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Biomedical subjects

W Eechaute

Publications and source records attributed to W Eechaute.

At least 37 records · Page 2Linked to original sources
PubMed1981

Role of testosterone levels and of hypophysis in the HCG-induced modifications of the 7 alpha-hydroxylation and 5 alpha-reduction processes in incubated rat testes.

The role of a direct or a hypophysis-mediated influence of increased testosterone levels in the effects of a long-term high-dose HCG administration (10 IU/day) upon the 7 alpha-hydroxylation and 5 alpha-reduction activities of incubated testes of mature rats was investigated. Administration of high doses of HCG to hypophysectomized rats resulted in the same metabolic changes as in normal rats, namely, a large decrease in the 7 alpha-hydroxylation and an increase in the 5 alpha-reduction processes. Administration of testosterone-propionate (0.2 mg and 20 mg/day) for several days to hypophysectomized rats and to normal rats receiving and substitutive dose of 1 IU HCG/day, did not modify the testicular metabolization pattern. These findings indicate that the decrease in testicular 7 alpha-hydroxylation activity induced by long-term administration of high doses of HCG is probably not mediated by the hypophysis nor by the extracellular testosterone levels.

Androgens↗
PubMed1980

Kinetic study of HCG induced decrease of microsomal 7 alpha-hydroxylase activity in rat testes.

Microsomes from rat testes were incubated with varying concentrations of 14C labelled testosterone and androstenedione. The production of 7 alpha-hydroxytestosterone and 7 alpha-hydroxyandrostenedione was followed; Km and Vm values were calculated from Lineweaver-Burk curves. A sustained treatment of rats with HCG resulted in a considerable decrease of the maximal 7 alpha-hydroxylation rats (Vm) whereas the Km value was not changed. Vm of microsomes from normal rats, when incubated with microsomes from HCG-treated animals, was also decreased substantially. It is concluded that HCG-induced depression of 7 alpha-hydroxylation capacity of testicular microsomes is at least in part due to non-competitive inhibition of the enzyme.

Androstenedione↗
PubMed1979

Estradiol metabolism by liver homogenates and microsomes of normal and cirrhotic male rats.

Incubation experiments show that homogenates and microsomes obtained from CCl4-induced cirrhotic livers of male rats metabolize an estradiol load at a much slower rate than preparations from normal livers. The decreased metabolic capacity results in a slower disappearance of estradiol from the incubation medium, and in a slower transformation of metabolized estradiol to polar extractable and to highly polar nonextractable metabolites.

Animals↗
PubMed1978

Metabolism of testosterone by isolated semiferous tubules and interstitial tissue of rat testes.

In prepubertal rat testes the main metabolisation of testosterone, which consists in 5alpha-reduction, is located predominantly in the Leydig-cells and is low in the seminiferous tubules. In adult rats, this metabolisation pattern has shifted to increased 7alpha-hydroxylation which is located mainly in the Leydig-cells, while 5alpha-reduction is performed in the seminiferous tubules. After prolonged treatment with HCG the 7alpha-hydroxylase activity in the Leydig-cells is strongly depressed while the metabolism of the seminiferous tubules is not influenced.

Animals↗
PubMed1976

Modification of testicular steroid metabolism in the rat during gonadotrophin administration.

The administration of human chorionic gonadotrophins to adult rats stimulates the formation of testosterone, 7alpha-hydroxy-testosterone and 5alpha-androstanediol in incubated testes. When the gonadotrophins are injected for several days, the testosterone formation is maintained at a high level; however, the transformation to 7alpha-hydroxy-testosterone decreases progressively to subcontrol levels, while 5alpha-androstanediol is produced in greater amounts.

Androstane-3,17-diol↗
PubMed1976

18-hydroxylated steroids in human hypertension - clinical study.

The detection of two unknown urinary steroids called x and y in various patients was previously reported. Compound x was tentatively characterized as a derivative of dihydro-18-hydroxy-DOC with two additional polar groups. In this communication clinical observations of a set of 25 hypertensive patients are presented. Compound x alone was found in 4 cases, compound y alone 4 cases and both compound x and y in 5 cases. In several other cases, hypokalemia and/or a decreased urinary Na+/K+ ratio were found.

18-Hydroxydesoxycorticosterone↗
PubMed1975

The metabolism of estradiol by perfused livers and liver slices of normal and cirrhotic rats.

The metabolism of estradiol- 17 beta and cirrhotic (CC14 -induced) rat livers was studied in isolated perfused livers and in incubations of liver slices. In these experiments the cirrhotic livers show a reduced clearance of estradiol, an accumulation of extractable metabolites and a delayed transformation to non-extractable metabolites. It is concluded that these changes in the metabolism of estradiol are caused not only by an altered circulation of the blood through intrahepatic shunts, but also by disturbances in the uptake and/or metabolism of the estrogens by the liver cells.

Animals↗