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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immature hypophysectomized rats were injected with 2mg of diethylstilbestrol to increase granulosa cell numbers and with 20 IU of PMS to stimulate ovarian growth. Steroid 17 alpha-hydroxylase activity of cultured granulosa cell, harvested from mature follicles 48 h after injection of PMS, was demonstrated using a tritium exchange assay with 17 alpha 3H-pregneneolone as substrate. For comparison, aromatase activity of the same cells was examined by a similar assay using 1 beta 3H-testosterone as the substrate. The activities of the two enzymes were similar when expressed in terms of the amount of substrate converted per unit time. While an NADPH generating system in the incubation medium was essential for demonstrating any hydroxylase activity, 10-15% of the total aromatase activity could be found without added cofactor. Attempts to alter hydroxylase activity of granulosa cells by inclusion of LH, FSH or prolactin in the incubation medium were unsuccessful. However, activity could be change by prostaglandins (PG) or agents which can alter PG synthesis. Activity was increased by low concentrations of phospholipase A2 (PLA2), histamine, and arachidonic acid (AA). Large doses of PLA2, or AA, were inhibitory. PGE2, but not PGF2 alpha, increased, while indomethacin decreased, hydroxylase activity. The results clearly indicate that granulosa cells in the rat have a potent 17-hydroxylase system and therefore do not support the widely held contention that lack of this enzyme is one of the bases for the need for two kinds of cells for ovarian estrogen production.
Steroids 1981 Nov
PMID:Steroid 17 alpha-hydroxylase activity of ovarian granulosa cells from hypophysectomized immature rats treated with pregnant mare's serum gonadotropin (PMS). 679 17

The influence of androgens on the FSH modulation of progestin biosynthetic enzymes was studied in vitro. Granulosa cells obtained from immature, hypophysectomized, estrogen-treated rats were cultured for 3 days in a serum-free medium containing FSH (20 ng/ml) with or without increasing concentrations (10(-9)-10(-6)M) or 17 beta-hydroxy-5 alpha-androstan-3-one (dihydrotestosterone; DHT), 5 alpha-androstane-3 alpha,17 beta-diol (3 alpha-diol), or the synthetic androgen 17 beta-hydroxy-17-methyl-4,9,11-estratrien-3-one (methyltrienolone; R1881). FSH treatment increased progesterone and 20 alpha-hydroxy-4-pregnen-3-one (20 alpha-OH-P) production by 10.2- and 11-fold, respectively. Concurrent androgen treatment augmented FSH-stimulated progesterone and 20 alpha-OH-P production in a dose-related manner (R1881 greater than 3 alpha-diol greater than DHT). In the presence of an inhibitor of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), the FSH-stimulated pregnenolone (3 beta-hydroxy-5-pregnen-20-one) production (a 20-fold increase) was further enhanced by co-treatment with R1881, 3 alpha-diol or DHT. Furthermore, FSH treatment increased 4.4-fold the activity of 3 beta-HSD, which converts pregnenolone to progesterone. This stimulatory action of FSH was further augmented by concurrent androgen treatment. In contrast, androgen treatment did not affect FSH-stimulated activity of a progesterone breakdown enzyme, 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSD). These results demonstrate that the augmenting effect of androgens upon FSH-stimulated progesterone biosynthesis is not due to changes in the conversion of progesterone to 20 alpha-OH-P, but involves an enhancing action upon 3 beta-HSD/delta 5,delta 4-isomerase complexes and additional enzymes prior to pregnenolone biosynthesis.
Steroids 1982 Dec
PMID:Androgen regulation of progestin biosynthetic enzymes in FSH-treated rat granulosa cells in vitro. 682 Dec 86

We have characterized the degree of asymmetry of ovarian steroid secretion in the luteal phase of the menstrual cycle in rhesus and cynomolus monkeys. Femoral blood levels of FSH, LH, progesterone, estradiol and 17-hydroxyprogesterone were determined. In addition, laparotomies were performed in the early, mid or late luteal phase to facilitate localization of the corpus luteum and collection of ovarian venus blood. We conclude that: 1) the ovary bearing the active corpus luteum contributes virtually all of the progesterone entering peripheral circulation in the luteal phase; 2) the ipsilateral ovary secretes more 17-hydroxyprogesterone one than the contralateral one, although both are active in the luteal phase; and 3) the asymmetrical secretion of estradiol was manifest only in the early and mid-luteal phase, with ovarian symmetry being reestablished in the late luteal phase.
Steroids 1982 Apr
PMID:Asymmetric secretion of principal ovarian venous steroids in the primate luteal phase. 717 54

