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PubMed1983

Release of progesterone from perifused, highly luteinized ovarian cells of rats: effects of luteinizing hormone and bovine serum albumin.

Release of progesterone from enzymatically dispersed luteal cells of superovulated rats was studied using a multi-channeled perifusion system. Cells were perifused with protein-free medium for up to 5 h. Basal release of progesterone showed a steady decline during the first h of perifusion to a stable baseline where it remained throughout the experiment. A 30-min exposure of the luteal cells to increasing amounts of luteinizing hormone (LH) stimulated a dose-dependent increase in progesterone release. Similar results were observed when luteal cells were exposed to 0.2 or 1.0 mM dibutyryl (Bu)2 cAMP for 30 min. Exposure of the cells to 0, 1, 10, and 100 ng LH/ml protein-free medium for 230 min showed increased release of progesterone, although the dispersed cells perifused with 100 ng LH/ml protein-free medium were unable to maintain the maximal levels of progesterone release. The effect of bovine serum albumin (BSA) in the perifusion medium on the basal and LH-stimulated progesterone release was examined. Low concentrations of BSA (0.05%) had no effect, but 0.5% and 2.0% BSA significantly increased the basal release of progesterone. However, the addition of 0.05% BSA to the medium resulted in an increased progesterone release in response to 10 ng LH/ml medium. These results suggest that the in vitro perifusion system maintains physiologically viable cells which are responsive to either LH or (Bu)2 cAMP for at least 5 h. The effect of protein in the perifusion medium or progesterone release was demonstrated by the addition of BSA.

Animals↗
PubMed1986

Secretion of oxytocin and progesterone by ovine corpora lutea in vitro.

The mechanisms involved in the control of oxytocin and progesterone secretion by the ovine corpus luteum have been investigated in vitro using luteal slice incubations. Oxytocin and progesterone were secreted at constant rates from luteal slices for 2 h of incubation (366 +/- 60 pg X mg X h and 18.9 +/- 0.18 ng X mg X h, respectively). Secretion of progesterone, but not of oxytocin, was significantly (p less than 0.02) stimulated in the presence of ovine luteinizing hormone. Incubation of luteal slices in medium containing 100 mM potassium, however, resulted in increased secretion of oxytocin and, to a lesser extent, of progesterone (294 +/- 59% and 142 +/- 15%, respectively, p less than 0.05). Basal oxytocin secretion was reduced during incubation in calcium-free medium, compared to secretion in the presence of calcium (70 +/- 15 and 175 +/- 25 pg X mg X 20 min, respectively, p less than 0.01), whereas progesterone secretion was not altered in the absence of calcium. Secretion of both hormones by luteal slices was stimulated by the addition of the calcium ionophore A23187 (p less than 0.05). Addition of prostaglandin F2 alpha (2.8 microM) had no effect on secretion of either oxytocin or progesterone. We have demonstrated that oxytocin and progesterone can be stimulated, independently, from corpus luteum slices incubated in vitro. The pattern of release is consistent with the proposal that oxytocin, but not progesterone, is associated with and actively released from luteal secretory granules. Our results also indicated that prostaglandin F2 alpha does not directly stimulate release of oxytocin or progesterone from luteal cells in vitro.

Animals↗
PubMed1987

Ovum transport in pregnant rats is little affected by RU486 and exogenous progesterone as compared to cycling rats.

In cycling and pregnant rats, the eggs stay in the oviduct for approximately 66 and 90 h, respectively. The influence of progesterone in these timings was investigated. An excess or a simulated deficit of progesterone was induced with exogenous progesterone or the antiprogesterone RU486, respectively, beginning on the day of ovulation. The effect of these treatments on egg transport in cycling and pregnant rats was assessed in detail and complemented with determinations of estradiol and progesterone circulating levels and progesterone receptor levels in the oviduct. Accelerated transport of ova followed treatment with RU486 in cycling and pregnant rats but with different features. In cycling rats, acceleration began 24 h after the onset of treatment and was not associated with changes in estradiol levels; in pregnant rats, it started 72 h after treatment and was associated with a 5-fold increase in estradiol circulating levels. Thus, RU486 failed to accelerate ovum transport during the first three days of treatment in pregnant rats, in spite of the fact that no progesterone receptors were available in the oviduct as early as 24 h of treatment. Progesterone administration caused egg retention in the oviducts and a 50% reduction in circulating estradiol levels in cycling rats, whereas in pregnant rats progesterone excess did not change estradiol circulating levels and had no effect on the location of embryos on Days 4 and 5. These results demonstrate a different physiological importance of endogenous progesterone in slowing down oviductal ovum transport in cycling and pregnant rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Progesterone secretion by corpora lutea of the isolated perfused rabbit ovary during pseudopregnancy.

