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Query: UMLS:C0338671 (
Steroids
)
9,479
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Corpus luteum function in cynomolgus monkeys (Macaca fascicularis) during the menstrual cycle and immediately following parturition was evaluated through in vitro studies on progesterone production by dispersed luteal cells in the presence and absence of human
chorionic gonadotropin
(hCG) or human prolactin (hPRL). Luteal cells isolated between days 17-20 of the menstrual cycle secreted progesterone (P) during short-term incubation (21.6 +/- 1.2 ngP/ml/5 X 10(4) cells/3 hr, X +/- S.E., n = 7) and responded to the addition of 1-100 ng hCG with a significant (p less than 0.05) increase in P secretion. Cells removed the day of delivery secreted large, but variable (27.9-222 ng/ml, n = 4) amounts of P during short-term incubation. Moreover, hCG (100 ng/ml) stimulation of P production by cells at delivery (176 +/- 19% of control) was less than that of cells from the cycle of (336 +/- 65%). The presence of hPRL (2.5-5000 ng/ml) failed to influence P secretion by luteal cells during short-term incubation in the presence or absence of hCG. P production by luteal cells obtained following delivery declined markedly during 8 days of culture in Ham's F10 medium: 10% fetal calf serum. Continual exposure to 100 ng/ml of hCG or hPRL failed to influence P secretion through Day 2 of culture. Thereafter hCG progressively enhanced (p less than 0.05) P secretion to 613% of control levels at Day 8 of culture. In contrast, hPRL significantly increased P secretion (163% of control levels, p less than 0.05) between Day 2-4 of culture, but the stimulatory effect diminished thereafter. The data indicate that dispersed luteal cells from the cynomolgus monkey provide a suitable model for in vitro studies on the primate corpus luteum during the menstrual cycle, pregnancy, and the puerperium, including further investigation of the possible roles of gonadotropin and PRL in the regulation of luteal function in primates.
Steroids
1980 May
PMID:Progesterone production by luteal cells isolated from cynomolgus monkeys: effects of gonadotropin and prolactin during acute incubation and cell culture. 677 95
A major component of sexual maturation in the male rat is a progressive decline in serum concentrations of 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) and a concomitant increase in testicular testosterone biosynthesis and secretion. Chronic administration of synthetic luteinizing hormone releasing hormone (LHRH) or luteinizing hormone (LH)/human
chorionic gonadotropin
(hCG) to immature male rats has been shown to result in a delay in sexual maturation as evidenced by decreased sex accessory gland weights and altered testicular testosterone production. We have examined the postulate that such treatments may either reverse or retard the normal developmental pattern of serum testosterone and 3 alpha-diol concentrations. Chronic in vivo treatment of 28 day old immature male rats for 2 weeks with daily injections of either 0.5 micrograms of LHRH, 1.0 micrograms of LHRH, or 30 micrograms of LH was found to result in significant reductions in weights of the seminal vesicles and ventral prostate glands and diminutions in serum testosterone concentrations. Serum content of 3 alpha-diol was either unchanged or slightly elevated in the LHRH treated animals and increased significantly in the LH treated animals. These data suggest that either a reversal of or retardation in the normal developmental pattern of serum testosterone and 3 alpha-diol content has been achieved in the immature male rat by chronic LHRH or LH treatment.
Steroids
1980 Sep
PMID:Alteration in the normal pattern of serum testosterone and 5 alpha-androstane-3 alpha, 17 beta-diol in the immature male rat following chronic treatment with luteinizing hormone releasing hormone or luteinizing hormone. 700 79
The effect of steroids contained in oral contraceptives, namely ethinylestradiol:17 alpha-ethinyl-1,3,5,(10)-estratriene-3, 17-diol (E) and norethindrone acetate:17 beta-acetoxy-17-ethinyl-4-estren-3-one (N), on cell replication and human
chorionic gonadotropin
(hCG) secretion by choriocarcinoma cells in monolayer culture and by hydatidiform mole tissue maintained in organ culture were studied. The steroids were added to the culture medium individually or in combination to achieve a range of concentrations (10-10 to 10-4), within and beyond the presumed concentration of these substances in the blood of women taking oral contraceptives. The effect of luteinizing hormone releasing hormone (LHRH) on hCG secretion by choriocarcinoma cells in monolayer culture also was investigated. The rate of hCG production by either choriocarcinoma cells in monolayer culture or by hydatidiform mole tissue maintained in organ culture was not affected by the hormones used in this study; indeed hCG secretion remained reasonably unchanged even with high concentrations of steroids (up to 10-4 M) or LHRH (up to 10-4 mg x ml-1). Cell replication, as measured by increase in amount of cellular protein and DNA, was not stimulated by either of these compounds.