Androgens influence some immunological processes, including the differentiation of T-cells in CD4+ (helpers) or CD8+ (suppressors/cytotoxic) phenotype. In nine postmenopausal osteoporotic women the effect of stanazolol on lymphocyte counts, CD3+ and the immunoregulatory index (CD4+/CD8+) were investigated. In the placebo group, ten postmenopausal osteoporotic women of similar age were included. The means of the investigated indices after stanazolol as compared with the values before treatment were as follows: lymphocyte counts (cells/microL +/- SEM) 2974 +/- 225 versus 2313 +/- 166, CD3+ (%) 54.3 +/- 5.5 versus 70.9 +/- 1.6 (P < 0.05); CD4+/CD8+ ratio 1.8 +/- 0.02 versus 2.5 +/- 0.28 (P < 0.05). The values after placebo as compared with the values before placebo were: 2558 +/- 201 versus 2370 +/- 256, 62.9 +/- 2.1 versus 64.8 +/- 1.7 and 1.6 +/- 0.2 versus 1.6 +/- 0.1 in sequence. The treatment was controlled by the serum stanazolol levels before and after steroid administration (unmeasurable versus 20.8 +/- 3.4 nmol/L, P < 0.01). The good compliance of the therapy was confirmed by a decline of serum LH (U/L; 30.1 +/- 3.1 versus 24.7 +/- 2.8, P = 0.014), FSH (U/L; 108.9 +/- 13.1 versus 93.3 +/- 12.8, P = 0.012) and serum sex hormone binding globulin (SHBG; nmol/L; 53.3 +/- 13.3 versus 11.2 +/- 1.9, P < 0.01). The decline of SHBG indicates a good tissue sensitivity to the androgen. There were no significant differences between hormonal parameters before and after placebo treatment. In conclusion, the immunosuppressive effect of the androgen, stanazolol, was confirmed in the investigated postmenopausal osteoporotic women.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1995 Jul
PMID:A decreasing CD4+/CD8+ ratio after one month of treatment with stanazolol in postmenopausal women. 748 25

The preovulatory gonadotropin surge is induced by progesterone in the cycling female rat or in the ovariectomized estrogen-treated female rat after adequate estrogen-priming activity is present. The source of progesterone under physiological conditions could be the ovary and/or the adrenal. Since the GnRH neuron does not possess estrogen and progesterone receptors, its function is modulated by other CNS neurotransmitters and neurosecretory products. Among these, excitatory amino acids (EAAs) have now been shown to play an important role in the regulation of pulsatile gonadotropin release, induction of puberty and preovulatory and steroid-induced gonadotropin surges. Glutamate, the major endogenous EAA exerts its action through ionotropic and metabotropic receptors. The ionotropic receptors consist of two major classes, the NMDA (N-methyl-D-aspartate) and non-NMDA: kainate and AMPA (DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors. EAA receptors are found in hypothalamic areas involved with reproduction. While both NMDA and non-NMDA receptors are involved in the regulation of LH secretion, the NMDA receptors appear to be involved with the regulation of puberty and FSH secretion as well. Steroids increase the release rates of glutamate and aspartate in the preoptic area during the gonadotropin surge. Steroids may also regulate the hypothalamic AMPA receptors.
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PMID:Glutamate: a major neuroendocrine excitatory signal mediating steroid effects on gonadotropin secretion. 762 74

The present study was designed to explore the steroidogenic responsiveness of ovine antral follicles of different sizes when cultured for varying time-periods with different doses of pregnenolone. Antral follicles of different sizes were isolated from sheep ovaries and cultured in medium 199 with or without pregnenolone in the presence or absence of FSH for 1, 6, 10, and 24 hours at 37 C. The levels of progesterone and estradiol in the spent medium were estimated. In the absence of pregnenolone, steroid production by the follicles did not increase significantly beyond 1 hour of culture. However, in the presence of pregnenolone there was a significant increase in progesterone production at 6, 10, and 24 hours of culture compared to controls. Estradiol levels were unaffected. Addition of FSH in combination with pregnenolone failed to increase progesterone or estradiol levels beyond that seen with pregnenolone alone. These data demonstrate that short-term incubation of follicles is sufficient for the secretion of steroids into the culture medium and supplementation of the culture medium with an immediate precursor is essential for optimal steroidogenesis in vitro.
Steroids 1993 Aug
PMID:Steroidogenesis in sheep ovarian antral follicles in culture: time course study and supplementation with a precursor. 821 88