An ovarian in vitro perfusion method was adapted to examine rabbit corpus luteum (CL) function during pseudopregnancy. Ovaries were perfused in vitro with tissue culture Medium 199 with or without 3% bovine serum albumin (BSA). Samples were obtained from both arterial and venous cannulae, allowing rates of progesterone secretion to be determined. Two perfusion methods were compared: a closed system in which perfusion medium continuously recirculated through the tissue, and an open system in which the ovarian vein cannula was left outside the perfusion chamber. The addition of 3% BSA was found to prevent edema and distortion of the interstitial space, and to result in increased progesterone secretion. With the closed perfusion system, the progesterone secretion rate measured over the 6-h perfusion was significantly higher on Day 11 than on Day 1 of pseudopregnancy and had declined significantly on Day 18. There was no difference in secretion rates whether the perfusion system was open or closed, and the results obtained with both systems closely approximated in vivo progesterone secretion rates. Measurements of CL tissue progesterone content before and after in vitro perfusion indicated that the changes in progesterone secretion seen during pseudopregnancy resulted from differences in the synthesis and secretion of progesterone and not from leakage of progesterone already present in the CL prior to perfusion. Taken together, these results indicate that the modified in vitro perfused rabbit ovary preparation described herein is an appropriate model to examine progesterone secretion by ovaries bearing CL.

Animals↗
PubMed1988

Pattern of ovarian progesterone secretion during the luteal phase of the ovine estrous cycle.

Pulsatile secretion of progesterone has been observed during the late luteal phase of the menstrual cycle in the rhesus monkey and human. As the luteal phase progresses in each of these species, there is a pattern of decreased frequency and increased amplitude of progesterone pulses. The present study was designed to determine the pattern of progesterone secretion during the late luteal phase (Days 10-16) of the normal ovine estrous cycle. Five unanesthetized ewes, each bearing an indwelling cannula in the utero-ovarian vein, were bled every 15 min from 0800 h on Day 10 through 0800 h on Day 16 of the estrous cycle. With the computer program PULSAR, it was determined that progesterone secretion was episodic, with pulsations observed on all days. Analysis of variance was used to determine differences in frequency, amplitude, and interpeak interval (IPI) of progesterone pulses among ewes and days. The ewes averaged 8.0 +/- 0.63 pulses of progesterone per 24 h. Mean frequency of pulses was not different between days but showed differences between ewes. Mean amplitude of progesterone pulses was 7.0 +/- 0.27 ng/ml, with no differences observed either between days or between ewes. Mean IPI was 197 +/- 7.1 min, and, like frequency, the IPI was not different between days, but varied between ewes. No consistent temporal relationship was found between progesterone pulses and luteinizing hormone (LH), as determined by bioassay and radioimmunoassay, on Day 14 of the cycle in one ewe. The results indicate that progesterone secretion is episodic during the luteal phase of the ovine estrous cycle and is independent of LH pulses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Antagonism of estrogen-induced prolactin release by progesterone.

