not affect the enzymatic activity. Repeated administration of lithium (50 mg/kg) within 10 days did not affect the tryptophane pyrrolase activity and did not alter the content of 11-hydroxycorticosteroids in rat blood plasma. The data obtained suggest that the increase in the tryptophane pyrrolase activity, caused by lithium, is mediated through the elevation in content of 11-hydroxycorticosteroids in blood.

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PubMed1990

Failure of industrial noise to change the patterns of vanilmandelic acid and 17-hydroxycorticosteroids in the urine of the female weavers with hearing loss.

The field experiments were undertaken on two consecutive working days on seven female weavers with noise-induced hearing loss (NIHL), and a control group of seven sewers with normal hearing. The first day, urine was collected during the shift (06:00-14:00 h) and at home (17:00-05:00 h) for measurements of 17-hydroxycorticosteroids (17-OH) levels. The following day, the procedure was repeated, but for vanilmandelic acid (VMA) analysis. No significant changes in the hormone levels were found, both concerning the different occupational noise exposure and the periods of a working day.

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PubMed1986

Hydrolysis of conjugated steroids by beta-glucuronidase from Ampullaria and application to the determination of urinary 17-hydroxycorticosteroids.

The usefulness of Ampullaria beta-glucuronidase as a reagent for the hydrolysis of steroid glucuronides was examined. The purified enzyme showed an optimum pH of 4, and was stable between pH 4.5 and 7.5. The enzyme from Ampullaria and Helix pomatia hydrolyzed various artificial substrates and conjugated steroids. Affinity of the Ampullaria enzyme for 17-hydroxycorticosteroid glucuronide was 7-fold the affinity of the Helix pomatia enzyme. Hydrolysis of urinary steroid conjugates was completed by an incubation with 320 Fishman units of Ampullaria beta-glucuronidase at 60 degrees C for 1 h. A close correlation was obtained between the values of steroid conjugates hydrolyzed by the Ampullaria enzyme and those by the bovine liver enzyme used conventionally. Ampullaria beta-glucuronidase is suitable for hydrolysis of urinary steroid conjugates because of its higher affinity for steroid substrate and the thermal stability.

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PubMed1992

The excretion of 17-ketosteroids and 17-hydroxycorticosteroids in night urine of elite rowers during altitude training.

During an altitude training camp (23 days, 1850 m above sea level) we collected night urine from 36 German elite rowers in order to measure the excretion of urea, creatinine, 17-ketosteroids (17-KS), and 17-hydroxycorticosteroids (17-OHCS). 17-KS and 17-OHCS represent the major metabolites from endogenous anabolic and catabolic steroid hormone systems. There was no significant change in the excretion of 17-OHCS during the training camp (mean value: females 0.0025 +/- 0.0011, males 0.0033 +/- 0.0012 mg/kgbw.h). Significant increases in the excretion of 17-KS (mean value: females 0.007 +/- 0.003, males 0.0092 +/- 0.0039 mg/kgbw.h) and in the ratio 17-KS/17-OHCS (mean value: females 3.13 +/- 1.65, males 3.11 +/- 1.71) were found during the first week and towards the end of the training camp. To investigate training effects on the excretion of these hormone metabolites, we used a recently described classification for rowing training (categories I to IV of rowing-specific training according to lactate levels and non-rowing specific categories) and a corresponding rowing data base. More than 80% of training was performed at a lactate level lower than 2 mmol/l. Using multiple regression analysis, the general finding was that in males the ratio of 17-KS/17-OHCS increased with rowing specific and non specific training regimes where a lactate level below 2 mmol/l was observed. Training at higher lactate levels caused a decrease in the ratio that may be interpreted as a shift in the production from endogenous androgenic steroid hormones to cortisol. No significant effects of single training variables were found in female rowers, which indicates major training influences on testosterone metabolism. The influence of further factors such as a relationship between urine urea and 17-KS in males are described and need further explanation.

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PubMed1975

The effect of sodium bisulfite on the removal of drugs and their metabolites interfering with the Porter-Silber reaction in the determination of urinary 17-hydroxycorticosteroids.

