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Biomedical subjects

E Steinberger

Publications and source records attributed to E Steinberger.

At least 55 records · Page 3Linked to original sources
PubMed1979

Effect of age and estrogen therapy on the immunoreactive human chorionic gonadotropin content of testes.

Levels of human chorionic gonadotropin (HCG) were determined in testicular tissue of young, apparently normal men; older men with carcinoma of the prostate; male transsexuals treated with estrogens; and also in seminal plasma of normal and vasectomized patients. In all samples with one exception (a 76-year-old male with cancer of the prostate), immunoreactive HCG activity could be detected. The immunoassayable HCG content was higher in testicular extracts from young adults as compared with older men with cancer of the prostate. In transsexuals receiving estrogen therapy, testicular HCG levels were also very low. A possible relationship between quantitatively normal spermatogenesis and the testicular HCG level has been discussed. HCG was detected in seminal plasma from both normal and vasectomized men. The origin of this HCG activity may be extratesticular, and the possible role of the prostate and seminal vesicle in the production of HCG-like activity has to be considered.

Adult↗
PubMed1979

The relation between plasma testosterone levels and the lengths of phases of the menstrual cycle.

Plasma testosterone levels were measured in 331 women of reproductive age. The incidence of clinical signs of hyperandrogenism (hirsutism, acne) was recorded. Ovulatory activity was evaluated clinically by basal body temperature and frequent observation of changes in the appearance of the cervical os and cervical mucus. Plasma testosterone levels were abnormally elevated in patients with clinical signs of hyperandrogenism. The highest mean testosterone levels were noted in the group of hyperandrogenic women with amenorrhea. Significant prolongation of the follicular phase and shortening of the luteal phase were demonstrated to be associated with clinical signs of hyperandrogenism and elevated plasma testosterone levels. Statistically significant correlations between plasma testosterone levels and duration of phases of the menstrual cycle were observed. Testosterone levels were directly related to the length of the follicular phase and inversely related to the length of the luteal phase. A significant inverse correlation between the lengths of the two phases of the menstrual cycle was also demonstrated. These results suggest an association between hyperandrogenism and prolongation of the follicular phase and shortening of the luteal phase of the menstrual cycle, possibly related to the high incidence of infertility and menstrual irregularity reported for hyperandrogenic women.

Adult↗
PubMed1979

Effect of prednisone on plasma testosterone levels and on duration of phases of the menstrual cycle in hyperandrogenic women.

A group of 106 women of reproductive age with laboratory and clinical evidence of hyperandrogenism was treated with prednisone. The daily dosage varied between 7.5 and 10 mg. Ovulatory activity was assessed prior to and during therapy by basal body temperature and observation of changes in the cervical os and cervical mucus. Plasma testosterone levels were significantly suppressed by prednisone therapy. This was associated with initiation of ovulatory activity in 5 of 14 (35.7%) amenorrheic patients and 10 of 11 (90.9%) anovulatory patients. In 81 ovulatory patients, prednisone therapy resulted in statistically significant shortening of the follicular phase and lengthening of the luteal phase of the menstrual cycle. The mean length of the menstrual cycle was unchanged. Significant correlations between percentage suppression of plasma testosterone and shortening of the follicular phase or lengthening of the luteal phase were observed. Suppression of plasma testosterone by prednisone was maximal after 2 months of treatment, while the effect on the phases of the menstrual cycle was progressive with duration of treatment. The effects of prednisone at daily dosages of 7.5 or 10 mg were not significantly different. These results suggest that prednisone therapy in hyperandrogenic women exerts an effect on both phases of the menstrual cycle, possibly related to suppression of plasma testosterone levels.

Adult↗
PubMed1979

Testicular steroidogenesis in the rhesus monkey (Macaca mulatta.

Studies were undertaken to investigate testicular steroidogenesis in the Rhesus monkey Macaca mulatta. Testicular fragments (50 mg) were incubated for 3 hr with pregnenolone-7-3H or with progesterone-7-3H. The major metabolite of pregnenolone was progesterone (70.1%), with a lesser conversion to 17-hydroxyprogesterone (1.6%), androstenedione (3.3%), and testosterone (7.2%). The delta-5 intermediates 17-hydroxypregnenolone (4.6%) and dehydroepiandrosterone (8.6%) were also identified in the pregnenolone incubates. A majority of the progesterone substrate was not metabolized by the testicular fragments (80.1%), while some conversion to 17-hydroxyprogesterone (3.4%), androstenedione (4.8%), and testosterone (11.7%) occurred in the incubates. These results suggest that testicular fragments from the Rhesus monkey may convert pregnenolone to testosterone through both the delta-4 and the delta-5 pathways.