Previous work from our laboratory has shown that during the process of nuclear occupancy of the progesterone receptor complex (1-2 h), nuclear estradiol receptors of the anterior pituitary are depleted. The purpose of this study was to determine whether the depletion of nuclear estradiol receptors by progesterone had functional biological significance. The ovariectomized (26 days of age) immature rat was used as the model for analysis of this question. The ability of estradiol to release prolactin from the anterior pituitary was the function chosen to determine the biological significance of the progesterone and estradiol interactions. In response to estradiol exposure (2 micrograms/rat), prolactin release reached peak values from 8 h to 12 h and returned to control levels by 24 h. A second injection of estradiol 13 h after the initial injection stimulated a second increase in serum prolactin at 25 h. This model of two injections of estradiol 13 h apart served to provide adequate levels of anterior pituitary progesterone receptors and elevated serum prolactin levels upon which superimposed progestin modulation could be examined. A single injection of progesterone (0.8 mg/kg BW) 1 h before the second estradiol injection blocked the increase in serum prolactin. This action was a receptor-mediated event because progesterone had no effect without estrogen priming or when the progesterone antagonist RU486 was used. Finally, when the interval between the progesterone and second estradiol injection was extended to 4 h, a time period when progesterone does not deplete pituitary nuclear estrogen receptors, the estrogen-induced increase in serum prolactin was not blocked.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Regulation of 11beta-hydroxysteroid dehydrogenase type 2 by progesterone, estrogen, and the cyclic adenosine 5'-monophosphate pathway in cultured human placental and chorionic trophoblasts.

Human placenta and fetal membranes contain two types of 11beta-hydroxysteroid dehydrogenase (11beta-HSD). 11Beta-HSD1 interconverts cortisol and cortisone and is the predominant isoform found in the fetal membranes. 11Beta-HSD2, which predominates in the placenta syncytiotrophoblast, converts cortisol to cortisone. It has been proposed that placental 11beta-HSD protects the fetus from high levels of maternal glucocorticoids. In this study, cultured term human placental and chorionic trophoblasts were used to examine the regulation of 11beta-HSD1 and 11beta-HSD2 activities and mRNA expression by progesterone, estrogen, and activators of adenylate cyclase (forskolin) and protein kinase C (phorbol 12-myristate 13-acetate, PMA). Placental trophoblast displayed mainly type 2 oxidase activities. 11Beta-HSD in the chorionic trophoblast was exclusively an 11beta-HSD1 reductase. Progesterone (0.001-1 microM) inhibited 11beta-HSD2 activity in a dose-dependent fashion. Inhibition of endogenous progesterone production with trilostane enhanced 11beta-HSD2 activity. The inhibitory effect of progesterone on 11beta-HSD2 activity was not reversed by the progesterone receptor antagonists RU-486 or onapristone. Progesterone (1 microM) also reduced levels of 11beta-HSD2 mRNA, an effect that was attenuated by both RU-486 and onapristone. Estradiol (1 microM) inhibited type 2 oxidase activity as well. Activation of adenylate cyclase by forskolin (100 microM) up-regulated both 11beta-HSD2 activity and mRNA expression; there was no effect of PMA (1 microM) on 11beta-HSD2. 11Beta-HSD1 reductase activity was unaffected by progesterone, estrogen, forskolin, or PMA in either the placental or chorionic trophoblasts. We conclude that both progesterone and estrogen are inhibitors of 11beta-HSD2 activity in term human placenta in vitro. Levels of 11beta-HSD2 activity and mRNA are increased by activation of the cAMP pathway. Progesterone also suppresses levels of 11beta-HSD2 mRNA.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1998

Both prolactin and progesterone in proestrus are necessary for the induction of apoptosis in the regressing corpus luteum of the rat.

This study was conducted to analyze the roles of prolactin (PRL) and progesterone in the induction of luteal cell apoptosis and accumulation of macrophages in the regressing corpus luteum. We studied the number of apoptotic cells and macrophages in regressing corpora lutea in estrus 1) in cycling rats or after blocking PRL secretion with the dopaminergic agonist CB154, and 2) after blocking progesterone actions with the progesterone receptor antagonists RU-486 or ZK98299. Cells showing the morphological features characteristic of apoptosis contained fragmented DNA as indicated by in situ 3' end labeling. In cycling rats, a 100-fold increase in the number of apoptotic cells and a 4-fold increase in the number of macrophages was found from the evening (1600 h) of proestrus to the morning (1100 h) of estrus. Both increases were blocked by PRL suppression with CB154. Furthermore, blocking progesterone actions with progesterone receptor antagonists RU-486 or ZK98299 without affecting PRL secretion inhibited apoptosis but did not affect the accumulation of macrophages, whether treatment was started on the morning of metestrus (blocking diestrous and proestrous progesterone) or on proestrus (blocking only proestrous progesterone). Otherwise, exogenous progesterone was not effective in inducing apoptosis in the absence of PRL. These results indicate that both PRL and progesterone in proestrus are necessary for the induction of apoptosis in the regressing corpora lutea, whereas the accumulation of macrophages seemed to be dependent exclusively on the PRL surge.

