Biomedical subjects
C Scorticati
Publications and source records attributed to C Scorticati.
L-dopa malabsorption in a parkinsonian patient with Strongyloides stercoralis duodenitis.
We report a parkinsonian patient initially responding to L-dopa who developed a severe loss of drug efficacy due to Strongyloides stercoralis duodenitis. The patient was put on mebendazole and metronidazole, and the parasitosis abated, allowing L-dopa reduction by 33%. Our patient illustrates the advisability of searching for Strongyloides stercoralis when L-dopa malabsorption is suspected in Parkinson's disease.
Further characterization of a model system for the study of human epididymal physiology and its relation to sperm maturation.
Some preliminary speculations about the possible participation of epididymal antigens in sperm function may be supported by the above data. On the one hand, the reduction in the amount of antigens and their abnormal localization on spermatozoa from infertile patients may be coincident with our view about participation of epididymal antigens in the development of zona pellucida binding ability and fertilizing capacity by spermatozoa during maturation. This hypothesis is derived from experiments showing that immature hamster spermatozoa gain their ability to recognize and bind to zona pellucida and to penetrate homologous oocytes when exposed to preparations enriched in androgen-dependent epididymal secretory proteins or preincubated in conditions that favor their interaction with these proteins. Supporting our viewpoint for such a role in humans is evidence showing the progressive development of the ability to interact with hamster denuded oocytes as human spermatozoa pass along the epididymis. On the other hand, the apparent correlation between the loss of epididymal antigens during capacitation and the increased fertilization of human oocytes in vitro may be reminiscent of the removal of a decapacitation or acrosome stabilizing factor known to occur in many species and that must be removed prior to fertilization. Pending further understanding of their physiological role, the androgen-dependent epididymal proteins may become a useful marker of epididymal function and/or of sperm capacitation in humans. Within this context, we wish to stress the potential value of the model system that we have developed for the study of human epididymal physiology.
Increased recovery of androgen receptors from human prostate through the use of mersalyl: evidence for androgen regulation of the binding sites in carcinomatous prostate.
With a technique adapted for needle biopsies from human prostate, androgen receptors have been quantitated in normal, hyperplastic, and carcinomatous samples. An important improvement in the yield of cytosol specific binding sites was obtained when samples were pre-incubated with the mercurial reagent mersalyl, which dissociates endogenously bound hormone receptor complexes, before the binding assay with 3H-methyltrienolone (3H-R1881). Androgen receptors in normal prostate tissue were found to be highest (7.81 +/- 1.12 pmoles/g tissue), and significantly different from hyperplastic prostate (2.02 +/- 0.55 pmoles/g tissue, p less than 0.025), but not from carcinomatous samples (4.47 +/- 0.79 pmoles/g tissue). Mean values for hyperplastic and carcinoma were not statistically distinguishable (p less than 0.1). The clinical response to hormone therapy in 85% of 13 patients with prostatic adenocarcinoma reflected the prostatic androgen receptor content. Orchidectomy followed by estrogen administration for several months leads to a dramatic fall (8-fold) in total androgen receptors in carcinomatous prostate, while estrogen alone did not seem to produce a significant effect. These preliminary data suggest that androgen could directly regulate its binding sites, as demonstrated earlier for other animal target organs.
Androgen metabolism in the human epididymis. Effect of in vivo estrogen administration.
Androgen metabolism in human epididymis was studied by incubating tissue fragments with isotopically labeled testosterone (T) and androstenedione (A) under batch and superfusion conditions. Epididymides were obtained from 16 patients with prostatic cancer, 5 of them treated with diethylstilbestrol (2.5 mg/d) for several months prior to castration. Results from batch incubations with [3H]T (100 nM) for 2 h at 25 degrees C indicated a markedly lower 5 alpha-reductase activity in tissues from estrogen-treated patients, as evaluated by measuring the amounts of radioactive 5 alpha-dihydrotestosterone, 5 alpha-androstanediols and 5 alpha-androstanedione present in tissue and medium at the end of the incubation period. Superfusion experiments confirmed this estrogen effect and also showed a shift of the interconversion between A and T towards the reductive direction and a diminished tissue retention of DHT after estrogen treatment. These effects may contribute to the marked regression of the epididymal epithelium that was noted in the estrogen-treated patients, which is thought to be mainly the result of the inhibition of androgen biosynthesis caused by chemical hypophysectomy.
