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At least 19 recordsLinked to original sources
PubMed2002

Direct ovarian effects and safety aspects of GnRH agonists and antagonists.

The wide application of gonadotrophin-releasing hormone (GnRH) analogues in assisted reproduction has raised concerns about their potential extra-pituitary actions. Although data from animal studies support the presence of ovarian GnRH receptors and of direct ovarian effects of GnRH analogues, this has not been unequivocally demonstrated in humans. Available evidence suggests, however, the existence of GnRH receptors in human granulosa-luteal cells, while the majority of the studies performed showed that progesterone is inhibited by GnRH agonists in vitro. On the other hand, no difference seems to exist between agonists and antagonists in terms of granulosa-luteal cell steroidogenesis under basal conditions. So far, no studies have suggested an adverse effect of GnRH analogues on the developing human follicle. Moreover, the physiological significance of a direct in-vitro ovarian effect of GnRH analogues remains to be established.

Amino Acid Sequence↗
PubMed2005

Metabolic and ovarian effects of rosiglitazone treatment for 12 weeks in insulin-resistant women with polycystic ovary syndrome.

BACKGROUND: Insulin sensitizers have favourable metabolic and ovarian effects in polycystic ovary syndrome (PCOS). This study examined rosiglitazone, a thiazolidinedione, in PCOS. METHODS: In a prospective, open-label study, the effects of rosiglitazone on metabolism and ovarian function were examined in 42 non-diabetic women with PCOS classified according to the National Institute of Child Health and Human Development criteria and insulin resistance (IR) by steady-state plasma glucose (SSPG) > or =10 mmol/l on octreotide-modified insulin suppression testing. Participants were randomized to rosiglitazone 2, 4 or 8 mg daily for 12 weeks. Endpoints included ovulation and menstrual pattern; serum testosterone, sex hormone-binding globulin (SHBG), and LH; and changes in IR and glucose-insulin responses on 8 h mixed-meal profile. RESULTS: After rosiglitazone 8 mg daily for 12 weeks, SSPG declined and insulinaemia fell by 46%; lower doses gave lesser effects. Serum LH, total and free testosterone were unchanged; SHBG increased. With rosiglitazone, ovulation occurred in 23/42 women (55%), without significant dose dependence. Both before and during treatment, ovulators on rosiglitazone had lower circulating insulin and free testosterone and higher SHBG than non-ovulators. Testosterone declined only in a subgroup of ovulators with early vaginal bleeding after starting rosiglitazone. CONCLUSIONS: Rosiglitazone in insulin-resistant PCOS promoted ovulation and dose-dependently decreased IR and insulinaemia; ovulators had lower circulating insulin and testosterone.

Blood Glucose↗
PubMedDate not supplied

Interaction of estradiol and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in an ovulation model: evidence for systemic potentiation and local ovarian effects.

Immature rats were treated with estradiol cypionate, (ECP, 0, 0.1, 1, or 2 mg/kg s.c.) followed 24 h later by TCDD (0 or 10 microg/kg orally). Follicular development was induced with eCG [5 or 10 IU subcutaneously (s.c.)] followed by an ovulatory dose of hCG (10 IU s. c.). Inhibition of ovulation by TCDD was potentiated by ECP in hypophysectomized but not intact rats. Only hypophysectomized rats exposed systemically to TCDD and ECP exhibited weight loss. Pair feeding mimicked the combined effects of TCDD and ECP in hypophysectomized rats. In another experiment, intact rats received ECP s.c. (0 or 2 mg/kg) and TCDD into the ovarian bursa (0 or 250 ng). Another group of intact rats received TCDD orally (10 microg/kg) and ECP into the ovarian bursa (0 or 1.5 microg). Blockade of ovulation by systemic or local TCDD was alleviated by ECP pretreatment. Estrogen increased the systemic toxicity of TCDD in rats whereas antagonizing its direct ovarian effects.

Administration, Oral↗
PubMed1985

Direct ovarian effect of clomiphene citrate in the rabbit.

The effects of clomiphene citrate (CC) on ovulation and ovum maturation were studied using the isolated perfused rabbit ovary. CC (10(-5) M) added to the perfusate with human chorionic gonadotropin (50 IU) did not affect ovulatory efficiency, ovulation time, oocyte maturation, or degeneration of ovulated ova and follicular oocytes. During perfusion without human chorionic gonadotropin, the percentage of follicular oocytes with germinal vesicle breakdown was significantly increased in response to CC (10(-5) M or 10(-7) M); a greater percentage of follicular oocytes was degenerated. Estradiol (100 ng/ml) added to the perfusate reversed the effect of CC on degeneration of follicular oocytes. Of follicular oocytes from ovaries perfused with CC, 79.3% were degenerated; in contrast, 25% were degenerated in ovaries treated with CC plus estradiol. These data suggest that CC has a direct ovarian effect and that ovum degeneration associated with CC may be related to an antiestrogenic action.