Animals↗
PubMed2002

Progesterone blocks the estradiol-stimulated luteinizing hormone surge by disrupting activation in response to a stimulatory estradiol signal in the ewe.

The preovulatory surges of GnRH and LH are activated by increased concentrations of circulating estradiol, but ovulation is blocked when progesterone concentrations are elevated. Although it is has been shown that this action of progesterone is due to a central inhibition of the GnRH surge, the mechanisms that underlie the blockade of the GnRH surge are poorly understood. In this study we investigated whether progesterone can block the estradiol-dependent activation stage of the GnRH surge induction process, and thus prevent expression of the LH surge. The results demonstrated that exposure to progesterone for half or the full duration of the activation stage can prevent the stimulation of LH surges by estradiol (experiment 1), whereas exposure to progesterone midway though a period of estradiol exposure, which in itself is sufficient to activate the surge, did not block the LH surge (experiment 2). These results suggest that progesterone 1) disrupts activation of the surge induction system in response to a stimulatory estradiol signal and 2) does not compromise the ability of animals to respond to a stimulatory estradiol signal applied immediately after progesterone exposure. Because the disruptive effects of activated progesterone in response to estradiol are rapid but transient, it may be that progesterone directly interferes with the activation of estradiol-responsive neural systems to block the GnRH/LH surge.

Animals↗
PubMed2002

Direct inhibitory effect of progesterone on oxytocin-induced secretion of prostaglandin F(2alpha) from bovine endometrial tissue.

The effect of progesterone on oxytocin-induced secretion of prostaglandin (PG) F(2alpha) from bovine endometrial tissue explants was examined. Endometrial tissue from the late luteal phase were preincubated for 20 h in control medium. Explants were then treated for 6 h with control medium, oxytocin (10(-7) M), progesterone (10(-5) M), or both hormones. Oxytocin increased the medium concentration of 13,14-dihydro-15-keto-PGF(2alpha), whereas progesterone completely suppressed the stimulatory effect of oxytocin. In experiment 2, isolated endometrial epithelial cells were incubated with progesterone (10(-5) M), oxytocin (10(-7) M), and combinations of these hormones with or without actinomycin D (1 ng/ml). Only oxytocin stimulated secretion of PGF(2alpha), and this response was suppressed by progesterone. Oxytocin induced a rapid increase in intracellular concentrations of Ca(2+) detected within 1 min of exposure of epithelial cells from the same cows. Progesterone pretreatment diminished this response. In experiment 3, direct effects of progesterone (2 nM-20 microM) on binding of (3)H-oxytocin to the membrane preparation from epithelial cells were determined by saturation analysis. Oxytocin binding was suppressed by progesterone at every dosage tested. Progesterone is capable of suppressing the ability of oxytocin to induce endometrial secretion of PGF(2alpha). This effect appears to be mediated through a direct interference in the interaction of oxytocin with its own receptor.

Animals↗
PubMed1992

Effects of progesterone on the cardiac electrophysiologic action of bupivacaine and lidocaine.

