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PubMed1998

Bovine ovarian non-genomic progesterone binding sites: presence in follicular and luteal cell membranes.

We have shown recently that the bovine corpus luteum (CL) possesses specific luteal cell surface membrane binding sites for progesterone. We have now confirmed and extended these observations to compare the subcellular distribution of these binding sites in developing, mature and regressing CL. The median buoyant densities of luteal progesterone binding sites from early-, mid- and late-luteal phase CL were similar (though three of five density profiles for late-luteal phase CL showed association of steroid binding with a fraction with a lower density), and clearly resolved from nuclear, mitochondrial, lysosomal, peroxisomal, Golgi-endoplasmic reticulum-lysosomal and smooth endoplasmic reticulum markers. Specific binding of [3H]progesterone overlapped with the distributions of 5'-nucleotidase and luteinizing hormone receptor (luteal cell surface membrane markers) in both control and digitonin-treated gradients at all stages of the luteal phase. Since steroidogenic 'large luteal' and 'small luteal' cells of the CL are derived from the granulosa cells (GC) and theca of the preovulatory follicle, we also investigated whether similar receptors were present in the follicle, and describe for the first time specific membrane binding sites for progesterone in purified GC and thecal membranes from healthy bovine follicles of different sizes. Specific binding increased linearly with GC and thecal membrane protein concentration; however, it was detectable only when digitonin was included in the binding incubation. Binding sites were specific for progesterone; unlabelled progesterone competed for [3H]progesterone binding at low concentrations (IC50, 35 and 31 nmol/l) compared with testosterone (IC50, 905 and 870 nmol/l) and delta4-androstenedione (IC50, 1050 and 660 nmol/l) for GC and thecal receptors respectively. In contrast, oestradiol, oestrone, pregnenolone, cortisol, cholesterol, and a genomic progesterone receptor antagonist, RU486, competed poorly. Steroid binding was present in GC and thecal membranes of follicles of all sizes, but [3H]progesterone binding to GC membranes decreased significantly with increasing follicle size (P<0.02), perhaps indicating developmental regulation of GC membrane non-genomic progesterone receptors in the preovulatory bovine follicle. We suggest that these membrane steroid receptors may be involved in the autocrine/paracrine regulation of follicular function by progesterone.

Animals↗

PubMed2001

Immunolocalization of progesterone receptors in the canine ovary and their relation to sex steroid hormone concentrations.

The aim of the present study was to describe the normal cellular distribution of progesterone receptors in the canine ovary at different stages of the oestrous cycle. Samples of both ovaries were obtained from 75 healthy adult bitches of various breeds and ages, including five pregnant bitches and three bitches that had just delivered. The presence of progesterone receptors was visualized by immunohistochemistry on paraffin wax sections using a monoclonal antibody. Nuclear staining for progesterone receptors was observed in the surface epithelium, cortical tubules, rete ovarii, follicle cells, thecal cells, luteal cells, granulosa cell cords and ovarian stroma. The staining intensity for progesterone receptors in the follicle cells increased with the stage of follicle development, indicating an intrafollicular role of progesterone in the mechanism of ovulation and luteinization. The stronger staining intensities for progesterone receptors in thecal cells compared with follicle cells may be explained by the fact that thecal cells mediate some effects of steroid hormones on the follicle cells in secondary and tertiary follicles. Little correlation was found between the expression of progesterone receptors in follicle cells and oestradiol, progesterone or testosterone concentrations. This finding indicates a different regulating mechanism for progesterone receptors in canine ovarian follicles compared with other tissues of the genital tract. During pregnancy all groups of ovarian cells had lower staining intensity scores than during the oestrous cycle, although the sex steroid hormone concentrations in pregnant bitches were similar to those in non-pregnant bitches during the luteal phase of the oestrous cycle. The lower expression of progesterone receptors during pregnancy may be due to higher tissue concentrations of progesterone that are not reflected in the serum because of haemodilution and increased metabolism and clearance during pregnancy.

Animals↗

PubMed2006

Progesterone for Premenstrual Syndrome.