Androstenedione↗
PubMed1979

Leydig cell density and function and their relation to gonadotropins in infertile oligospermic men with varicocele.

Circulating gonadotropin and testosterone levels in infertile men with varicocele and sperm counts of less than 10(7)/ml were correlated with testicular Leydig cell density and in vitro testosterone synthesis. A significant correlation was found between Leydig cell density and both plasma testosterone levels and in vitro testosterone synthesis. Luteinizing hormone (LH) levels paralleled the in vitro testosterone synthesis. Although in the majority of patients, in vitro testosterone synthesis and Leydig cell density were low, plasma testosterone and LH levels were within the normal range. The only abnormal circulating hormonal level was high follicle-stimulating hormone in the most severely oligospermic patients. No difference were found between the right and left testes with regard to in vitro testosterone synthesis or Leydig cell density, and no correlation with patient age or site or degree of varicocele could be demonstrated. These findings suggest that Leydig cell dysfunction was the mechanism responsible for the oligospermia and infertility of these patients.

Adult↗
PubMed1978

Testicular steroidogenesis in the baboon Papio anubis.

We recently reported that the baboon testis converts pregnenolone to testosterone through the delta-4 pathway. The present studies were to determine the metabolism of intermediates of the delta-4 and delta-5 pathway by the baboon testis. Fragments (50 mg) were incubated for 3 hr with 10 muCi of the following tritium-labelled substrates: pregnenolone, progesterone, 17-hydroxypregnenolone, 17-hydroxyprogesterone, dehydroepiandrosterone, androstenedione, or testosterone. Pregnenolone was converted to testosterone primarily through the delta-4 pathway, with accumulation of progesterone, 17-hydroxyprogesterone and 20alpha-dihydroprogesterone as predominant intermediates. Similar results were obtained in progesterone incubations. 17-hydroxyprogesterone was not efficiently metabolized by the fragments, while 17-hydroxypregnenolone and dehydroepiandrosterone were efficiently converted into testosterone and androstenedione. Androstenedione was metabolized primarily to testosterone, while testosterone was not a suitable substrate. Some 5alpha-androstanediol was identified in each incubate. These results suggest that although testosterone is formed from pregnenolone through the delta-4 pathway, the delta-5 intermediates are more suitable substrates for testosterone synthesis in the baboon testis.

17-alpha-Hydroxypregnenolone↗
PubMed1978

Prostaglandin inhibition of testosterone production induced by luteinizing hormone, dibutyryl cyclic AMP or 3-isobutyl-1-methyl xanthine in dispersed rat testicular interstitial cells.

Testicular interstitial cells were utilized to study the effects of prostaglandins (PG) on in vitro testosterone production and to examine the role of cyclic adenosine-3',5'-monophosphate (cAMP) in this process. Testosterone production was assessed after 3 hour incubations while cAMP accumulation was examined after a 0.5 hour incubation period. Testosterone and cAMP were measured by radioimmunoassay. None of the PGs tested (PGA, PGA2, PGB1, PGE1, PGE2, PGF1alpha PGF2alpha) altered basal testosterone production when present in incubates at concentrations of 1.3 X 10(-8) M to 1.3 X 10(-4). However, at concentrations of 1.3 X 10(-4) M all of these PGs were capable of decreasing Luteinizing Hormone (LH; 100ng)-induced testosterone production. The inhibition of LH-induced testosterone production by the B, E and F series PGs was less pronounced than that for the A series. PGA1 and PGA2 exhibited 80% and 95% inhibition, respectively, at 1.3 X 10(4) M. The inhibitory action of 4 X 10(5) M PGA1 or PGA2 was evident within 30 minutes. Preincubation of interstitial cells with indomethacin (10(-5) or 10(-6) M) for 30 minutes did not alter subsequent basal or LH (100ng)-induced testosterone production. Accumulation of cAMP was stimulated by LH (10 microgram) or by PGs (1.3 X 10(-4) M PGA1, PGA2, PGB1, PGE1 or PGF2alpha). The PG-induced cAMP accumulation thus occurred at concentrations where LH-stimulated testosterone production was inhibited. Furthermore, PGA1 and PGA2 (1.3 X 10(-4) M) inhibited testosterone production induced by either 3-isobutyl-1-methyl xanthine (MIX; 10(-4) M or 10(-3) M) or dibutyryl cAMP (dbcAMP; 10(-4) M or 10(-3) M). These results indicate that PGs can block testosterone production by a direct effect on testicular interstitial cells and suggest that PGs exert their inhibitory action distal to stimulation of cAMP formation. PGs do not appear to play a role in the mechanism of LH action.