Pregnancy is accompanied by an increased cardiac and neural sensitivity to some local anesthetic agents such as bupivacaine. The current study was initiated to investigate the relationship between increased progesterone concentrations and the electrophysiologic effects of bupivacaine, and lidocaine in isolated Purkinje fiber (PF)-ventricular muscle (VM) preparations. Twenty-four oophorectomized female white rabbits were killed after receiving 30 mg.kg-1.day-1 of progesterone intramuscularly or peanut oil alone for 4 days. PF and VM action potentials were recorded using standard electrophysiologic procedures. Plasma progesterone concentrations were 5 +/- 2.9 ng/ml in control animals compared to 59.8 +/- 11.0 ng/ml in progesterone-treated animals (P less than 0.05). Bupivacaine (3.5-17.4 microM) depressed the maximal rate of depolarization (Vmax) of PF to a significantly greater extent in tissues from progesterone-treated animals as compared to control animals. For example, at 3.5 microM bupivacaine decreased PF Vmax 52% in progesterone-treated tissues compared to 32% in controls (P less than 0.05); the Vmax of VM was also depressed to a greater extent in tissues from progesterone-treated animals (P less than 0.001). Lidocaine did not demonstrate an enhanced depressant effect in tissues from progesterone-treated animals. These results indicate that progesterone selectively increases the cardiac membrane depressant effects of bupivacaine but not lidocaine. This may contribute to the enhanced toxicity of bupivacaine in pregnant animals.

Action Potentials↗
PubMed1992

Effect of progesterone on the cardiac electrophysiologic alterations produced by ropivacaine and bupivacaine.

Bupivacaine-induced cardiotoxicity is enhanced in pregnant laboratory animals and in progesterone-pretreated isolated cardiac tissues. Ropivacaine is a new local anesthetic chemically related to bupivacaine. Although clinically equipotent with bupivacaine, ropivacaine is less cardiodepressant. Progesterone levels are elevated during pregnancy, and exogenously increasing progesterone levels in rabbits has increased bupivacaine's depressive effects on excitability. In neural tissues, bupivacaine's increased onset of block and depression of compound action potentials in tissues from progesterone-treated animals was similar to its effect in nerves from pregnant animals. This study determined whether exogenously increased progesterone levels can increase myocardial sensitivity to ropivacaine. Female ovariectomized rabbits were pretreated with progesterone for 4 days. After killing, the hearts were removed and Purkinje fibers (PFs) and ventricular muscle (VM) action potential parameters recorded. Tissues from animals receiving either progesterone or placebo were exposed to either ropivacaine or bupivacaine at concentrations ranging from 3.5 to 18.7 microM. Preparations were routinely paced at 2 Hz except where rate-dependent effects on the maximal rate of depolarization of phase zero (Vmax) were determined. Progesterone increased depression of myocardial Vmax only to bupivacaine (P less than 0.05). Ropivacaine was generally 3-5 times less potent in depressing cardiac electrophysiologic parameters. Bupivacaine demonstrated rate-dependent depression of Vmax that at higher frequencies was greater than ropivacaine's effects (P less than 0.05). Ropivacaine is less cardiodepressant than bupivacaine in this isolated PF-VM preparation. Exogenously increasing progesterone levels in vivo does not increase ropivacaine's depression of myocardial Vmax in isolated PF-VM tissues as it does to bupivacaine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amides↗
PubMedDate not supplied

Absence of progesterone effects on chlamydial genital infection in female guinea pigs.

The effect of progesterone alone and in combination with estradiol was investigated in ovariectomized and gonadally intact female guinea pigs infected with the chlamydial agent of guinea pig inclusion conjunctivitis (GPIC). The course of the infection, as determined by the percentage of cells with GPIC (chlamydia) inclusions in Giemsa-stained vaginal scrapings, was not affected in animals receiving 5.0 mg of progesterone daily. Progesterone had no influence on the enhancement of infection by estradiol. In comparison with sesame oil-treated controls, infection was prolonged by four to six days (P less than .05) in animals receiving a combination of 5.0 mg of progesterone plus 1.0 microgram of estradiol or 1.0 microgram of estradiol alone each day. In ovariectomized animals, estradiol delayed the appearance of IgA antibody in genital secretions, whereas progesterone alone had no effect. Guinea pigs treated with estradiol or progesterone plus estradiol manifested an acute endometritis not observed in animals treated with progesterone alone or in controls receiving sesame oil. Although cervical ectopy, analogous to that seen in women with high levels of progesterone, was identified by histopathology in animals treated with progesterone, no enhancement of the chlamydial infection was observed.