Steroids
1981 Jun
PMID:Failure of contraceptive steroids to modify human chorionic gonadotrophin secretion by hydatidiform mole tissue and choriocarcinoma cells in culture. 702 40
To characterize Leydig cell steroidogensis, we examined the metabolism of [3H]pregnenolone (3 beta-hydroxy-5-pregnen-20-one) to androgens in the presence and absence of human
chorionic gonadotropin
(hCG) as a function of culture duration. Approximately 20-30% of the (3H)pregnenolone was converted to testosterone (17 beta-hydroxy-4-androsten-3-one) by purified Leydig cells at 0, 3 and 5 days (d) of culture. Androstenedione (4-androstene-3,17-dione) and dihydrotestosterone (17 beta-hydroxy-5 alpha-androstan-3-one) were also produced while on day 5 of culture, significant amounts of progesterone (4-pregnene-3,20-dione) were isolated. The delta 5 intermediates, 17-hydroxypregnenolone (3 beta, 17-dihydroxy-5-pregnen-20-one) and dehydroepiandrosterone (3 beta-hydroxy-5-androsten-17-one), accounted for less than 1% of substrate conversion, indicating a clear preference for Leydig cells to metabolize (3H)pregnenolone via the delta 4 pathway. On day 0 of culture, unidentified metabolites considered of predominately polar steroids while on day 5 of culture, the unidentified metabolites consisted of predominately nonpolar steroids. In the presence of hCG, (3H-pregnenolone metabolism did not differ from basal on day 0 or 3 of culture. HCG increased the conversion of pregnenolone to progesterone and 17-hydroxyprogesterone (17-hydroxy-4-pregnene-3,20-dione) on 5d. This suggests that Leydig cells cultured for 5d have decreased C17-20 desmolase activity or that hCG acutely stimulates 3 beta-hydroxysteroid dehydrogenase and delta 5-delta 5 isomerase activities.
Steroids
1982 Nov
PMID:Steroid metabolism by purified adult rat Leydig cells in primary culture. 718 85
Corpus luteum (CL) function and control during pregnancy and early lactation in the pigtailed macaque was investigated. Peripheral concentrations of progesterone (P) on day 10 of pregnancy were 12.98 +/- 2.21 ng/ml and decreased progressively to 7.96 +/- 1.27 ng/ml by day 21 of pregnancy. The concentration of P increased around day 27 of gestation and reached peak levels of 18.48 +/- 2.45 ng/ml on day 37, thereafter gradually decreasing to a nadir at about midgestation. Ten days before parturition P concentrations increased again (P < 0.05). Concentrations of P decreased from 6.62 +/- 1.48 ng/ml on the day of delivery to 2.16 +/- 0.43 ng/ml on day 2 of lactation and remained low thereafter. Ovariectomy on day 35 did not affect the normal course of gestation or the patterns of P secretion during pregnancy. However, in these ovariectomized animals, in spite of suckling, P was not detectable after parturition. In intact monkeys, serum concentrations of P in the utero-ovarian vein at days 80 and 159 of pregnancy were higher relative to the uterine vein. Incubation studies utilizing 3H-cholesterol as a substrate revealed that the CL were capable of synthesizing P on days 35 and 159 of gestation. Histologically, the CL contained active luteal cells at late pregnancy. Low serum concentrations of
chorionic gonadotropin
were detected on day 10 of gestation; concentrations of this hormone reached high levels between days 18 and 24 and the titers were nondetectable after day 40 of pregnancy. Luteinizing hormone was present in constant amounts in the circulation during pregnancy and lactation. These data suggest that the CL of pregnancy in the pigtailed monkey is functional or capable of functioning during various stages of pregnancy. However, the fetoplacental unit is the primary source of P during the latter 4.5 months of gestation. As in other primates, a functional CL is not required for maintenance of pregnancy after implantation nor for lactation. Thus, the physiological significance of CL function during pregnancy is unclear.
Steroids
1980 Oct
PMID:Serum progesterone and corpus luteum function in pregnant pigtailed monkeys (Macaca nemestrina). 744 98
The effect of human
chorionic gonadotropin
(hCG) on intact Leydig cell phospholipid methylation was studied. Hormonal stimulation of rat Leydig cells increased the incorporation of [methyl-3H]methionine into phospholipids threefold. This effect was observed after 10 minutes of incubation time and was time and dose dependent with a maximal stimulation at 67 ng/ml of hCG. In the presence of hCG, 3H-labeled methyl groups were preferentially incorporated into phosphatidyl-N-monomethylethanolamine. This effect of hCG was not reproduced by dibutyryl cyclic adenosine monophosphate (cAMP), cholera toxin, or forskolin. Purified hCG beta subunit but not hCG alpha subunit had stimulatory activity on Leydig cell phospholipid methylation. We conclude that luteinizing hormone (LH)/hCG stimulates specifically Leydig cell phospholipid methylation, because LH-releasing hormone or [Arg8]-vasopressin did not modify these reactions. We postulate that these reactions are occurring at a cellular level that involves hormone-receptor interaction. It is also suggested that this biological response involves hCG beta subunit receptor interaction and does not require cAMP synthesis.