Animals↗
PubMedDate not supplied

Direct ovarian effects and safety aspects of GnRH agonists and antagonists.

In in-vitro fertilization programmes, gonadotrophin releasing hormone (GnRH) agonists are now routinely used in order to prevent the undesired pre-ovulatory spontaneous luteinizing hormone surge. The first publications are now appearing in which GnRH antagonists are used with the same purpose. More attention should be addressed to the safety aspects of these drugs. This review aims to summarize studies on direct ovarian effects of GnRH agonists and GnRH antagonists in non-primates and primates with respect to the functional and morphological aspects in-vitro as well as in-vivo. We conclude that there is a wide variety of functional and morphological effects of GnRH analogues on the ovary. The sometimes paradoxical effects indicate that a variety of factors may be involved in the various processes. Those factors are: (i) the type and dose of the analogue, (ii) the different regimens of administration, (iii) ovarian status at the time of exposure, (iv) ovarian cell types in in-vitro systems, (v) hormonal pre-treatment of these cultures, (vi) the type of hormonal stimulation added to the in-vitro culture, (vii) further methodological differences in the experiments and finally (viii) physiological variations in GnRH receptor abundance which depends on species and/or timing in the cycle. With the increasing number of patients using GnRH analogues in assisted reproduction treatments, there will be an increasing number of pregnancies exposed to these drugs. So far, there does not appear to be an increased risk of birth defects or pregnancy wastage in human pregnancies exposed to daily low-dose GnRH agonist therapy in the first weeks of gestation.

Animals↗
PubMed1975

Extra-ovarian effects of bovine prolactin and growth hormone on the vagina of the mouse.

Hypophysectomized-ovariectomized mice receiving oestrogen and progesterone were treated with and without bovine prolactin and growth hormone (GH). Prolactin significantly increased vaginal weight and vaginal sialic acid content, but had no effect on vaginal sialic acid concentration, an indicator of vaginal mucification. Growth hormone significantly increased all three vaginal parameters. For vaginal sialic acid content and concentration, the synergism between oestrogen and progesterone was found to be greater in the presence than in the absence of GH and the maximum response to GH was obtained when between 20 and 100 mug GH was administered daily. It was concluded that GH but not prolactin has an extra-ovarian effect on vaginal mucification in the mouse.

Animals↗
PubMed1988

Ovarian effects of SK&F 86002-A2 in the rat: site of action.

In a preliminary 30-day study, oral administration of SK&F 86002-A2, an inhibitor of prostaglandin and leukotriene synthesis, blocked ovulation and altered ovarian structure and hormone production in rats. The purpose of the present study was to determine if the locus of action of SK&F 86002-A2 for these effects was the ovary or some other site in the female reproductive system, using a number of experimental approaches. A single sc or intraovarian injection of SK&F 86002-A2 did not block spontaneous or gonadotropin-induced ovulation in proestrous rats, whereas indomethacin, a positive control, acutely disrupted the ovulatory process. Since neither route of administration blocked ovulation, integrated pituitary and ovarian events were not negatively affected by a single injection of SK&F 86002-A2 at doses which caused ovarian dysfunction when administered repeatedly for 30 days. In contrast to a single dose, oral administration of SK&F 86002-A2 to hypophysectomized rats for 2 weeks suppressed follicular growth and estradiol production in response to sc administration of pregnant mare serum gonadotropin. Although ovarian function was suppressed in hypophysectomized rats, LH surges induced by estradiol in ovariectomized rats were not affected by administration of SK&F 86002-A2 for 2 weeks. Thus, hypothalamic/pituitary dysfunction did not contribute to the ovarian effects of SK&F 86002 that occurred after repeated dosing. In conclusion, these results indicate that disruption of ovarian cycles by SK&F 86002-A2 is related to a direct effect on the ovary, and not to altered hypothalamic/pituitary function and LH release. Specifically, SK&F 86002-A2 may suppress the ovarian response to gonadotrophin, retarding follicular growth and estrogen production. The ovarian effects are consistent with a pharmacological expression of the inhibitory action of SK&F 86002-A2 on prostaglandin and leukotriene synthesis.

Administration, Oral↗
PubMedDate not supplied

Ovarian effects of a high lactose diet in the female rat.

