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Biomedical subjects

H Breuer

Publications and source records attributed to H Breuer.

At least 145 records · Page 8Linked to original sources
PubMed1977

Factors involved in the uptake of corticosterone by rat liver cells.

Isolated rat liver cells take up corticosterone rapidly; the initial rates increase with increasing temperature. A plot of the initial rates against the concentration of corticosterone indicated the presence of saturable and nonsaturable uptake systems. The Eadie-Hofstee plot showed the presence of two saturable and one nonsaturable uptake components. The apparent Kt values of the saturable systems were 64 +/- 40 nM (n = 3) and 1085 +/- 313 nM (n = 12). The nonsaturable system, probably diffusion, contributed 12% to the total uptake between 15 and 72 nM corticosterone, the physiological concentration of the free corticosterone in rat serum. Metabolic inhibitors did not influence the uptake of corticosterone. N-Ethylmaleimide, 1-fluoro-2,4-dinitrobenzene and sodium ethyl mercurithiosalicylate (1 mM each) decreased the uptake by 40%. Iodoacetate did not have any influence. Treatment of cells with phospholipase A inhibited the uptake 35--45%. In the presence of cortisone, cortisol, dexamethasone, aldosterone, testosterone, estradiol-17beta and estrone (2 muM each) the uptake decreased 30--50%. The presence of serum proteins in the external medium inhibits the uptake of corticosterone. These results suggest that corticosterone is transported into the cell and is accumulated. Only the free hormone is available for uptake which in turn may be regulated by protein and lipid components in the plasma membrane of the liver cell.

Animals↗
PubMed1977

Studies on the metabolism of oestrone sulphate. Comparative perfusions of oestrone and oestrone sulphate through isolated rat livers.

The metabolism of [4-(14)C]oestrone and of [6,7-(3)H(2)]oestrone sulphate was studied during cyclic perfusion and once-through perfusion of the isolated rat liver. The following results were obtained. 1. As shown by once-through perfusion, the two steroids are metabolized differently during the first passage through the organ. [4-(14)C]Oestrone was taken up by the liver and partly delivered as oestradiol-17beta and oestriol into the medium. After uptake of [6,7-(3)H(2)]oestrone sulphate, only oestrone, liberated by hydrolysis, was delivered into the medium; no oestradiol-17beta or oestriol could be detected in the medium after one passage through the organ. This indicates that intracellular oestrone, which was taken up as such, and oestrone, which derived from intracellular hydrolysis, may be metabolized in different compartments of the liver cell. 2. The results of the cyclic perfusion showed that intracellular oestrone is preferentially conjugated with glucuronic acid, and subsequently excreted into the bile. Intracellular oestrone sulphate is preferably reduced to oestradiol sulphate, thus indicating that oestrone sulphate is a better substrate for the 17beta-hydroxy steroid oxidoreductase than is oestrone. 3. Albumin-bound oestrone sulphate acts as a large reservoir, and in contrast with free oestrone is protected from enzyme attack by its strong binding to albumin. 4. Oestrone sulphate is partly converted into the hormonally active oestrone by liver tissue. This suggests that liver not only inactivates oestrogens, but also provides the organism with oestrone, which is subsequently readily taken up by other organs.

Animals↗
PubMed1977

[Simultaneous occurrence of primary hyperparathyroidism and pituitary Cushing's syndrome (author's transl)].

A case of primary hyperparathyroidism and coincidental Cushing's syndrome of hypothalamic-hypophyseal origin is reported. The hyperparathyroidism was based on an adenoma of the parathyroid glands and produced a severe hypercalcaemia (4.5 mmol/l) and calcinosis of kidneys and lungs. The Cushing's syndrome was caused by a hyperplasiogenic ACTH cell-adenoma of the pituitary which had induced a regulative hyperplasia of the ACTH-dependent zones of the adrenal cortex. The ultrastructure of the zona fasciculata and reticularis showed a conspicuous activation of the steroid hormone-producing organelles. The two endocrine diseases added together in skeleton, heart, duodenum, and pancreas. As a sign of hyperparathyroidism the osteoclastic absorption of the bone was strongly increased, whereas the bone formation was reduced due to the hypercortisolism. The pancreas showed a severe acute recurrence of chronic pancreatitis which was induced by a parathyrotoxic crisis. This was the immediate cause of death.

