Search PubMed⌕ Search

Biomedical subjects

E Lacroix

Publications and source records attributed to E Lacroix.

At least 37 records · Page 2Linked to original sources
PubMed1987

Influence of neonatal androgenization on the testicular steroidogenesis in the adult rat.

The in vitro testicular steroidogenesis of male rats, androgenized on the third postnatal day by a single injection of 1 mg testosterone propionate, was investigated when the animals were 100 days old. The neonatal androgenization resulted in a 25% lower testes weight, significantly increased plasma levels of FSH (P less than 0.01) and LH (P less than 0.02), and normal levels of testosterone. Although the testes were hypotrophic, the incubation of the testes pairs yielded the same amounts of testosterone, 7 alpha-hydroxytestosterone and 5 alpha-androstane-(3 alpha + 3 beta), 17 beta-diol as in the control animals. However, the steroidogenic response to an acute hCG stimulation was reduced. From incubations of testes homogenates with various labelled steroid precursors it could be inferred that the activity of the 17 alpha-hydroxylase, the 3 beta-hydroxysteroid dehydrogenase-isomerase and the 17 beta-hydroxysteroid dehydrogenase, expressed per unit of incubated protein, was significantly increased in the testes of the androgenized rats. These data indicate that the basal steroidogenesis in neonatally androgenized male rats is maintained by an increased synthesis per unit of tissue, possibly under influence of an increased gonadotrophic stimulus, but that the maximum steroidogenic capacity is reduced.

17-alpha-Hydroxyprogesterone↗
PubMed1984

Testosterone metabolism by incubated rat testes after chronic LHRH treatment.

Adult male rats were injected 4 or 8 days with LHRH agonist. After sacrifice the testes were incubated in vitro with or without [4-14C]testosterone. After LHRH-administration the endogenously produced amounts of testosterone and of 7 alpha-hydroxytestosterone, the main testosterone metabolite normally found on incubation of adult rat testes, were drastically reduced when compared with controls. hCG, injected to rats 2 h before sacrifice, increased steroid production. In the LHRH-treated rats, however, the amounts of testosterone and of 7 alpha-hydroxytestosterone produced were much less while an important formation of 5 alpha-androstanediol was observed. The testes of LHRH treated rats metabolized [4-14C]testosterone to a large extent to 5 alpha-reduced and unextractable metabolites while the formation of 7 alpha-hydroxylated metabolites was much reduced. It is concluded that prolonged LHRH treatment provokes not only a depression of the testosterone production but has also an influence on the testicular metabolism pattern of testosterone resulting in a proportionally increased production of 5 alpha-reduced steroids and unextractable metabolites while the formation of 7 alpha-hydroxylated steroids is inhibited.

Androgens↗
PubMed1984

Metabolism of [4-14C]testosterone and precursors by homogenates of rat testes after chronic LHRH-treatment.

Adult male rats were injected daily for 8 days with an LHRH agonist. Twenty-four hours after the last injection testes-homogenates were incubated in the presence of a 4-14C-labeled steroid, either progesterone, 17 alpha-hydroxyprogesterone, dehydroepiandrosterone, androstenedione or testosterone. The activity of several enzymes involved in the androgen biosynthetic pathway was inferred from the amount of metabolites produced under these conditions. After LHRH-treatment a significant increase in the 17,20-lyase activity was observed without any significant change in the activity of 17 alpha-hydroxylase, 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4-isomerase and 17 beta-hydroxysteroid dehydrogenase. The results of the experiments indicate that the decreased testosterone secretion observed in rats after chronic LHRH-administration is not due to an inhibition of the enzyme-systems studied.

Androstenedione↗
PubMed1983

Steroid metabolism and steroid receptors in dimethylbenz(a)anthracene-induced rat mammary tumors.

Mammary tumors were induced in rats by treatment with dimethylbenz(a)anthracene. Cytosol receptors for 17 beta-estradiol and progesterone were estimated by means of sucrose density gradient centrifugation, and the metabolism of [14C]progesterone, [14C]testosterone, and 17 beta-[14C]estradiol by minced tumor tissue was studied. The estradiol receptor (ER) and progesterone receptor (PR) levels of the tumors varied considerably from less than 5 to 48 fmol/mg protein for ER and to 243 fmol/mg protein for PR. Considering a receptor level lower than 5 fmol/mg protein to be negative, four groups of tumors were found: ER-negative and PR-negative; ER-positive and PR-negative; ER-negative and PR-positive; ER-positive and PR-positive. In dimethylbenz(a)anthracene-induced tumor tissue, high 5 alpha-reductase and 20 alpha-hydroxysteroid dehydrogenase activities and somewhat lower 3 alpha-hydroxysteroid dehydrogenase and 6 alpha-hydroxylase activities were found. No aromatization was detectable. Steroids, especially estradiol, were also metabolized in a high degree to unextractable metabolites. It was concluded that steroid metabolism of dimethylbenz(a)anthracene-induced rat mammary tumors was not related to the ER and/or PR concentration of tumor tissue.

9,10-Dimethyl-1,2-benzanthracene↗
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↗
PubMed1979

[Cardiovascular effects of a single injection of fentanyl in dogs under acute experimental conditions].

Experimental studies carried out in unselected dogs often face the problem of instabilit of various parameters both in terms of haemodynamics as well as acid-base balance. It is possible, with the injection of a single dose of Fentanyl of 0.35 mg.kg-1 given over a period of ten minutes to obtain, from the 30th minute after the injection, satisfactory cardiovascular stability (confirmed during 120 minutes in 9 dogs and 360 minutes in 2 of them). This haemodynamic state at T + 30 is obtained with a fall in mean blood pressure of -40 per cent, and an increase in peripheral resistance of +38 per cent and stroke volume of +11 per cent. This stability, obtained at the price of a stable normacapnia, correction of any possible metabolic acidosis and maintenance of body temperature, makes it possible to study the cardiovascular effects of certain types of treatment or of induced pathology.

Acid-Base Equilibrium↗
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↗