THE SERUM LEVELS OF PROGESTERONE AND 20α-DIHYDROPROGESTERONE, AND THE OVARIAN LH, FSH AND PRL BINDING DURING LUTEOLYSIS OF THE SUPERLUTEINIZED RAT OVARY

1977 ◽  
Vol 86 (1) ◽  
pp. 162-172 ◽  
Author(s):  
Peter A. Torjesen ◽  
Asbjørn Aakvaag
Keyword(s):  
Binding Sites ◽  
Ovarian Tissue ◽  
Serum Levels ◽  
Plasma Progesterone ◽  
Luteal Function ◽  
Prostaglandin Analogues ◽  
Prostaglandin F ◽  
Serum Gonadotropin ◽  
Rat Ovary

ABSTRACT The process of luteolysis has been studied in immature rats in which superluteinization had been induced with pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotrophin (HCG). Following prostaglandin F2α and the prostaglandin analogues, and at the end of the pseudopregnancy, the plasma levels of progesterone and 20α-dihydroprogesterone were measured and used as parameters of luteal function in relation to the capacity of the ovarian tissue to bind LH, FSH and prolactin (PRL) in vitro. On day 19 after HCG a marked decrease in the progesterone level from the day 8 level was observed concomitant with a marked increase in 20α-dihydroprogesterone. The capacity of the ovarian tissue to bind LH in vitro was markedly reduced on day 19 compared to day 8. Identical changes were observed 21 h after 1 mg prostaglandin F2α or prostaglandin analogues. Progesterone decreased from about 600 ng/ml to about 50 ng/ml, whereas the increase in 20α-dihydroprogesterone was from about 200 ng/ml to 500–1000 ng/ml and the reduction in LH binding sites was from 1.7 × 10−12 to 0.5 × 10−12 mol/mg protein. Nanogram amounts of the analogues were as effective as 1 mg of prostaglandin F2α. The number of FSH or PRL binding sites was not affected by spontaneous luteolysis or the treatment given. By the use of graded doses of the prostaglandin analogues a negative correlation (r=−0.81) was found between plasma progesterone and 20α-dihydroprogesterone levels, and a positive correlation (r = 0.84) between LH binding sites and plasma progesterone levels. The luteolysis induced by prostaglandin F2α or prostaglandin analogues was indistinguishable from the spontaneous luteolysis using these parameters.

Induction of transient functional luteolysis in cyclic sheep by a 3 β-hydroxysteroid dehydrogenase inhibitor

1984 ◽  
Vol 100 (1) ◽  
pp. 61-66 ◽  
Author(s):  
G. Jenkin ◽  
R. T. Gemmell ◽  
G. D. Thorburn
Keyword(s):  
Luteal Phase ◽  
Competitive Inhibition ◽  
Ovarian Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Oestrous Cycle ◽  
Morphological Examination ◽  
Plasma Progesterone ◽  
Luteal Regression ◽  
Luteal Function ◽  
Prostaglandin F

ABSTRACT The mechanism by which prostaglandin F2α terminates luteal function in the sheep is unclear even though it is used extensively in animal husbandry. At the time of luteal regression, a decrease in 3β-hydroxysteroid dehydrogenase (3β-HSD) activity is apparent in the corpus luteum, but it is not known whether the decrease in enzyme activity is the primary cause of structural luteolysis. The effect of trilostane, a 3β-HSD inhibitor, on luteal function and morphology has therefore been investigated. Intravenous injection of trilostane in the mid-luteal phase of the oestrous cycle caused a decrease in ovarian tissue progesterone content. A transient decrease in peripheral and utero-ovarian vein plasma progesterone was observed but there was no significant effect on the length of the luteal phase of the cycle. There was no significant change in plasma 13,14-dihydro-15-oxo-prostaglandin F2α during the period when plasma progesterone was depressed. Morphological examination of the corpora lutea revealed a decrease in the concentration of electron-dense granules without any other features of impending luteal regression. When plasma progesterone was reduced for more than 10 h by two injections of trilostane 4 h apart, there was again no subsequent effect on the length of the oestrous cycle or on the return to oestrus. Plasma progesterone returned to preinjection levels within 24 h of injection. This evidence suggests that competitive inhibition of 3β-HSD activity, per se, is ineffective in bringing about structural luteolysis. J. Endocr. (1984) 100, 61–66

Oxytocin receptor concentrations, inositol phosphate turnover and prostaglandin release by endometrium from ewes induced to ovulate during the early post-partum period