Androgen receptor assay in small biopsies of human prostate. Preservation of nuclear receptor from rat ventral prostate by lyophilization.
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Sex hormone binding globulin in arterial, and in peripheral, hepatic, renal and spermatic venous blood of children and adults.
Human sex hormone binding globulin (SHBG) was measured in arterial serum and in serum obtained from different venous territories. In 6 children, SHBG ranged from 44.4 +/- 4.8 (mean +/- SD) in arterial blood to 55.3 +/- 5.3 in the hepatic vein (P less than 0.01), while it did not change significantly in renal or peripheral tissue venous blood. In 6 male adults, no significant arteriovenous differences were found either in the peripheral tissues or in the splanchnic circulation. In the spermatic vein of 8 subjects, SHGB was significantly lower (17.1 +/- 5.7) than in the arterial blood (22.8 +/- 7.5), P less than 0.025. The arterio-venous difference found in the splanchnic circulation of children supports the hepatic origin of SHBG, and also suggests extra-hepatic clearance of the binding globulin. Testicular uptake of SHBG might be necessary to regulate delivery of androgens to Sertoli cells in the seminiferous tubules.
[Biological markers in testicular cancer].
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Development and characterization of a model system for the study of epididymal physiology in man.
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Testosterone, dihydrotestosterone, and zinc concentrations in human testis and epididymis.
Tissue testosterone, dihydrotestosterone, and zinc concentrations have been determined in testis and epididymis of 13 patients with carcinoma of the prostate, 1 patient with carcinoma of the penis, and 3 patients with carcinoma of the prostate on estrogens. The 13 patients not receiving estrogens had the following testicular levels: testosterone, of 529 +/- 63.1 ng/g (mean +/- SE); dihydrotestosterone, 23.7 +/- 2.58 ng/g; and zinc 62.2 +/- 7.6 micrograms/g. The epididymal levels were as follows: testosterone, 40.6 +/- 3.4 ng/g; dihydrotestosterone, 20.5 +/- 2.36 ng/g; and zinc, 67.2 +/- 11.1 micrograms/g. Patients on estrogen therapy showed much lower androgen values in the two organs but zinc was not changed significantly. Concentrations of androgens were not significantly different in the epididymal fractions of caput, corpus, and cauda. In testis, there was a positive correlation between zinc and androgens contents, while the opposite was suggested by the data in the epididymis. Even though these patients were not normal, there was no evidence of testicular or epididymal disturbances.
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.
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.
The effect of in vitro androgen stimulation upon androgen metabolism and trophic parameters in cultured human epididymis.
Previous results obtained with a model system of human epididymal tubules maintained in organ culture suggested that androgenic stimulation of this tissue resulted in responses similar to those obtained in epididymides of experimental animals under physiological conditions, as well as in other human androgen-dependent tissues. In this instance we have explored the possible influence of androgens on the activity of the androgen-converting enzymes 5 alpha-reductase and 17 beta-dehydrogenase. Activity of the former enzyme increases significantly during the culture period but no differences were found among the cultured groups, regardless of the addition of androgen. On the other hand, the activity of 17 beta-dehydrogenase was unchanged in all the experimental conditions tested. The co-culture of the tissue with explants of human testis was without effect. More than 85% of the activity of both enzymes was found localized in a fraction enriched in epithelial cells. Histological observation of the cultured tissues showed a marked disorganization of the pseudostratified epithelium in the absence of androgen while the inclusion of DHT in the media partially prevented these changes. We conclude that, under the conditions employed in these experiments, the activity of the enzymes studied is not influenced by androgens.
[Acute gastrointestinal hemorrhages in postoperative urologic patients].
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[Uronephrosis caused by periureteral endometriosis].
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[Cancer of the female urethra (9 cases)].
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[Long-term incoercible hemorrhagic pyelonephritis].
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