BACKGROUND: Premenstrual Syndrome (PMS) is the term for severe symptoms experienced by about 5% of menstruating women up to two weeks before their menstrual periods, but not at other times. Treatment with progesterone may restore a deficiency, or balance the level of progesterone with other menstrual hormones. Progesterone therapy may reduce the effects of falling progesterone levels on the brain or on electrolytes in the blood. OBJECTIVES: The objectives were to determine if progesterone has been found to be an effective treatment for all or some premenstrual symptoms, and if adverse events associated with this treatment have been reported. SEARCH STRATEGY: We last searched the Cochrane Menstrual Disorders and Subfertility Group's Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, Issue 1, 2005), MEDLINE (1966 to 2005) and EMBASE (1980 to 2005) in March 2005, and PsycINFO (1806 to 2006) in April 2006. We contacted pharmaceutical companies for information about unpublished trials. SELECTION CRITERIA: We included randomised double-blind, placebo-controlled trials of progesterone on women with PMS diagnosed by at least two prospective cycles, without current psychiatric disorder. DATA COLLECTION AND ANALYSIS: Two reviewers (BM and OF) extracted data independently, and decided on the trials to be included. OF wrote to the trial investigators to ask for missing data. MAIN RESULTS: We considered 17 studies. We included two trials totaling 280 participants aged from 18 to 45 years. Of these 115 yielded analysable results. Both studies measured outcomes using subjective scales of symptom severity but made calculations as if they were interval data. The two studies differed in design, participants, dose of progesterone, how and when the dose was administered and in outcome measures. It was impossible to combine data in a meta-analysis. Adverse events which may or may not have been the side effects of the treatment, were generally described as mild. Both trials intended to exclude women whose symptoms continued after their periods; unfortunately the larger multicentre study had some ineligible participants. Overall, participants benefited more from progesterone than placebo. This was statistically significant in per protocol analysis but not in the intention-to-treat analysis, except for the first cycle. The smaller, crossover study found no statistically significant difference between oral progesterone, vaginally absorbed progesterone and placebo. AUTHORS' CONCLUSIONS: We could not say that progesterone helped women with PMS, nor that it was ineffective. Neither trial distinguished a subgroup of women who benefited.

Female↗

PubMed1997

The hyperventilation of cirrhosis: progesterone and estradiol effects.

Progesterone and estradiol are metabolized in the liver and are elevated in patients with cirrhosis. Progesterone stimulates ventilation by activating progesterone receptors in the central nervous system; estradiol may facilitate progesterone's actions by increasing progesterone receptors. This study evaluated whether progesterone and estradiol contribute to the respiratory alkalosis common in cirrhotic patients. Arterial blood gases and progesterone and estradiol levels were obtained in 50 patients with cirrhosis. Multiple linear regression revealed a statistically significant correlation between PaCO2 and progesterone and estradiol (r = .54, P < .05). Patients with severe hyperventilation (PaCO2 < or = 30 mm Hg) had statistically higher levels of progesterone and estradiol than did patients with mild hyperventilation (30 < PaCO2 < or = 35) or normal ventilation (PaCO2 > 35) (P < .05). Although the progesterone levels were two orders of magnitude lower than those associated with hyperventilation in pregnant patients, the increased ventilatory effect may be because of the altered blood-brain barrier (BBB) present in cirrhotic patients. Progesterone and estradiol appear to contribute to the hyperventilation in cirrhotic patients.

Adult↗

PubMed2002

Progesterone attenuates the inhibitory effects of cardiotonic digitalis on pregnenolone production in rat luteal cells.

Previous studies have shown that digoxin decreases testosterone secretion in testicular interstitial cells. However, the effect of digoxin on progesterone secretion in luteal cells is unclear. Progesterone is known as an endogenous digoxin-like hormone (EDLH). This study investigates how digitalis affected progesterone production and whether progesterone antagonized the effects of digitalis. Digoxin or digitoxin, but not ouabain, decreased the basal and human chorionic gonadotropin (hCG)-stimulated progesterone secretion as well as the activity of cytochrome P450 side chain cleavage enzyme (P450scc) in luteal cells. 8-Br-cAMP and forskolin did not affect the reduction. Neither the amount of P450scc, the amount of steroidogenic acute regulatory (StAR) protein, nor the activity of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) was affected by digoxin or digitoxin. Moreover, in testicular interstitial and luteal cells, progesterone partially attenuated the reduction of pregnenolone by digoxin or digitoxin and the progesterone antagonist, RU486, blocked this attenuation. These new findings indicated that (1) digoxin or digitoxin inhibited pregnenolone production by decreasing the activity of P450scc enzyme, but not Na(+)-K(+)-ATPase, resulting in a decrease on progesterone secretion in rat luteal cells, and (2) the inhibitory effect on pregnenolone production by digoxin or digitoxin was reversed partially by progesterone. In conclusion, digoxin or digitoxin decreased progesterone production via the inhibition of pregnenolone by decreasing P450scc activity. Progesterone, an EDLH, could antagonize the effects of digoxin or digitoxin in luteal cells.

