PubMed Health⌕ Search

Biomedical subjects

R S Calandra

Publications and source records attributed to R S Calandra.

At least 73 records · Page 4Linked to original sources
PubMed1980

Uptake and metabolism of androgen by the human epididymis in vitro.

Uptake and metabolism of [3H]testosterone, mainly to 5 alpha-dihydrotestosterone (5 alpha-DHT and 5 alpha-androstanediol were higher in the caput than in the cauda epididymidis in vitro. The metabolites represented 57, 49 and 47% of the total radioactivity in the caput, corpus and cauda epididymidis, respectively; subcellular distributions of the metabolites in each segment showed 67% of total radioactivity in cytosol and 18% in the nuclei. In both fractions, the amount of 5 alpha-DHT was greater than that of androstanediol while the reverse was true for the mitochondria and microsomes. The distribution of 5 alpha-reductase activity in subcellular fractions was similar to that of the microsomal marker enzyme NADPH: cytochrome C reductase, whilst 3 alpha-hydroxysteroid dehydrogenase was found mainly in the cytosol. Maximal 5 alpha-reductase activity was at pH 5.3, apparent Km values in the microsomal and nuclear fractions were 1.65 +/- 0.7 and 1.75 +/- 0.36 x 10(-6) M respectively, and the Vmax in these preparations was 5.28 +/- 1.19 and 3.1 +/- 0.52 pmol/mg protein/min, respectively. The activity of 5 alpha-reductase was inhibited by Zn2+, Cu2+, Ba2+ and Cd2+ and by epitestosterone, progesterone and 4-androstene-3-one 17 beta-carboxylic acid.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

Hormonal regulation of 5alpha-reductase activity in rat epididymis.

The specific activity of epididymal 5alpha-reductase (pmol 5alpha-reduced products mg protein-1 h-1) decreased by 17, 44, 58 and 83% of the initial value and its total activity (nmol 5alpha-reduced products organ-1 h-1) decreased by 66, 85, 94 and 98% 2, 4, 8 and 14 days respectively, after castration. The loss of total activity always exceeded the decrease in organ weight and protein content. The decline in enzymic activity could be prevented by implantation of testosterone at the time of castration. Administration of testosterone propionate (200 microgram/day) for 12 days starting 1 month after castration was associated with the weights of the accessory organs returning to the control values and although the specific activity of 5alpha-reductase was almost completely restored by this treatment, the total activity of the nuclear fraction remained at 49% of the control value. Recombination experiments demonstrated that the effect of androgens is not mediated by a factor present in the soluble fraction and the concomitant administration of androgen and either cycloheximide or actinomycin D blocked the effect of androgen. These data suggest that androgens stimulate the synthesis of epididymal 5alpha-reductase.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1975

The effect of castration and testosterone replacement on specific proteins and androgen levels of the rat epididymis.

The normal weight increase of the epididymis during sexual maturation and its maintenance through adulthood were found to be dependent on the provision of androgens. Binding of [3H]dihydrotestosterone (DHT) to the epididymal 8S cytoplasmic receptor gradually decreased after castration to become undetectable after 25 days. Binding to the androgen binding protein (ABP) was absent 4 days after castration and was not reinduced by 3 weeks of testosterone (T) administration. Unilateral castration for periods of up to 27 days showed the disappearance of ABP with preservation of the 8S receptor on the castrated side, indicating a testicular source for ABP and the epididymal origin of the 8S receptor. The tissue concentrations of T and DHT in the epididymis became undetectable 30 days after castration and were restored to normal values by administration of testosterone in large doses (1.5 mg/100 g BW). Similar results were obtained in rats castrated at 10 days of age and injected with testosterone until 60 days old. The ratio DHT/T was depressed in the castrate and increased with testosterone treatment. The protein content of the epididymis (mg of protein/g wet weight) was also found to be influenced by androgens. Our results show evidence of some mechanisms involved in the trophic effect of androgens upon the epididymis and suggest the possible androgenic control of epididymal 5alpha-reductase activity. They also indicate that a testicular factor is required for the maintenance of the 8S cytoplasmic androgen receptor. It is not known whether this factor is testosterone or some other testicular secretion.

Androgens↗
PubMed1970

Hormonal and metabolic studies in pheochromocytoma.