1993 ◽  
Vol 136 (1) ◽  
pp. 17-NP ◽  
Author(s):  
J. M. Wallace ◽  
M. G. Thompson ◽  
R. P. Aitken ◽  
M. A. Cheyne
Keyword(s):  
Receptor Binding ◽  
Inositol Phosphate ◽  
Post Partum ◽  
Oxytocin Receptor ◽  
Receptor Expression ◽  
Luteal Function ◽  
Induction Of Ovulation ◽  
Release Device ◽  
Prostaglandin F

ABSTRACT Induction of ovulation early post partum in sheep is associated with a high incidence (30–40%) of premature luteolysis. The present study was designed to characterize oxytocin receptor levels, oxytocin-stimulated inositol phosphate (IP) turnover (second messenger) and oxytocin-stimulated prostaglandin F2α (PGF2α) release in the endometrium of post-partum ewes induced to ovulate 21 days after parturition and expected to exhibit a range of corpus luteal functions subsequently. Ovulation was induced on day 21 post partum using a controlled internal drug release device and pregnant mare serum gonadotrophin, and uterine tissues were collected on days 5, 10 or 15 of the cycle (n = 4/day). A further 12 ewes whose interval from previous parturition exceeded 150 days were similarly treated and acted as controls. Measurement of daily peripheral progesterone concentrations revealed that while all control ewes exhibited normal luteal function, abnormal luteal function was evident in two, two and one post-partum ewes studied on days 5, 10 and 15 of the cycle respectively. Oxytocin receptor binding was detected (by receptor-binding assay and in-vitro autoradiography) in the endometrium and myometrium of post-partum ewes at all three stages of the oestrous cycle but only at day 15 in control ewes. To determine IP turnover, 100 mg caruncular endometrium was incubated in duplicate for 2·5 h with 10 μCi [3H]inositol and treated with 0 or 2 μmol oxytocin/l for 30 min, then [3H]inositol mono-, bis- and trisphosphates were quantified. Oxytocin stimulated total IPs in all day-5 and day-15 post-partum ewes, in three of four day-10 ewes and in all day-15 control ewes. Basal endometrial PGF2α release measured in triplicate (100 mg/well) during a 2 h incubation was higher in post-partum versus control ewes on days 5 and 10 but not on day 15 of the cycle. Similarly, oxytocin stimulated PGF2α release to varying levels at all stages of the cycle in post-partum ewes but only on day 15 in control ewes. Irrespective of the treatment group endometrial oxytocin receptor number was significantly (P < 0·001) correlated with oxytocin-stimulated IP turnover and PGF2α release. Thus the induction of ovulation and the subsequent luteal phase in post-partum ewes is against a back ground of high oxytocin receptor expression and enhanced PGF2α release which in some ewes may contribute to abnormal luteal function. Journal of Endocrinology (1993) 136, 17–25

THE SEQUENCE OF HORMONAL CHANGES DURING PROSTAGLANDIN INDUCED LUTEOLYSIS OF THE SUPERLUTEINIZED RAT OVARY

1978 ◽  
Vol 87 (3) ◽  
pp. 617-624 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag
Keyword(s):  
Binding Sites ◽  
Limit Of Detection ◽  
Serum Levels ◽  
Female Rats ◽  
Serum Prolactin ◽  
Hormonal Changes ◽  
Subsequent Increase ◽  
Serum Progesterone ◽  
Serum Lh ◽  
Prostaglandin F

ABSTRACT Immature female rats were pre-treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve superluteinization. Eight days after the HCG administration luteolysis was induced by sc injection of 5 μg of the prostaglandin F2α (PGF2α) analogue cloprostenol (Estrumate®). The serum levels of progesterone, 20α-dihydroprogesterone (20α-DHP), prolactin (PRL) and luteinizing hormone (LH) as well as the number of ovarian LH binding sites were measured during the first 23 h after cloprostenol injection. The serum levels of progesterone decreased from 500 to 200 ng/ml within 25 min after cloprostenol administration. A further decrease to 20 ng/ml occurred during the next 4 h, and serum progesterone remained low for the rest of the period. An increase in serum prolactin (PRL) to values between 28 and 44 ng/ml was observed after 3 h and the values remained elevated for the next 7 h. Although the serum levels of progesterone declined immediately, the serum 20α-dihydroprogesterone (20α-DHP) levels remained at 60 to 140 ng/ml for the first 5 h and then gradually increased to values corresponding to the initial progesterone levels 14 to 23 h after treatment. The number of ovarian LH binding sites was between 1.2 and 1.4 × 10−12 mol/mg protein during the first 9 h after prostaglandin (PG) injection, and then decrreased to 0.8 and 0.5 × 10−12 mol/mg protein at 14 and 23 h, respectively. The serum LH levels remained below the limit of detection for the assay (10 ng/ml) throughout the observation period. PGF2α injection induced the same basic changes in the serum levels of progesterone and 20α-DHP as cloprostenol treatment. Thus, the first effect of PG treatment measured was an immediate decline in the serum levels of progesterone, and this decline probably initiated the subsequent increase in pituitay PRL and ovarian 20α-DHP secretion. Therefore, the decrease in the number of ovarian LH binding sites appeared to be a consequence rather than a mediator of luteolytic effects of the prostaglandins.