17-Hydroxysteroid Dehydrogenases↗

PubMed1986

Calcium effects on progesterone accumulation and oocyte maturation in cultured follicles of Rana pipiens.

Pituitary homogenates (FPH) provoke a cascade of responses in the amphibian ovarian follicle, culminating in progesterone biosynthesis and oocyte maturation (GVBD). Calcium may play an important role as an intracellular second messenger in regulating these physiological responses. Experiments were carried out on cultured, isolated follicles of Rana pipiens to assess the effects of varying extracellular calcium on follicular progesterone accumulation and oocyte maturation. In hormonally unstimulated follicles, an increase in extracellular Ca2+ alone produced a significant increase in progesterone in methanol extracts of follicles after 4 hours of culture, and in some cases also provoked oocyte maturation assessed after 24 hours of culture. In no case did elevated Ca2+ alone stimulate maximal progesterone accumulation as compared with FPH-stimulated follicles, although the time-course of accumulation was similar. The calcium ionophore, A-23187, similarly increased progesterone accumulation in a dose-dependent manner when introduced in amphibian Ringer's (1.35 mM Ca2+), but inhibited progesterone elevation caused by increasing calcium concentrations in the culture media and FPH stimulation. Depleting free calcium from the culture medium with graded doses of the chelator EGTA decreased FPH-induced progesterone accumulation and inhibited FPH- and progesterone-induced GVBD. The calcium channel blocker, verapamil, also inhibited FPH-induced progesterone accumulation and GVDB in a dose-dependent manner, while having no effect on progesterone-induced meiotic resumption. These data strongly implicate intracellular calcium levels regulating progesterone production by ovarian follicle cells and subsequent oocyte maturation.

Animals↗

PubMed1994

Progesterone modulation of estrogen receptors in microdissected regions of the rat hypothalamus.

One mechanism whereby progesterone opposes the regulatory actions of estrogen in the brain may include the down-regulation of estrogen receptors. A previous study has shown a small decrease in estrogen binding in the combined preoptic area-hypothalamic area in response to progesterone treatment. To determine if this effect is region specific, gonadectomized/adrenalectomized (GDX/ADX) estrogen-treated female rats were administered a single injection of progesterone (5.0 mg, sc) or a silastic capsule containing crystalline progesterone. Control animals were treated identically but without progesterone exposure. Animals were killed 24 or 72 h after initiating progesterone treatment and estrogen binding was measured in cytosol and cell nuclear extracts of the anterior pituitary, mediobasal hypothalamus (MBH), and preoptic area. A significant effect of progesterone injection on nuclear estrogen binding was observed in the MBH at 24 h. This effect had subsided by 72 h. No effect was observed when progesterone was administered in a continuous fashion. To further examine the regional specificity of the progesterone effect and to determine if males were similarly affected, nuclear-bound estrogen receptors were measured in microdissected brain regions from male and female estrogen-treated GDX/ADX rats treated with 5.0 mg progesterone or vehicle 24 h before sacrifice. A significant decrease in estrogen binding was found in the ventromedial nucleus of the female but not the male. A significant effect of progesterone treatment was found in the periventricular preoptic area of the male.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗

PubMed1983

Progesterone and estradiol in the saliva and plasma during the menstrual cycle.

Plasma and salivary progesterone and estradiol were measured throughout nine menstrual cycles and before and after intramuscular injection of progesterone in four women. Mean +/- standard error of the mean (SE) salivary progesterone increased significantly from 238.7 +/- 14.3 pg/ml in the proliferative phase to 475.3 +/- 39.8 pg/ml in the secretory phase (p less than 0.001). There was a highly significant correlation between plasma and salivary progesterone levels throughout the menstrual cycle (r = 0.5841, p = 0.001). The ratio of plasma to salivary progesterone was 6.4 during the proliferative phase and increased to 26.7 during the secretory phase. Free unbound progesterone as determined by equilibrium dialysis gave a mean +/- SE level of 126.8 +/- 6.9 pg/ml during the proliferative phase and increased significantly to 196.8 +/- 18.8 pg/ml during the secretory phase (p less than 0.001). The corresponding levels in the plasma were 88.5 +/- 11.2 pg/ml, which increased significantly to 332.2 +/- 39.2 pg/ml (p less than 0.001). Free progesterone constituted 53.7% and 41.4% of salivary progesterone during the proliferative and secretory phases, respectively, whereas the corresponding percentages in the plasma were 5.8% and 2.6%. Both plasma and salivary progesterone levels increased in a dose-dependent manner after an intramuscular injection of progesterone, with peak levels being attained from 2 to 3 hours after the injection. Salivary estradiol levels were 5 to 18 and 8 to 35 pg/ml in the proliferative and secretory phases, respectively, but showed no correlation with plasma estradiol levels. The findings are discussed in relationship to the origin of salivary progesterone and the potential use of it as an index of ovulation.