One patient with benign and another with malignant pheochromocytoma have been studied in an attempt to elucidate the effect of increased catecholamines on the response of blood sugar, unesterified fatty acids, insulin and growth hormone to a glucose load. The presence of increased catecholamines in both patients appeared to produce increased fasting plasma unesterified fatty acid levels, carbohydrate intolerance and an unusual plasma growth hormone response to glucose. There was no interference with the normal decrease in plasma unesterified fatty acids after glucose ingestion. The malignant tumour, but not the benign one, was associated with low plasma insulin levels.After removal of the benign tumour the fasting unesterified fatty acid levels became normal. In addition, following glucose ingestion there appeared to be a more normal plasma insulin and growth hormone response and improved glucose tolerance. After removal of the primary malignant tumour it is noteworthy that the distant metastases secreted abnormal amounts of both adrenaline and noradrenaline.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Induced hypoprolactinemia and testicular steroidogenesis in man.

The effects of short-term hypoprolactinemia on the pituitary-gonadal axis were evaluated in a group of patients with untreated prostatic carcinoma. Each patient was studied prior to and during 7-day oral administrations of bromocriptine (2.5 mg q.i.d.). Serum LH, prolactin (PRL), androst-4-ene-3,17 dione (androstenedione), testosterone, and 5 alpha-androstane-3 alpha, 17 beta-diol (5 alpha-Diol) levels, as well as intra-testicular testosterone, dihydrotestosterone (DHT), 5 alpha-Diol and zinc (Zn) concentrations, were determined. Daily administration of bromocriptine caused a marked suppression of serum PRL (mean +/- SEM, 23.8 +/- 2.5 vs. 6.4 +/- 1.0 ng/ml) without concomitant changes in serum LH levels (mean +/- SEM, 8.3 +/- 1.6 vs. 8.9 +/- 2.1 ng/ml). Hypoprolactinemia induced a significant decrease (P less than 0.05) in the mean peripheral testosterone levels; but 5 alpha-Diol and androstenedione remained unchanged. However, in testicular tissues, bromocriptine treatment resulted in significant increases in mean concentrations of total androgens (P less than 0.001), testosterone (P less than 0.001) and DHT (P less than 0.02). Testicular levels of 5 alpha-Diol were not significantly altered. There was no change in Zn levels in basal conditions and during bromocriptine administration. These results indicate that short-term suppression of serum PRL levels in man affects basal testicular function without altering serum LH. However, a direct action of bromocriptine on the human gonad cannot be excluded.

Aged↗
PubMedDate not supplied

Effects of induced hypoprolactinemia on testicular function during gonadal maturation in the rat.

We have evaluated the effects of hypoprolactinemia during gonadal maturation in the male rat. Intact 30-day-old rats were injected daily for 10 days with three different doses of bromocriptine (0.75, 1.5 or 3.0 mg/kg of body weight/day). At the end of the treatment period, the animals were sacrificed, serum was collected for prolactin (PRL), LH, and androgen measurements. Intratesticular testosterone and 5 alpha-androstanediol (androstanediol) were measured following celite column chromatography and a specific radioimmunoassay. In addition, the production of androgens by decapsulated testes and dispersed Leydig cells was also studied in vitro. Serum levels of PRL (9.4 +/- 1.9 ng/ml) were suppressed to undetectable levels in the three bromocriptine-treated groups, whereas LH levels were not altered. All three doses of bromocriptine markedly depressed serum testosterone (plus DHT) and androstanediol. Intra-testicular testosterone and androstanediol were diminished (25% and 35%, respectively, P less than 0.05) during hypoprolactinemia. Decapsulated testes and dispersed Leydig cells from bromocriptine-treated animals showed a significant reduction in the basal secretion of testosterone (plus DHT) and androstanediol, and in androgen responses to submaximal hCG stimulation. Maximal steroidogenic responses from bromocriptine-treated rats were similar to controls. The present findings show that, during puberty, bromocriptine influences testicular steroidogenesis, and these effects may be partly due to changes in PRL levels. A direct effect of this dopaminergic agonist on the male gonad cannot be completely ruled out.

Androgens↗
PubMedDate not supplied

Catecholamine distribution in adult rat testis.

Catecholamine distribution in the adult rat testis was examined using a sensitive radioenzymatic method. Norepinephrine was present in the capsule and the interstitial fluid, in higher concentrations than dopamine, while in the interstitial cell preparations only norepinephrine was found. Epinephrine was undetectable in all testicular compartments investigated. No catecholamines were found in the seminiferous tubules. Testicular denervation caused a significant decrease in capsular catecholamines, confirming the neural origin of these amines.

Animals↗