Development and regulation of the prostaglandin F2α receptor in the rat ovary

1981 ◽  
Vol 98 (3) ◽  
pp. 441-445 ◽  
Author(s):  
Ulrich Müller ◽  
Th. Bauknecht ◽  
Jan Willem Siebers
Keyword(s):  
Binding Sites ◽  
Specific Binding ◽  
Prostaglandin F2α ◽  
Cell Type ◽  
Adult Rats ◽  
Endogenous Prostaglandin ◽  
Prostaglandin F ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Specific Receptors ◽  
Rat Ovary

Abstract. Ovaries of adult rats specifically bind PGF2α while those of immature animals do not. Induction of luteinization by hCG in juvenile animals, however, results in specific binding of PGF2α It is suggested that luteal cells are the only cell type of the ovary, which is endowed with specific receptors for PGF2α The number of PGF2α binding sites varies during the ovarian cycle. Most free receptors are detectable in early pro-oestrus, least in the oestrus stage. The oscillation of receptors disappears after inhibition of prostaglandin synthesis by indomethacin. Therefore the apparent cyclic variation of prostaglandin receptors must be ascribed to occupancy of the receptors by varying amounts of endogenous prostaglandin F2α.

STEROID HORMONE FORMATION BY THE RAT OVARY.

1966 ◽  
Vol 51 (1) ◽  
pp. 131-139 ◽  
Author(s):  
Bernard F. Rice ◽  
Albert Segaloff
Keyword(s):  
Steroid Hormone ◽  
Ovarian Tissue ◽  
Female Rats ◽  
Male Rats ◽  
Corpora Lutea ◽  
Castrate Male ◽  
Rat Ovary ◽  
17 Hydroxyprogesterone ◽  
Hormone Formation

ABSTRACT Ovaries were transplanted to the spleens of castrate male rats. After 120 days, slices of ovarian tissue, composed predominantly of corpora lutea, were incubated in Krebs-Ringer bicarbonate medium containing 50 μc acetate-1-14C. Radioactive steroid formation was assessed quantitatively by reverse isotope dilution. The formation of radioactive progesterone and 20α-hydroxy-pregn-4-en-3-one was established. The formation of radioactive 3β-hydroxy-pregn-5-en-20-one, androst-4-ene-3,17-dione, 17-hydroxyprogesterone, testosterone, oestrone and 17β-oestradiol could not be established. It appears that the corpus luteum of the rat, induced by endogenous gonadotrophins, forms only progestins from acetate-1-14C. Contrary to results previously obtained with ovarian tissue transplanted to female rats, radioactive steroid formation in vitro appeared to be augmented by luteinizing hormone (NIH-LH-S1) added to the incubation flasks. Administration of human chorionic gonadotrophin (200 IU/day) for 5 days prior to autopsy did not enhance acetate-1-14C incorporation in vitro.

scholarly journals Decay-accelerating factor in the periovulatory rat ovary

2005 ◽  
Vol 186 (2) ◽  
pp. 303-313 ◽  
Author(s):  
Mary C Gieske ◽  
Gi Youn Na ◽  
Yongbum Koo ◽  
Misung Jo ◽  
Thomas E Curry ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Complement System ◽  
Northern Blot ◽  
Ovarian Tissue ◽  
Host Cells ◽  
Control Activity ◽  
Decay Accelerating Factor ◽  
Rat Ovary ◽  
The Complement System