Young women with galactosemia experience ovarian failure at a very early age raising concern about the ovarian toxicity of galactose. While galactose may be present in the diet as a monosaccharide, it is predominantly derived from cleavage of the disaccharide lactose within the intestine. Our previous studies in animals have shown that high galactose diets inhibit ovarian follicular development and long-term exposure to high lactose diets retards growth of rats. The objective of the present study was to determine whether galactose exposure in the form of dietary lactose mimics the effects found previously with diets rich in galactose. Sixty female Long-Evans rats (25-day-old) were randomly assigned to two groups and fed a control diet (41.9% glucose in AIN93G [American Institute of Nutrition], CON) before lactose treatment. Unilateral ovariectomy (uOVX) was performed on half of the rats in each group to determine baseline ovarian follicle numbers. The study diet was a high lactose diet (HLD) containing 41.9% lactose in AIN93G. Study diet exposure started 1 month after uOVX (3 months old) and continued for 7 months in the treatment group. The control group remained on the 41.9% glucose diet throughout. Vaginal cytology, ovarian morphometric analyses, and serum concentrations of estradiol and progesterone were examined. Long-term exposure to the HLD decreased the body weights of animals and progesterone concentrations in the serum but produced no harmful effects on ovarian morphology or function. Beginning at 5 months of age (two months of lactose treatment) increasing numbers of females began to cycle irregularly but there was no difference between the glucose and lactose diet groups. These negative findings imply that administration of galactose in the form of lactose seems to be much less toxic than when galactose is fed to animals. From a human health perspective, these results are somewhat reassuring, since in general, women eat lactose-containing foods rather than foods that contain large amounts of free galactose.

Aging↗
PubMed1975

Action of prostaglandin F2alpha on pregnancy in hamsters: luteolytic and extra-ovarian effects.

Pregnancies in hamsters may be terminated by 10 mug PGF2alpha administered b.i.d. on days 4, k and 6 of gestation. Small (250 mug and above) daily injections of progesterone on the same days will reverse this PG effect; in contradistinction, 10 mg of progesterone per day failed to maintain normal pregnancies in hamsters spayed on day 5. Daily administration of 3 mg of progesterone and 1 mug of estrone essentially normalized the gestation; administration of PGF2alpha at 10 mg on days 5, 6 and 7 of pregnancy in steroid-maintained rats, resulted in pregnancy termination in all animals, while 1 mg was partly effective. These data demonstrate an extra-ovarian site of action of prostaglandin F2alpha on pregnancy in hamsters.

Animals↗
PubMed1990

Insulin secretion in polycystic ovarian disease: effect of ovarian suppression by GnRH agonist.

Nine obese and ten non-obese women with polycystic ovarian disease (PCO), and seven obese and eight non-obese normal women, had an oral glucose tolerance test (OGTT) before and after treatment with GnRH agonist (buserelin 400 micrograms/day s.c. for 8 weeks) in order to investigate the effect of ovarian suppression on their insulinaemic secretion. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), oestradiol (E2), androstenedione (A), testosterone (T), DHEAS, cortisol and insulin (I) were measured at time 0 of OGTT; in all samples of OGTT, E2, T, A and I were also assayed. PCO patients showed higher basal androgen levels than control patients. All subjects showed a normal glycaemic response to OGTT. The mean fasting and areas under the curve (ISA) of plasma I were significantly greater in the obese PCO women than in non-obese PCO, the normal obese and non-obese women. All PCO patients showed significantly higher fasting I and ISA values in respect to all control patients. Hyperinsulinaemic responses were 89% in PCO obese, 30% in non-obese PCO and 29% in obese control patients. After buserelin treatment, these values did not change significantly in respect to pretreatment in all groups, in spite of a significant decrease of androgen secretion. During OGTT, no variations of steroid plasma concentrations were seen in both normal or hyperinsulinaemic PCO patients. The data of this study show that hyperandrogenism, hyperinsulinism and obesity were associated with different modalities in PCO patients and that a marked decrease of androgen secretion did not restore a normal insulinaemic response to OGTT, suggesting that hyperandrogenism does not produce hyperinsulinism.

Adult↗
PubMed1996

Ovarian effects upon maternal glucose tolerance.

Ovaries from homozygous diabetic (db/db) female mice were removed and transplanted into the empty left ovarian sacs of normal homozygous (m/m) female mice which had undergone left oophorectomies. To produce controls, the previously removed normal left ovaries were transplanted into the empty left ovarian sacs of other normal (m/m) left oophorectomized females. Glucose tolerance tests were done on the study and control mice before surgery, after surgery, during pregnancy, and after delivery. There were no significant differences in the glucose tolerance test results between study group and controls before or after surgery. However, the study group, when compared to the controls, had a statistically significant glucose intolerance during pregnancy. After delivery, the glucose levels returned to normal. The ovaries from diabetic (db/db) female mice may produce hormones which, by themselves or in concert with the fetal and placental hormones, may produce maternal glucose intolerance during pregnancy.

Animals↗
PubMedDate not supplied

Direct ovarian effect of growth hormone in the rabbit.