Animals↗
PubMed1999

Progesterone is neuroprotective after acute experimental spinal cord trauma in rats.

STUDY DESIGN: A standardized rat contusion model was used to test the hypothesis that progesterone significantly improves neurologic recovery after a spinal cord injury that results in incomplete paraplegia. OBJECTIVES: To compare the effect of progesterone versus a variety of control agents to determine its effectiveness in promoting neurologic recovery after an incomplete rat spinal cord injury. SUMMARY OF BACKGROUND DATA: Progesterone is a neurosteroid, possessing a variety of functions in the central nervous system. Exogenous progesterone has been shown to improve neurologic function after focal cerebral ischemia and facilitates cognitive recovery after cortical contusion in rats. METHODS: A standardized rat contusion model of spinal cord injury using the New York University impactor that resulted in rats with incomplete paraplegia was used. Forty mature male Sprague-Dawley rats were randomly assigned to four groups: laminectomy with sham contusion, laminectomy with contusion without pharmacologic treatment, laminectomy with contusion treated with dimethylsulfoxide and dissolved progesterone, and laminectomy with contusion treated with dimethylsulfoxide. Functional status was assessed weekly using the Basso-Beattie-Bresnehan (BBB) locomotor rating scale for 6 weeks, after which the animals were killed for histologic studies. RESULTS: Rats treated with progesterone had better outcomes (P = 0.0017; P = 0.0172) with a BBB score of 15.5, compared with 10.0 in the dimethylsulfoxide control group and 12.0 in the spinal cord contusion without pharmacologic intervention group. This was corroborated in histologic analysis by relative sparing of white matter tissue at the epicenter of the injury in the progesterone-treated group (P < 0.05). CONCLUSIONS: Rats treated with progesterone had a better clinical and histologic outcome compared with the various control groups. These results indicate potential therapeutic properties of progesterone in the management of acute spinal cord injury.

Acute Disease↗
PubMed1993

The contrasting effects of progesterone and oestrogen on the susceptibility of mice to genital infection with Mycoplasma pulmonis.

The genital tract of young female mice was rendered susceptible to colonisation with Mycoplasma pulmonis by pre-treating them with progesterone (usually 2.5 mg) given subcutaneously at weekly intervals for 4 weeks. Colonisation was influenced by the size of the inoculum and by the dose of progesterone; at least 2.5 x 10(4) organisms and at least 0.5 mg of hormone (administered on four occasions) were required. The duration of colonisation was related also to the size of the inoculum and the dose of progesterone. Similar results were obtained in TO, BALB/c and CBA strains of mice. Progesterone treatment induced the dioestrous stage of the reproductive cycle within 5 days and the cycle of the majority of untreated, mycoplasma-susceptible mice was also at this stage. However, mice, particularly of the CBA strain, were far less susceptible when not given progesterone and the mycoplasmas tended to persist for a shorter time. Mice treated with oestradiol, even in small doses, became completely refractory to infection with M. pulmonis. In vitro, progesterone inhibited the growth of M. pulmonis, as did oestradiol, but vaginal washings from progesterone-treated mice were no more inhibitory than those from untreated mice. Thus, the success of progesterone in enhancing colonisation could not be attributed to a direct stimulatory effect of the hormone at the mucosal surface and we suggest that it may be due to a greater availability of progesterone-induced receptors for mycoplasmas in the dioestrous phase of the reproductive cycle than in the oestrous phase.

Animals↗
PubMed1988

Positive and negative feed-back effect of progesterone on luteinizing hormone secretion in post-menopausal women.