Dose-Response Relationship, Drug↗

PubMed1976

Pentobarbital inhibition of progesterone-induced behavioral estrus in ovariectomized guinea pigs.

Administration of pentobarbital inhibits the facilitatory effects of progesterone on the release of gonadotropins. In this experiment facilitatory effects of progesterone on lordosis behavior in guinea pigs were examined with pentobarbital anesthesia. Two major animal groups were subjects: one was short-term ovariectomized (2 weeks) and the other was long-term ovariectomized (several months). All animals received estradiol benzoate (6.6 mug s.c.) followed by progesterone (0.4 mg s.c.) 40 h later. Lordosis behavior was induced by the manual stimulation method of Young et al.29 Sodium pentobarbital (30 mg/kg) was injected 8,4 or 2 h before, simultaneously or 1, 2, 6, or 7 h after progesterone. Animals which received pentobarbital slept for 4.5-5 h with subsequent drowsiness for an additional 0.5-1 h. Pentobarbital injections given 8 h before progesterone had no effect on latency to the first lordosis or on other parameters of estrous behavior. However, pentobarbital delayed the onset of heat in estrogen treated ovariectomized guinea pigs when given 4 h before, 2 h before, or simultaneously with progesterone. The delay was directly related to the length of time the animals remained asleep after the progesterone injection, since estrous behavior was invariably displayed with the latency of controls after the animal awoke. Moreover, in animals which were awake for 1-2 h immediately after the progesterone injection before receiving pentobarbital, the latency of recovery from anesthesia to the first display of lordosis was about 1-1.5 h shorter than in the other pentobarbital groups. In contrast to the latency effects of pentobarbital, the duration of heat was unaffected by the anesthetic for all groups mentioned. In animals which received pentobarbital after they were already in heat, pentobarbital injection terminated heat and abolished it completely, since lordosis behavior was not displayed in the hours after recovery from anesthesia. Gross hypothalamic uptake of progesterone was not influenced by pentobarbital administration. Thus, it is tentatively concluded that an incubation period is necessary for progesterone to mediate the display of estrous behavior in the guinea pig in addition to the time necessary for neural uptake. The way in which pentobarbital interferes with the period of progesterone incubation is not currently known.

Animals↗

PubMed1976

The head extractions, brain and pituitary uptake and metabolism of progesterone and 5alpha-dihydroprogesterone in anesthetized, female rabbits.

Three days after ovariectomy adult female rabbits were injected intramuscularly with either 2 mug estradiol/kg b.w., 0.5 mg progesterone/kg b.w., 2 mug estradiol plus 0.5 mg progesterone/kg b.w., or oil vehicle daily for 5 days. On the sixth day the animals were anesthetized and given a continuous infusion of [14C]progesterone and [3H]5alpha-pregnane-3,20-dione (5alpha-DHP) for 4 h via the femoral vein. Head extractions, calculated from the difference in blood concentrations of radioactive steriods between the femoral artery and jugular vein, were in the range of 60-75% for both progesterone and 5alpha-DHP and were unaffected by the hormone treatments. Nine brain areas and the pituitary were analyzed for [14C]progesterone, [3H]5alpha-DHP and [14C]-5alpha-DHP. Generally, the brain and pituitary retention and distribution of [14C]progesterone and [3H]5alpha-DHP and the brain and pituitary metabolism of [14C]progesterone were unaffected by hormone treatments. In the cerebellum, progesterone treatment increased [14C]progesterone retention as compared to oil treatment. All tissues contained 2-7 times more [14C]progesterone than arterial blood concentrations. [3H]5alpha-DHP tissue: arterial blood concentrations ratios were much lower ranging from 0.9 to 1.78. [14C]progesterone and [3H]5alpha-DHP showed similar brain distribution with highest concentrations in the pons, pons reticulum and midbrain reticulum. All tissues converted progesterone to 5alpha-DHP, but only the cerebellum contained more [14C]5alpha-DHP than [14C]progesterone.