One of the most prominent inflammatory reactions is the activation of the complement system. The activated complement system does not distinguish between pathogens and the host cell. In order to prevent autologous complement-mediated attack, host cells express a variety of both membrane-bound and fluid-phase complement regulatory proteins which control activity of the complement cascade by acting on convertase enzymes or the membrane-attack complex. Although the process of ovulation is facilitated by the inflammatory reaction, this reaction has the potential to cause serious damage to growing follicles, ovulated follicles, and other important ovarian tissues. This study was undertaken to characterize the expression and regulation of decay-accelerating factor (DAF), a complement regulator, as a potential mediator of ovarian tissue protection from ovulatory inflammation. DNA microarray and Northern blot analyses showed that an ovulatory gonadotropin stimulus dramatically yet transiently induced DAF mRNA expression in the immature rat ovary. Northern blot and PCR analyses revealed that of the three known DAF isoforms, glycosylphosphatidylinositol (GPI)-, soluble-, and transmembrane-(TM) DAF, GPI-DAF was the predominant form. In situ hybridization localized GPI-DAF mRNA expression in the theca-interstitial cells of the periovulatory ovary. Neither the anti-progestin RU486 nor the cyclooxygenase inhibitor indomethacin significantly inhibited human chorionic gonadotropin (hCG)-induced GPI-DAF mRNA expression in vivo. In vitro theca cell culture studies indicated that hCG induces GPI-DAF mRNA expression through the protein kinase A pathway. This study suggests that gonadotropin-induced GPI-DAF may be involved in the protection of ovarian tissues from the potential attack by the complement system activated by the inflammatory response associated with ovulation.

Feasibility of in vitro maturation of oocytes collected from patients with malignant ovarian tumors undergoing fertility preservation

2021 ◽  
Vol 31 (3) ◽  
pp. 475-479
Author(s):  
Ekaterina Bunyaeva ◽  
Anastasia Kirillova ◽  
Grigory Khabas ◽  
Alexandra Asaturova ◽  
Nona Mishieva ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Endometrial Cancer ◽  
Ovarian Tissue ◽  
Serum Levels ◽  
Tumor Burden ◽  
Ovarian Tumors ◽  
Cancer Stage ◽  
Cancer Antigen 125 ◽  
Large Tumor

ObjectiveIn vitro maturation of oocytes collected from oophorectomy samples might be a promising approach in the field of oncofertility. In this study, we evaluate the feasibility of in vitro maturation of oocytes collected from oophorectomy samples in patients with ovarian tumors.MethodsThis prospective observational study included 27 patients with malignant ovarian tumors. Patients underwent oophorectomy and ovarian tissue was examined for the presence of immature cumulus-oocyte complexes. These were matured in vitro for 48 hours. Mature oocytes were vitrified or used for fertilization. Serum anti-müllerian hormone (AMH) levels were analyzed in 11 patients and cancer antigen 125 (CA125) levels in 16 patients.ResultsIn this study, 99 cumulus-oocyte complexes were obtained from 17 patients (63%). The mean (SE) age of the patients was 33.47±1.86 years (range 16–44). A total of 14 patients had ovarian cancer (IA–IVB), one patient had ovarian cancer IC and endometrial cancer IA, one patient had endometrial cancer stage IA with metastasis into the ovary, and one patient had cervical cancer stage IIB with metastasis in the ovary. Oocytes were not obtained in 10 patients who had diminished ovarian reserve due to age (>38 years), chemotherapy, or previous surgical treatment. On average, 5.8 cumulus-oocyte complexes were obtained per patient. The maturation rate was 40.4% with an average of 2.8 metaphase II oocytes per patient. As a result of the study, 3 blastocysts in 3 patients and 22 oocytes in 9 patients were vitrified.ConclusionsIn vitro maturation of oocytes collected from oophorectomy samples in patients with malignant ovarian tumors may result in oocyte and blastocyst vitrification. However, it should be offered to patients before surgery and chemotherapy. This method might be most beneficial in patients younger than 38 years, with AMH serum levels >1 ng/mL and without a large tumor burden.

STUDIES WITH ANTISERA TO LUTEINIZING HORMONE IN VIVO AND IN VITRO ON LUTEAL STEROIDOGENESIS AND ENZYME REGULATION OF CHOLESTERYL ESTER TURNOVER IN RATS

1972 ◽  
Vol 52 (3) ◽  
pp. 419-426 ◽  
Author(s):  
H. R. BEHRMAN ◽  
N. R. MOUDGAL ◽  
R. O. GREEP
Keyword(s):  
Luteinizing Hormone ◽  
Cholesteryl Ester ◽  
Control Level ◽  
Enzyme Regulation ◽  
Serum Levels ◽  
Separate Experiment ◽  
Direct Role ◽  
Luteal Function