Physiological gonadotropin levels are modulated by complex interrelationships between the sex steroids and the hypothalamic GnRH pulse generator, and the steroids and GnRH individually regulate gonadotropin subunit (alpha, LH beta, FSH beta) gene expression. Steroids may act directly at the pituitary level or indirectly at the hypothalamus to alter GnRH pulses, and they can have positive or negative actions, depending on the model system and physiological state. GnRH pulse frequency and amplitude have subunit-specific effects on the gonadotropin genes, and alteration of pulse frequency during the reproductive cycle can selectively favor LH or FSH synthesis. The cloning of the gonadotropin subunit genes and sensitive molecular approaches to the study of transcriptional regulation have permitted insights into the sites of steroid and GnRH action and into the mechanisms by which such hormonal effects occur. This review describes several such approaches including the measurement of endogenous gene transcription by nuclear run-off assays, definition of hormone-sensitive gene regions by transient transfection analysis, and the use of transgenic animal technology to verify hormonal and tissue-specific control of gene expression. Recent studies in the rat model suggest that some steroid actions, such as estrogen stimulation of LH beta gene transcription and alteration of estrogen and GnRH receptor number, occur directly at the level of the pituitary, while suppressive effects of estrogen on gonadotropins may occur at least partly if not primarily via hypothalamic effects. Changes in GnRH pulses may also alter GnRH receptor number, thus modifying the potential signal received by the gonadotroph. Current and emerging molecular technologies will probably identify additional targets of steroid and GnRH action and allow greater insight into gonadotropin regulation and reproductive function.
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PMID:Gonadotropin gene modulation by steroids and gonadotropin-releasing hormone. 878 77

Estradiol secreted by growing ovarian follicle(s) has been considered classically to be the neural trigger for the preovulatory surge of gonadotropins. The observation that the estradiol-induced gonadotropin surge in ovariectomized rats is of lesser magnitude and duration than that found in the cycling rat at proestrus has resulted in a search for other steroid regulators. Progesterone is a major regulator of the preovulatory gonadotropin surge. It can only act in the presence of an estrogen background, which is necessary for the synthesis of progesterone receptors. In the estrogen-primed ovariectomized rat, progesterone is able to initiate and enhance the gonadotropin surge to the magnitude observed on the day of proestrus and limit it to 1 day. The physiological role of progresterone in the induction of the preovulatory gonadotropin surge has been demonstrated by the attenuation of the progesterone-induced surge and the endogenous proestrus surge by progesterone receptor antagonist RU486 and the progesterone synthesis inhibitor trilostane. The promoter region of the follicle-stimulating hormone (FHS)-beta gene contains multiple progesterone response elements and progesterone brings about FSH release as well. The reduction of progesterone in the 5 alpha-position appears to be important for the regulation of progesterone secretion. Corticosteroids appear to play a significant role in the secondary FSH surge on late proestrus and early estrus.
Steroids 1998 Dec
PMID:Regulation of the preovulatory gonadotropin surge by endogenous steroids. 987 Feb 58

Products of Chicken Embryo (PCE) such as Ji-Pei-Jing is a kind of food for Chinese children prepared from chicken embryo. Female rats on 21 days were administered with aqueous solutions of Ji-Pei-Jing (1.2%, 3%, 12%, and 48%, respectively) by gavage up to their onsets of puberty. The rats in the control group were treated with distilled water. However, Ji-Pei-Jing treatment exerted some effects on sexual maturation in the immature female rats. Essentially, the effects showed a dose-response tendency with an inverted "U" shape. The age of vaginal opening for group treated with Ji-Pei-Jing was significantly earlier than that to the control. Its uterus weight/b.w. ratio also significantly increased on day 30 and at the first estrus. There were significantly increases in the adrenal weight/b.w. ratio of 30-day-old rats that were treated with 3%, 12%, and 48% Ji-Pei-Jing. The rats treated with 48% Ji-Pei-Jing had significantly lesser ovary weight/b.w. ratio on day 30, too. The rats treated with Ji-Pei-Jing could normally ovulate at the first estrus, and no significant differences were observed during estrous cycles. The effects of PCE on serum levels of E2, P, LH in 30-day-old rats and FSH in 28-day-old rats were elevated significantly by 3% Ji-Pei-Jing treatment. It appears that the effects of PCE result from interaction of contained complex physiologically active substances. Steroids, especially estradio-17 beta, possibly play a key role, and polypeptide hormones may also exert important effects.
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PMID:Effects of "products of chicken embryo" on growth and sexual development in rats. 1056 May 38

Progesterone (P) is secreted by the corpus luteum under the control of gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH). Progesterone (P) is essential for reproduction because: (1) it induces in the endometrium the transcription of specific genes involved in the implantation of the blastocyst, (2) it modulates GnRH/LH secretion by decreasing GnRH pulse frequency, which in turn enriches the gonadotroph cells in FSH and avoids a second LH surge. Using the ewe as a model, we investigated the immediate GnRH and LH responses to acute changes of circulating P levels. Our results show that P changes cause dramatic modifications in GnRH pulse frequency: P removal induces an acceleration of the pulse generator, while P administration slows the pulse frequency. LH secretion was modified in parallel to the changes in GnRH. Other experiments proved that these neuroendocrine effects of P are mediated by P itself, not by its hydroxylated metabolites, and occur at the level of P receptors. Finally, these effects require priming by estradiol. Additionally, in the final stage of the follicular phase, P plays a role in the triggering of the LH surge. This has been shown in rodents, non-human primates, and in women. Such a phenomenon is not observed in ewes, although in these species luteal P modulates the amplitude of the estradiol-induced LH surge.
Steroids
PMID:Neuroendocrine effects of progesterone. 1110 67


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