20-alpha-Dihydroprogesterone↗

PubMed1989

Inhibitory effects of the antiprogestin, RU 486, on progesterone actions and luteinizing hormone secretion in pituitary gonadotrophs.

The effects of RU 486 on the modulation of LH release by progesterone were investigated in cultured anterior pituitary cells from ovariectomized adult female rats. The inhibitory effect of progesterone on LH secretion was demonstrable in estrogen-treated pituitary cells, in which addition of 10(-6) M progesterone to cells cultured in the presence of 10(-9) M estradiol for 52 h reduced the LH response to GnRH (10(-11) to 10(-7) M). When RU 486 was superimposed upon such combined treatment with estradiol and progesterone, the suppressive effect of progesterone on GnRH-induced LH release was completely abolished. The converse (facilitatory) effect of progesterone on LH secretion was observed in pituitary cells pretreated with 10(-9) M estradiol for 48 h and then with 10(-6) M progesterone for 4 h. When RU 486 was added together with progesterone during the 4 h treatment period, the facilitatory effect of progesterone was blocked and LH release fell to below the corresponding control value. The direct effect of RU 486 on LH secretion in the absence of exogenous progesterone was evaluated in cells cultured in the absence or presence of 10(-9) M estradiol and then treated for 4 to 24 h with increasing concentrations of RU 486 (10(-12) to 10(-5) M) and stimulated with GnRH (10(-9) M) during the last 3 h of incubation. In estrogen-deficient cultures, 4 h exposure to RU 486 concentrations of 10(-6) M and above decreased the LH response to GnRH by up to 50%. In cultures pretreated with 10(-9) M estradiol, GnRH-stimulated LH responses was inhibited by much lower RU 486 concentrations, of 10(-9) M and above. After 24 h of incubation the effects of RU 486 were similar in control and estradiol-pretreated pituitary cell cultures. Thus, RU 486 alone has a significant inhibitory effect on LH secretion that is enhanced in the presence of estrogen. The antiprogestin is also a potent antagonist of both the inhibitory and the facilitatory actions of progesterone upon pituitary gonadotropin release in vitro.

Animals↗

PubMed1991

Metabolic regulation of plasma apolipoprotein E by estrogen and progesterone in the baboon (Papio sp).

Apolipoprotein (apo) E plays an important role in the metabolism of lipoproteins. To determine the effects of estrogen and progesterone on plasma levels and metabolism of apo E, we used 12 ovariectomized baboons fed a cholesterol- and fat-enriched diet. These baboons were divided into four groups and treated with estrogen, progesterone, estrogen + progesterone, and a placebo control. After 10 months, although the lipid levels were not different among the treatment groups, low-density lipoprotein (LDL)/high-density lipoprotein (HDL) ratios in the estrogen + progesterone group were significantly lower than those in the control and progesterone groups. Estrogen alone or in combination with progesterone decreased plasma apo E levels significantly compared with those in the control group. Plasma apo E levels in the progesterone group were similar to those in the control group. In all groups, most (greater than 60%) of the apo E was present in HDL. HDL apo E concentrations in the estrogen and estrogen + progesterone groups were significantly lower than those in the control and progesterone groups. To determine the metabolic mechanisms of these changes in apo E levels, turnover studies were conducted by injection of iodinated apo E-labeled very-low-density lipoprotein (VLDL) and HDL. Residence times were calculated using multicompartment modeling. Progesterone alone and in combination with estrogen decreased residence times of apo E injected in both HDL and VLDL compared with estrogen alone and control groups. Progesterone alone also increased the apo E production rate compared with other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Effects of Silastic progesterone implants on activity cycles and steroid levels in ovariectomized and intact female rats.