In the determination of urinary 17-hydroxycorticosteroids, the urine is saturated with NaHSO3 after hydrolysis with beta-glucuronidase and then extracted with methylene chloride. Sodium bisfulfite removes almost all non-steroidal impurities in the urines from patients medicated with acetylspiramycin, leucomycin, erythromycin, triacetylolenadomycin, rifampicin and tranquilizers such as chlorpromazine, which interfere with the absorption at 410 nm. in the subsquent Porter-Silber reaction. In order to increase the specificity of a routine method, a procedure conducted by Allen has been often employed: The sum of 370- and 450-nm. absorbances is subtracted from twice absorbance at 410 nm. However, the procedure could not be used in the medicated urines mentioned above, because the spectral absorption curve of these drugs and their metabolites in the Porter-Silber reaction was not a straight but a strongly convex or concave line in the 370-450-nm. range. Using the present method, interference with the Porter-Silber reaction was not found in the urines from patients medicated with chloramphenicol, minocycline, chlordiazepoxide, meprobamate, methyprylon, nitrazepam, synthetic penicillins such as hetacillin, oxacillin and cloxacillin, or cephalosporins such as cephalexin and cephalothin. However, to obtain correct values in urines from patients medicated with spironolactone, it was necessary to subject the urines to treatment with methylene chloride before enzyme hydrolysis.

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PubMed1976

Overnight urinary 11-hydroxycorticosteroid estimations in diagnosis of Cushing's syndrome.

Overnight specimens of urine were collected from control, obese, and hirsute women and from 11 women with Cushing's syndrome. Urinary 11-hydroxycorticosteroid levels in the group with Cushing's syndrome were significantly higher than in the other three groups. This simple test has proved invaluable when screening for Cushing's syndrome in a busy outpatient clinic.

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PubMed1978

Angiotensin II infusion increases vasopressin, ACTH, and 11-hydroxycorticosteroid secretion.

The effects of intravenous infusion of Asp1. Ile5-angiotensin II on blood pressure, plasma vasopressin, ACTH and 11-hydroxycorticosteroid levels and on plasma renin activity were studied in five trained, conscious dogs. The dogs were prepared with bilateral carotid loops. Infusion of angiotensin II at rates of 5, 10, and 20 ng/kg.min raised its plasma concentration from 23 +/- 7 to 48 +/- 8, 125 +/- 8, and 187 +/- 21 pg/ml, respectively. The lowest rate of infusion was mildly pressor, the two higher rates more so. All rates of infusion promptly increased vasopressin levels and depressed renin levels. The two higher rates also stimulated ACTH, although with a latency of 30-45 min. Since the rates of infusion of angiotensin II employed produced plasma levels within the physiological range, it is suggested that peripherally generated angiotensin II may play an important role in the regulation of vasopressin, and ACTH secretion.

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PubMed1978

Effects of exogenous acetylcholine upon adrenal 17-hydroxycorticosteroid secretion of intact and head X-irradiated dogs.

Adrenocortical response to exogenous acetylcholine (Ach) was investigated, under anesthetized conditions, in intact, hypophysectomized and head X-irradiated dogs. Intravenous injection of Ach (1 mg/kg b.w.) to intact dogs resulted in marked increases in the secretion of 17-hydroxycorticosteroids (17-OHCS) by the adrenal gland. The maximum response was seen at 10 min after the injection and a return to preinjection levels tended to occur by 60 min. This effect was abolished completely by hypophysectomy. In dogs whose heads had been irradiated with 200 and 1,000 R of X-rays 1 day previously, a considerably lower response to Ach was found; 17-OHCS output at the time when the secretion had been maximum was 44--53% less than that in non-irradiated dogs.

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PubMed1977

Ratio of urinary 6beta-hydroxycortisol to 17-hydroxycorticosteroids in patients with liver disease.

The ratio of 6beta-hydroxycortisol to 17-hydroxycorticosteroids in the urine of 73 patients with liver disease, and 53 controls has been measured. The mean ratio was significantly greater in the liver disease group (p less than 0.001), this elevation being most marked among patients with liver metastases and patients with acute hepatitis. We feel that the use of the ratio as a test of early liver cell dysfunction requires further evaluation, in particular in the early recognition of metastatic liver disease.

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