SUMMARY The effect of antiserum to luteinizing hormone (LH) on progesterone and 20α-dihydroprogesterone output and on the enzymes regulating luteal cholesteryl ester turnover was measured in pseudopregnant rats to provide information on the role of LH in regulating luteal function. Progesterone synthesis was reduced when antiserum was added directly to an incubation system of luteinized ovarian slices from animals which had received intravenous saline or 10 μg LH. Steroidogenesis was stimulated in vitro when LH was previously given in vivo, and also on incubating luteinized ovaries from animals treated with antiserum. Treatment in vivo with antiserum alone, however, increased progesterone and 20α-dihydroprogesterone synthesis in vitro but this appeared to be an effect of incubation since in a separate experiment peripheral serum levels of both progesterone and 20α-dihydroprogesterone were reduced after antiserum treatment. Ovarian levels of cholesteryl ester and cholesterol were increased after antiserum treatment in vivo. The level of ovarian cholesteryl esterase was reduced to only 10% of the control level 24 h after antiserum treatment and in this period the level of cholesteryl ester synthetase increased 1·5 times. From these results LH appears to play a direct role in regulating the activity of enzymes controlling cholesteryl ester turnover and thereby regulates the availability of cholesterol for conversion to steroids.

PROLACTIN AND THE REGULATION OF 20α-DIHYDROPROGESTERONE SECRETION OF THE SUPER-LUTEINIZED RAT OVARY DURING LUTEOLYSIS INDUCED BY A PROSTAGLANDIN F2α ANALOGUE

1978 ◽  
Vol 87 (3) ◽  
pp. 625-631 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag
Keyword(s):  
Prostaglandin F2α ◽  
Serum Levels ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Female Rats ◽  
Serum Progesterone ◽  
Prostaglandin F ◽  
Rat Ovary ◽  
Pre Treatment ◽  
Observation Period

ABSTRACT Twenty-five day old female rats were treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve a state of luteinization. Eight days after the HCG administration luteolysis was induced by a subcutaneous injection of 5 μg of the prostaglandin F2α analogue cloprostenol (Estrumate®, ICI 80996). In animals treated with 2-Br-α-ergocryptine (BEC), administration of cloprostenol decreased serum progesterone levels from 580 to 20 ng/ml in 5 h and progesterone remained low for the next 18 h. The serum levels of 20α-dihydroprogesterone (20α-DHP) and prolactin (PRL) remained at pre-treatment values (20α-DHP 85 to 170 ng/ml; PRL less than 5 ng/ml) throughout the observation period. When animals treated with both BEC and cloprostenol were given PRL 5 h after the prostaglandin injection, an increased 20α-DHP level (630 ng/ml) was found 23 h after the cloprostenol administration, while the progesterone level was decreased (70 ng/ml). These findings were similar to the observations following cloprostenol treatment alone. The study indicates a causal relationship between the increase in the serum levels of PRL and 20α-DHP observed after PGF2α induced luteolysis in rats with superluteinized ovaries.

scholarly journals Regulation of Ascorbic acid by gonadotropins in rat Ovary

2019 ◽  
Author(s):  
Shah Saddad Hussain ◽  
Taruna Arora ◽  
Madan Mohan Chaturvedi ◽  
Sharmila Basu-Modak ◽  
Rajesh Chaudhary ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Specific Activity ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Transcriptional Level ◽  
Immature Female ◽  
Serum Gonadotropin ◽  
Rat Ovary ◽  
Dose Dependent

AbstractThe dose dependent depletion of ovarian Ascorbic acid (AA) in rat ovaries, has been used as a bioassay for measurement of Luteinizing Hormone (LH). However, the mechanism of action of gonadotropin (LH, FSH) on ascorbic acid depletion is not completely clear in biochemical terms. To elucidate the mechanism, we looked for the pathways; one, where L-GulonateDehydrogenase (L-GuDH) catalyzes the conversion of L-Gulonic acid (L-GuA) to L-Xylulose, and, in the second the pathway conversion of L-GuA to AA, in a cats, dogs and Rats. Kinetic analysis of the enzyme L-GuDHin vitroshowed the inhibitory effect of AA on L-GuDH. Therefore, we hypothesized that gonadotropins (FSH and LH) may regulate the L-GuDH maintain level of AA in ovary. LH administration to super-ovulated immature female rats caused depletion of ovarian AA but did not result in any change in the specific activity of the ovarian L-GuDH. Further, we administrated a surrogate FSH like hormone (PMSG) to immature female rats which, resulted in increased specific activity of ovarian L-GuDH. However, microarray data on RNA from ovaries exposed to FSH like hormone such as Pregnant Mare serum Gonadotropin (PMSG) did not reveal any increased expression of L-GuDH transcript. It is therefore concluded from the results obtained that; that neither LH, in decreasing the ovarian AA, nor FSH, in increasing the ovarian AA do so by regulating the activity of enzyme L-GuDH at transcriptional level. The results obtained have also been discussed by giving emphasis on the mechanism of ovarian ascorbic acid regulation of LH and FSH.

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