We have previously shown that although Silastic implants of progesterone reduce the amount of running of animals living in activity wheels, progesterone-treated animals continue to show periodic fluctuations or peaks in activity. We hypothesized that although progesterone treatment inhibited estrous cycles, ovaries of animals treated with Silastic implants of progesterone continued to secrete estradiol in amounts adequate to stimulate moderate levels of running. In the present study we tested this hypothesis by removing ovaries from progesterone-treated animals and comparing their running behavior and steroid levels to progesterone-treated animals who received sham ovariectomies. Although progesterone treatment significantly inhibited running activity, removal of ovaries in progesterone-treated animals further suppressed running activity. In addition, both estradiol and progesterone levels were significantly reduced following removal of ovaries in progesterone-treated animals. We conclude that although Silastic progesterone implants inhibit normal ovarian and estrous activity cycles, ovaries produce sufficient estradiol to stimulate running behavior.

Activity Cycles↗

PubMed1983

Androgenic modulation of progesterone metabolism by rat granulosa cells in culture.

Effects of androgens on progesterone accumulation, utilization of exogenous progesterone and accumulation of [4-14C]progesterone metabolites by rat granulosa cells in culture were studied. Androgen increased progesterone accumulation in cultures without exogenous progesterone and slowed the overall decline of progesterone concentration in cultures supplemented with exogenous progesterone. Both aromatizable testosterone and nonaromatizable 5 alpha-dihydrotestosterone decreased [4-14C]progesterone utilization by granulosa cells by 12 to 30%. This effect was observed irrespective of whether the cells were continuously exposed to androgens or only pre-exposed. In he same experiments, androgens decreased conversion of radiolabeled progesterone to 20 alpha-hydroxy-4-pregnen-3-one by 11 to 50% and to 5 alpha-pregnane-3 alpha, 20 alpha-diol by 26 to 49%. Accumulation of 3 alpha-hydroxy-5 alpha-pregnan-20-one was not altered in 3 h incubations and was increased by up to 43% in 24 h incubations by androgen treatment. It is suggested that androgens alter progesterone catabolism by granulosa cells by decreasing 20 alpha-hydroxysteroid dehydrogenase activity and that this effect may contribute to overall stimulatory action of androgens on progesterone accumulation.

Animals↗

PubMedDate not supplied

Effect of drugs on progesterone metabolism in the female rat.

Various drugs brought about a reduction of serum progesterone level irrespective of whether or not a potent inducer (phenobarbital, 4-methyl-coumarin) or a hepatotoxin (carbon tetrachloride, alpha-naphthylisothiocyanate, coumarin) has been administered. The decrease by hepatotoxins was highly significant during the estrus phase of the cycle. These treatments affected the hepatic level of progesterone and altered the uptake of [4-14C]progesterone in vivo. The serum level of progesterone was significantly decreased by phenobarbital and carbon tetrachloride; however, the incorporation into the liver was enhanced by phenobarbital and reduced by carbon tetrachloride. This opposing hepatic action showed selectivity; phenobarbital increased the oxidative pathway of progesterone metabolism (formation of 6 beta-, 16 alpha-, 20 alpha-hydroxyprogesterone) but the reductive pathway remained unaltered (formation of pregnanediol, pregnanolone). Conversely, carbon tetrachloride diminished oxidation and raised reduction of progesterone. These results have been confirmed by measurements of progesterone metabolism in vitro using isolated microsomes. Phenobarbital brought about an induction of progesterone 16 alpha-, 6 beta- and 20 alpha-hydroxylase, did not affect progesterone delta 4-5 alpha-dehydrogenase, whereas carbon tetrachloride inhibited hydroxylase and raised dehydrogenase activities. The action of these test compounds on serum and liver levels of progesterone and on the variation of progesterone metabolism seemed to be related to changes manifest in the function of the hepatic endoplasmic reticulum. Similar changes might be associated with the development of mild hepatic lesions induced by various steroids.

1-Naphthylisothiocyanate↗

PubMed1981

Hormonal regulation of cytoplasmic estrogen and progesterone receptors in the beagle uterus and oviduct.

The hormonal regulation of uterine and oviductal cytoplasmic estrogen and progesterone receptors was studied in immature beagles that were untreated, treated with estradiol-17 beta, or treated sequentially with estradiol and progesterone. Estradiol treatment increased the concentration of estrogen receptors in both tissues. Progesterone receptors were not detectable in the reproductive tract of untreated animals, but increased dramatically under the influence of estradiol. Estrogen withdrawal following estrogen stimulation concomitant estrogen plus progesterone administration, and estrogen withdrawal plus progesterone administration all caused significant reductions in both estrogen and progesterone receptors in uterine oviductal cytosols when compared to estrogen treatment alone. Estrogen withdrawal resembled estrogen plus progesterone administration in reducing both estrogen and progesterone receptor levels, although estrogen withdrawal plus progesterone administration resulted in a further reduction in both receptor concentrations. The same positive and negative relationships between estrogen and progesterone receptor content were observed in uterine cytosols from cycling and ovariectomized adults. These data suggest that estrogen and progesterone regulate their respective receptors and that tissue sensitivity to both steroids may be controlled by mechanisms involving fluctuations in receptor concentration in the reproductive tract of the beagle.