Adenoma↗
PubMed1977

Steroid glucuronyltransferases of rat liver. Properties of oestrone and testosterone glucuronyltransferases and the effect of ovariectomy, castration and administration of steroids on the enzymes.

1. Microsomal preparations from rat liver, kidney and intestine were tested for UDP-glucuronyltransferase activity by using oestrone, oestradiol-17 beta, oestriol, testosterone, cortisol, cortisone, corticosterone, aldosterone, tetrahydrocortisol and tetrahydrocortisone as substrates. The microsomal preparation from the liver glucuronidated oestrone, oestradiol-17 beta and testosterone. 2. The specific activity of the enzyme was significantly higher in livers from female rats than in those from male rats. 3. Testosterone was actively glucuronidated by both sexes. Cortisol, cortisone, corticosterone, aldosterone, tetrahydrocortisol and tetrahydrocortisone were not glucuronidated by any of the three tissues. 4. The non-ionic detergent Lubrol WX activates liver microsomal UDP-glucuronyltransferase 2-3-fold with oestrone and testosterone as substrates. 5. Oestrone glucuronyltransferase was inhibited by oestradiol-17 beta, predominantly competitively and by testosterone non-competitively. Bilirubin was a non-competitive inhibitor of oestrone glucuronidation. p-Nitrophenol had no effect. 6. Oestrone glucuronyltransferase could not be stimulated by either acute or prolonged treatment of animals with phenobarbital, whereas a single dose of 3-methylcholanthrene led to a moderate stimulation. 7. Ovariectomy leads to a 56% decrease in oestrone glucuronyltransferase activity; administration of oestradiol-17 beta induces the enzyme to normal activity after 12 days, and after 15 days the activity is twice the control value. Actinomycin D and cycloheximide block the oestradiol-17 beta-induced increase in enzyme activity. 8. Castration has no effect on the activity of testosterone glucuronyltransferase, nor does administration of testosterone influence enzyme activity. The results provide strong evidence for the existence of multiple steroid glucuronyltransferases in the liver of the rat.

Animals↗
PubMed1977

An improved method for the simultaneous determination of individual 17-oxosteroids and of pregnanediol in urine by gas-liquid chromatography.

An improved method for the simultaneous gas-chromatographic determination of individual 17-oxosteroids and of pregnanediol in the same sample of urine is described. The method involves the following steps. The urinary sample is chromatographed on Amberlite XAD-2. The fraction containing the steroid conjugates is evaporated; the residue is dissolved in n-heptane and the organic phase extracted with water. The steroid glucuronides are hydrolysed by a bacterial beta-glucuronidase; subsequently, the steroid sulphates are solvolysed in ethyl acetate. Free 17-oxosteroids and pregnanediol are separated by two-dimensional thin-layer chromatography. The zone containing the steroids to be investigated is eluted; after evaporation, the residue is treat with N-methyl N-trimethyl silyl trifluoroacetamide. The reaction mixture is injected into a gas chromatograph; the trimethyl silyl ethers of the individual 17-oxosteroids and of pregnanediol are quantitated by measuring the peak heights.

17-Ketosteroids↗
PubMed1977

[Effect of immersion on the urinary excretion of aldosterone in trained and untrained male subjects (author's transl)].

Diuresis, the excretion of aldosterone-18-glucuronide and the excretion of sodium and potassium were measured before and during two periods of immersion in four male athletes in training and four untrained male subjects (age 20-27 years). The increase in diuresis during immersion was accompained by a concomitant decrease of aldosterone excretion and increase of sodium excretion in urine. These changes were more pronounced in untrained subjects than in trained subjects. From these results it may be concluded that trained subjects react more sensitive to slight changes in aldosterone secretion than untrained subjects.