Steroids
1993 Jul
PMID:Human chorionic gonadotropin and free beta subunits stimulate phospholipid methylation in intact rat Leydig cells. 769 25
Steroidogenesis-stimulating activity (SSA) was examined in testicular intertubular fluid from normal, and short-term and long-term (up to 12 months) experimentally cryptorchid rats, using an in vitro Leydig cell bioassay based on testosterone production over 20 h in the presence of a maximum dose of human
chorionic gonadotropin
. Total fluid volume increased throughout the period of cryptorchidism, while intertubular testosterone concentrations declined. SSA from cryptorchid rats was significantly greater (2- to 3-fold) than normal at all time-points; however, the major increase in activity occurred within the first 4 weeks after treatment. Similar concentrations of lipoproteins were recovered from both untreated and 4-week cryptorchid fluid by density ultracentrifugation, although the bioactivity of the cryptorchid testis lipoprotein fraction was 8-fold higher than the lipoprotein fraction from untreated testes. Moreover, removal of the lipoproteins led to a loss of SSA in the lipoprotein-deficient fraction of the intertubular fluid. Consequently, the in vitro bioassay conditions were modified by addition of a constant level of serum lipoproteins to all assay wells. Employing the lipoprotein-supplemented bioassay, multiple stimulatory and inhibitory activities were resolved by Sephadex G-100 gel filtration in intertubular fluid from both normal and cryptorchid testes: (i) an inhibitory activity eluting in the void volume (> 150 kDa), which decreased after cryptorchidism; (ii) a stimulatory activity (40-80 kDa), which did not appear to be affected by cryptorchidism; (iii) an inhibitory activity (20-40 kDa) which decreased after cryptorchidism, and (iv) a stimulatory activity (12-20 kDa) which increased after cryptorchidism.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids
1994 Dec
PMID:Multiple factors with steroidogenesis-regulating activity in testicular intertubular fluid from normal and experimentally cryptorchid adult rats. 790 Jan 65
The present study examined the effects of naloxone (N) and naltrexone-methobromide (NMB; an opioid receptor antagonist that does not cross the blood-brain barrier) on testicular steroidogenesis during acute immobilization stress (IMO; 2 h) in adult rats. Unstressed rats as well as IMO rats were treated by unilateral intratesticular injection of N (20 micrograms/testis), NMB (36 micrograms/testis), or vehicle at the beginning of and at 1 h of the IMO period. In IMO rats serum T levels were significantly reduced, while serum luteinizing hormone levels were not affected. N and NMB normalized serum T levels in IMO rats and had no effects in controls. In IMO rats the activities of 3 beta-hydroxysteroid dehydrogenase (HSD) and P450(17 alpha, lyase) were significantly reduced, while the activity of 17 beta-HSD was not affected. N and NMB antagonized the inhibitory effect of IMO on 3 beta-HSD and P450(17 alpha, lyase) but did not alter enzyme activity in freely moving rats. Acute IMO decreased basal and human
chorionic gonadotropin
-stimulated androgen production by hemitestis preparation, but N (10(-4) M) added directly to the incubation medium blocked the decrease and had no effect on testes from freely moving control rats. These results support the conclusion that endogenous opioid peptides are potentially important paracrine regulators of testicular steroidogenesis under stress conditions.
Steroids
1997 Nov
PMID:The effect of opioid antagonists in local regulation of testicular response to acute stress in adult rats. 936 9
A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism. With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. Hypogonadism returned, but was successfully treated with weekly injections of human
chorionic gonadotropin
for three months. Testicular function remained normal thereafter on no treatment. The use of human
chorionic gonadotropin
should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic
steroid abuse
.
...
PMID:Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin. 953 90
During the second half of the luteal phase, the human corpus luteum becomes responsive to regular luteinizing hormone (LH) pulses. These LH pulses stimulate progesterone secretion tonically, and during this tonic stimulation, additional LH-independent progesterone pulses occur, which are particularly pronounced in women with human
chorionic gonadotropin
-stimulated luteal function. No progesterone pulses are seen in women suffering from corpus luteum deficiency due to absent LH pulses. The corpus luteum thus has a progesterone pulse generator turned on by gonadotropins but functioning for several hours without further gonadotropic support. This pulse generator appears to be regulated by intraluteal auto-/paracrine mechanisms, which we have investigated in a porcine model using molecular, cellular, and in vivo tools. Luteal oxytocin and progesterone release occurs in tightly coupled pulses. In vivo, oxytocin and prostaglandin F2 alpha(PGF2 alpha) stimulate estradiol and progesterone release and estradiol itself further stimulates progesterone release. Analysis of the different luteal cell compartments (large luteal cells, small luteal cells, fibroblasts) suggests an intraluteal circuit that involves paracrine effects of estradiol, oxytocin, and PGF2 alpha. At the time of luteolysis, the luteotropic effects of estradiol are inhibited by tumor necrosis factor derived from invading macrophages and the intraluteal circuit is thereby disrupted, leading to luteolysis.
Steroids
PMID:Regulation of steroid production and its function within the corpus luteum. 961 90
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