Animals↗

PubMed1990

Role of 17 beta-hydroxysteroid dehydrogenase in the modulation of nuclear estradiol receptor binding by progesterone in the rat anterior pituitary gland and the uterus.

Progesterone has been shown to decrease occupied pituitary and uterine nuclear estradiol receptor (E2R) binding in mature and immature estrogen-primed rats. Progesterone has also been shown to stimulate pituitary but not uterine 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) in the rat. The conversion of estradiol to its less active metabolite estrone by 17 beta-HSD and activation of phosphatase are among mechanisms considered to be involved in the reduction of E2R. To determine if 17 beta-HSD stimulation was a mechanism by which progesterone induced nuclear E2R decrease, the synthetic estrogen ethinylestradiol, which is not oxidized by 17 beta-HSD, was used instead of estradiol to prime adult ovariectomized rats. When ethinylestradiol-primed rats received 0.8, 2.0 or 4.0 mg/kg body wt of progesterone 2 h before sacrifice, the total and occupied nuclear E2R accumulation in the anterior pituitary by a subsequent ethinylestradiol injection 1 h later did not show any decrease. This response was different from that observed previously in estradiol-primed animals in which progesterone showed a multiphasic decrease of occupied form of nuclear E2R. However, in the uterus of ethinylestradiol-primed rats, a partial decrease of total and occupied nuclear E2R accumulation was observed in the presence of the three doses of progesterone used. The decrease of uterine nuclear E2R with the three progesterone doses was different from the dose-dependent effect of progesterone observed in the uterus of estradiol-primed rats. Affinity constants of the interaction between [3H]estradiol and the nuclear E2R were similar among groups treated with ethinylestradiol, estradiol and progesterone. These results demonstrate the involvement of 17 beta-HSD in the reduction of anterior pituitary gland E2R by progesterone in the estradiol-treated animals. Furthermore, the mechanism of decrease of E2R by progesterone in the uterus appears to be different from the pituitary gland.

17-Hydroxysteroid Dehydrogenases↗

PubMed2005

Enzyme immunoassay of progesterone in the feces from beef cattle to monitor the ovarian cycle.

The present study was undertaken to measure fecal progesterone concentration of beef cattle using antibody against authentic progesterone and to examine whether this method can monitor the ovarian cycle in beef cattle. Rectal fecal samples collected from 14 beef cattle were mixed with 6 ml of 100% methanol and shaken for 15 min. After centrifugation, supernatant was extracted with petroleum ether followed by an enzyme immunoassay (EIA) for progesterone. Specificity of the assay was examined by HPLC separation of fecal solution followed by the EIA in each fraction. The present assay identified only progesterone but not other metabolites in the feces sample that was extracted with petroleum ether. Sensitivity of the assay was estimated to be 0.0055 ng/ml (0.11 ng/g). Coefficient variations of intra- and inter-assay were 9.6-10.9% and 10.8-16.6%, respectively. Recovery rates ranged between 73 and 84%. Patterns in the fecal progesterone concentrations during the ovarian cycle were almost parallel to the plasma concentrations. A significant positive correlation was established between the fecal and plasma progesterone concentrations in individual animal (r=0.59-0.84, P<0.001, n=10) as well as pooled data (r=0.70, P<0.001, n=65). Fecal progesterone concentrations of day 0 (showing the nadir of concentration) of the ovarian cycle were less than 50 ng/g, which increased significantly toward day 9 (P<0.01). From days 14 to 18, there was significant reduction of fecal progesterone concentration (P<0.01). Ovarian cycles had at least 48 ng/g (mean=74 ng/g) of difference between minimum and maximum fecal progesterone concentrations. All cattle at days 9, 11 and 14 had higher fecal progesterone concentrations by more than 20 ng/g compared with day 0. These results suggest that the present EIA is suitable to measure the progesterone in cattle feces and can monitor ovarian cycle.

Animals↗