Adaptation, Physiological↗
PubMed1977

[Effect of spirolactones on the urinary excretion of individual 17-oxosteroids and of pregnanediol in man (author's transl)].

The effect of spirolactones on the urinary excretion of individual 17-oxosteroids and of pregnanediol in man was investigated under various conditions. After purification by thin-layer chromatography, the 17-oxosteroids and pregnanediol were determined by gas chromatography. Eleven male subjects (age 21-34 years) received a daily dose of 200 mg spironolactone (Aldactone) orally on seven consecutive days. Five female subjects (age 20-35 years) and ten pregnant women (age 20-35 years; 28th.-39th. week of gestation) were given a daily intravenous injection of 600 mg potassium canrenoate (Aldactone pro injectione) on three consecutive days. In the male subjects, the excretion of individual 17-oxosteroids and of pregnanediol was significantly reduced during administration of spironolactone. In the nonpregnant female subjects, the excretion of etiocholanolone and dehydroepiandrosterone was diminished, whereas in the pregnant women, the excretion of pregnanediol and dehydroepiandrosterone was decreased during treatment with potassium canrenoate. These results suggest that the reduced urinary excretion of steroids may be due to an inhibition of steroid metabolising enzymes by spirolactones. It seems likely that spirolactones affect the enzymatic conversion fo cholesterol to pregnenolone.

17-Ketosteroids↗
PubMed1976

[Changes of the renin-angiotensin-aldosterone system under contraceptive steroids. Contribution to the etiology of hypertension under hormonal contraceptives].

Treatment with hormonal contraceptives leads to a considerable stimulation of the renin-angiotensin-aldosterone-system. First of all, there is a 2,5- to 4fold increase of renin substrate synthesis in the liver. As a consequence, more angiotensin I and angiotensin II are released. Angiotensin II stimulates the secretion of aldosterone in the adrenals, thus producing a higher aldosterone concentration in plasma. The urinary excretion of aldosterone is elevated to a lesser degree, probably because of the simultaneously increased binding of aldosterone to plasma proteins. The release of renin is suppressed to 50% by negative feedback mechanisms. Some possible factors in the etiology of hypertension induced by oral contraceptives are discussed.

Adult↗
PubMed1976

Investigations on the kinetic properties of estrone glucuronyltransferase from pig kidney.

The microsomal fraction of the pig kidney catalyzes the glucuronidation of estrone in the presence of UDP-glucuronic acid. This bireactant system exhibits a sequential type of reaction mechanism. Increasing concentrations of either substrate increase the affinity of the enzyme for the other substrate. The Hill coefficient, n, was calculated to be 1.0 for both estrone and UDP-glucuronic acid. The Kestrone and KUDP-glucuronic acid are 6.6 muM and 254 muM, respectively. The estrone glucuronyltransferase (UDP-glucuronate: 17 beta-oestradiol 3-glucuronosyltransferase, EC 2.4.1.59) exhibits high substrate specificity in that it is inhibited noncompetetively by estradiol-17 beta, estradiol-17 alpha, estriol, testosterone, phenolphthalein and bilirubin; p-nitrophenol and o-aminophenol do not inhibit the glucuronidation of estrone. Mg2+ and Ca2+ were found to be nonessential activators. One of the two products of the reaction, estrone glucuronide, inhibits the enzyme competitively in the presence of increasing concentrations of UDP-glucuronic acid. The other product of the reaction, UDP, inhibits the enzyme noncompetitively with varying estrone concentrations and uncompetitively with varying UDP-glucuronic acid concentrations. Under incubation conditions for the glucuronidation of estrone, the enzyme catalyzes the reverse reaction with estrone glucuronide and UDP as reactants to an extent of about 0.4% of the forward reaction; this reverse reaction is also of a sequential type.

Adenosine Triphosphate↗