1-Methyl-3-isobutylxanthine↗
PubMed1978

Quantitation of Leydig cells in testicular biopsies of oligospermic men with varicocele.

Leydig cell density was evaluated quantitatively in bilateral testicular biopsies from 16 oligospermic men with varicocele. The method utilized for this quantitation is based on the determination of the total number of Leydig cells, Leydig cell clusters, and seminiferous tubules in the entire histologic section of each biopsy, and the calculation of the following indices: mean Leydig cells per seminiferous tubule, mean Leydig cell clusters per seminiferous tubule, and mean Leydig cells per cluster. A significant correlation between Leydig cells per tubule and Leydig cell clusters per tubule was demonstrated, suggesting that determination of Leydig cell clusters per seminiferous tubule in testicular biopsies is an objective and clinically applicable method for quantitative evaluation of Leydig cell density. An association of varicocele with Leydig cell hyperplasia was not noted for the 16 patients studied. In addition, no significant differences in Leydig cell density between right and left testes were found, and no correlation between Leydig cell density and site or degree of varicocele, or age of the patients could be demonstrated. To our knowledge this is the first report of quantitative analysis of Leydig cell density in men with varicocele.

Biopsy↗
PubMed1978

Quantitative analysis of the seminiferous epithelium in human testicular biopsies, and the relation of spermatogenesis to sperm density.

Quantitative analysis of the seminiferous epithelium was performed in bilateral testicular biopsy specimens from 14 patients with sperm counts ranging from 0 to 89 million/ml. All Sertoli cells and germ cells within each seminiferous tubule cross-section were counted in all biopsies. Results were expressed either as number of cells per unit length of seminiferous tubule circumference or as number of cells per Sertoli cell. Results were correlated with sperm count (millions per milliliter), total sperm count (millions per ejaculate), and age. A significant correlation between sperm density and germ cell counts was demonstrated. Coefficients of correlation were higher when results were expressed per unit of tubular wall length than when expressed per Sertoli cell. In men with sperm counts below 5 million/ml the number of germ cells in the biopsy was lower than in men with higher sperm counts. Spermiogenesis appeared to be most affected. In this group of patients an adverse effect of age on spermatogenesis was noted.

Adolescent↗
PubMed1978

A possible mechanism for the detrimental effect of varicocele on testicular function in man.

Seminiferous epithelium histology, Leydig cell density, and in vitro testosterone synthesis were quantitated in bilateral testicular biopsies from men with varying degrees of unilateral or bilateral varicoceles. Results were correlated with plasma levels of gonadotropins (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) and testosterone (T), as well as with semen quality. In patients with bilateral varicoceles, spermatogenesis, Leydig cell density, plasma T levels, and in vitro T synthesis were significantly lower than in patients with unilateral varicoceles. Varicoceles appeared to affect maximally the latest stages of spermatogenesis. A negative correlation between FSH and LH levels and spermatogenesis was observed; however, a dissociation between the two gonadotropins occurred when spermatogenesis declined. Plasma T levels were within the normal range in all patients. The T:LH ratio was significantly correlated with spermatogenesis and sperm motility. Leydig cell density was abnormally low in oligospermic patients, and it was significantly correlated with in vitro T synthesis, spermatogenesis, sperm motility, and semen volume. Sperm count and motility were significantly correlated in this group of patients, suggesting a common pathophysiology for the effect of varicocele on spermatogenesis and sperm motility. This common pathophysiology appears to be disturbed Leydig cell function resulting in decreased testicular androgen production, in turn causing inadequate spermatogenesis and epididymal function.

Adolescent↗
PubMed1978

Stimulation of cyclic adenosine 3':5'-monophosphate accumulation in human testes in vitro by luteinizing hormone, follicle-stimulating hormone, and prostaglandins.

The gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH) stimulate cyclic adenosine 3':5'-monophosphate (cyclic AMP) accumulation in human testicular incubates. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine acts synergistically with LH and FSH to enhance cyclic AMP accumulation. These studies indicate that cyclic AMP accumulation may be involved in the mechanism of action of LH and FSH in the human testes, as has been proposed for rat testes. The prostaglandins (PG PGE1, PGE2, PGA1, and PGF2alpha stimulate cyclic AMP levels at 10(-4) M in human testes. The E type prostaglandins are the most potent. They induce half-maximal stimulation of cyclic AMP at 7 x 10(-7) M.

1-Methyl-3-isobutylxanthine↗