Progesterone is known to exert a biphasic feedback effect on luteinizing hormone (LH) secretion in animals and it has been demonstrated that this effect is dependent upon both duration of exposure to progesterone and the dose administered. In this paper we sought to determine whether a similar biphasic effect exists in humans. The pattern of LH secretion was assessed in six healthy oestrogen treated post-menopausal women before and after they were given progesterone (50 mg/day) for 1 and 7 days. Progesterone treatment for 1 day resulted in a significant elevation in the basal serum LH concentration and in individual LH pulse amplitude with no change in LH pulse frequency. In contrast, progesterone treatment for 7 days increased LH pulse amplitude with no change in basal serum LH concentrations and a significant reduction in LH pulse frequency. We concluded that firstly, progesterone does exert a biphasic feedback effect on LH secretion and that the nature of this effect is determined by the duration of exposure to the progesterone stimulus. Secondly, as LH pulsatility has been shown to be an accurate indicator of GnRH pulsatility, that the reduction in LH pulse frequency after a long exposure to progesterone is due to a hypothalamic effect of progesterone whereas the positive feedback effect may be the result of a pituitary or hypothalamic action.

Aged↗
PubMed1996

Effects of progesterone on human spermatozoa prepared for in-vitro fertilization.

Progesterone has been tested in vitro with human spermatozoa to verify its physiological effects and its possible therapeutic use in cases of male infertility. Progesterone induced a rapid, dose-dependent influx of calcium in capacitated and non-capacitated spermatozoa with a half-maximally effective dose of 30 nM. The agonist, 19-nortestosterone, was much less potent that progesterone itself. Progesterone-induced calcium influx was not inhibited by a similar concentration (0.1 microgram/ml) of RU 486, a classical progesterone antagonist. The increase in intracytoplasmic calcium levels was unable to induce the acrosome reaction (AR) even after incubation for 5 h, when this was evaluated by double staining, using a monoclonal antibody GB24 raised against the inner acrosome membrane and ethidium homodimer as a vital probe. However, after incubation for 5 h, progesterone was able to enhance the tyrosine phosphorylation of a 95 kD sperm protein, which is phosphorylated progressively during capacitation in well-defined culture media. Incubation of spermatozoa with 1 or 10 micrograms/ml progesterone for 3 or 30 min did not induce major modifications of hyperactivated movement when analysed by computer-assisted semen analysis. Progesterone secreted by cumulus cells may physiologically increase sperm intracytoplasmic free calcium during capacitation. This priming effect may facilitate the acrosome reaction, induced by binding to the zona pellucida, without enhancing spontaneous acrosome reaction prematurely. It therefore seems useful to propose progesterone as a means of accelerating capacitation during in vitro fertilization in cases of male infertility.

Acrosome↗
PubMed1987

Production of testosterone from progesterone by rat testicular microsomes without release of the intermediates 17 alpha-hydroxyprogesterone and androstenedione.

It has been shown that during the in vitro conversion of progesterone to androstenedione, 17 alpha-hydroxyprogesterone is not an obligatory intermediate which equilibrates with freely diffusible steroids in the incubation medium. Recently a cytochrome P-450 was purified that catalyzed, in addition to hydroxylase/lyase activities, reduction of androstenedione to testosterone. In order to determine whether progesterone could be transformed to testosterone without both intermediates (17 alpha-hydroxyprogesterone and androstenedione) being equilibrated with steroids in the medium, several double-label double-substrate experiments were performed. When rat microsomes were incubated with an equimolar mixture of [14C]progesterone and 17 alpha-hydroxy[3H]progesterone, androstenedione was isolated with a 11-fold higher 14C/3H ratio than 17 alpha-hydroxyprogesterone, indicating that androstenedione could not be produced from free, diffusible 17 alpha-hydroxyprogesterone. Incubation of an equimolar mixture of 17 alpha-hydroxy[3H]progesterone and [14C]androstenedione with testicular microsomes resulted in the incorporation of 3-4-fold more 17 alpha-hydroxyprogesterone into testosterone than of androstenedione, although the latter is the immediate precursor of testosterone. In an experiment in which equimolar concentrations of [3H]progesterone and [14C]androstenedione were incubated with testicular microsomes, the large pool of progesterone inhibited competitively lyase activity, but still the label of progesterone was incorporated into testosterone to the same extent as that of androstenedione. These results indicate that testosterone can be produced by immature rat testicular microsomes from added progesterone on an organized unit without the intermediates equilibrating with the incubation medium.

17-alpha-Hydroxyprogesterone↗