PROBLEM: This study was undertaken to assess whether growth hormone (GH) can stimulate follicle growth and ovarian steroidogenesis via putative GH receptors. METHOD: In vitro perfused rabbit ovary. RESULTS: Ovulation occurred in neither the control ovaries nor experimental ovaries treated with 100 ng/ml of GH, whereas all ovaries exposed to 50 IU of human chorionic gonadotropin (hCG) ovulated. The addition of GH to the perfusate significantly stimulated the follicle growth in the absence of gonadotropin. The percent change in follicle diameter in GH-treated ovaries did not differ significantly from that in hCG-treated ovaries. Exposure to GH significantly stimulated the meiotic maturation in the follicular oocytes, as compared with the contralateral control ovaries. Although the concentration of progesterone in the perfusate did not differ significantly between GH-treated and control ovaries, GH stimulated estradiol production by the perfused rabbit ovaries. Rabbit ovary membranes exhibited high affinity binding sites of hGH (Kd = 6.1 x 10(-9) M). CONCLUSION: GH acts on the rabbit ovary to stimulate the follicle growth, oocyte maturation, and ovarian estradiol production by interacting with the specific receptors located in ovarian plasma membranes.

Animals↗
PubMed1985

In vitro study of the direct ovarian effects of gonadotropin-releasing hormone (GnRH) in the frogs, Rana pipiens and Rana catesbeiana.

Ovaries from the leopard frog, Rana pipiens, and bullfrog, R. catesbeiana, were used to study potential direct extrapituitary effects of gonadotropin-releasing hormone (GnRH). GnRH alone did not alter steroid secretion from ovaries in either species. Ovarian fragments containing mature follicles from R. pipiens were incubated in several submaximal doses of homologous pituitary homogenate or purified bullfrog luteinizing hormone (LH) together with 1000 ng/ml GnRH. The addition of GnRH failed to alter testosterone (T) or progesterone secretion or germinal vesicle breakdown over a wide dose range of gonadotropin. The effects of supramaximal doses of pituitary homogenate on R. pipiens and the effects of homologous LH on T secretion by fragments of R. catesbeiana ovaries were also unaffected by the presence of GnRH. The lack of a GnRH effect on the dynamics of T secretion in the bullfrog was further confirmed in a superfusion system with homologous pituitary homogenate. This study fails to demonstrate an action of GnRH at the level of the ovary in two ranid species.

Animals↗
PubMed1988

Ovarian effects of an anti-inflammatory-immunomodulatory drug in the rat.

The purpose of this study was to determine whether a 30-day administration of SK&F 86002-A2, an inhibitor of cyclooxygenase and 5-lipoxygenase pathways of arachidonate metabolism, adversely affected reproductive cycles, ovarian structure, and/or pituitary/ovarian hormone secretion. Cyclooxygenase and 5-lipoxygenase enzymes catalyze the reactions leading to the synthesis of prostaglandins and leukotrienes, respectively, which are physiological regulators of ovarian function. Female rats were dosed once daily by gavage with 0, 1, 5, 10, 30, or 60 mg (base)/kg/day of SK&F 86002-A2 for 30 consecutive doses beginning on the day of vaginal proestrus. Vaginal smears were then examined daily until necropsy, when ovaries and uteri were collected for macroscopic and histological examination. In addition, serum concentrations of estradiol, progesterone, luteinizing hormone, follicle stimulating hormone, and prolactin were estimated by radioimmunoassay. Estrous cycle irregularity, resulting from a dose-related lengthening of the interestrous interval, significantly (p less than 0.05) reduced the number of cycles in rats receiving 60 mg/kg/day of SK&F 86002-A2 compared to controls. Furthermore, the ovaries from this group of rats weighed significantly more (p less than 0.05) than controls, apparently due to an increased occurrence of enlarged, cystic follicles that occasionally contained blood. Luteinized follicles with entrapped ova were also detected during histological examination. Dilatation of the uterine lumen was observed in some rats receiving doses of SK&F 86002-A2 greater than 1 mg/kg/day. Serum progesterone in rats receiving 60 mg/kg/day of SK&F 86002-A2 was significantly (p less than 0.05) lower than controls. In contrast, mean levels of serum estradiol were elevated in rats receiving 30 mg/kg/day of SK&F 86002-A2. Serum concentrations of FSH, LH, and prolactin were not significantly different in any group. The results of this study suggest that SK&F 86002-A2 disrupts cyclic ovarian function by a local, cumulative action that inhibits ovulation and alters steroid secretion.

Animals↗
PubMed1982

Dominant lethal and ovarian effects of plutonium-239 in female mice.

In two separate experiments (C3H x 101)F1 female mice were injected intravenously with 239Pu in trisodium citrate, then mated in pairs to strain CBA males, to test for dominant lethality. In the first experiment 10 muCi kg-1 and in the second 20 muCi kg-1 body mass was injected. Matings were after 6 days in the first experiment (estimated ovarian absorbed dose of 0.1 Gy) and after 3, 6 or 12 weeks in the second (estimated ovarian doses of 1.11, 2.45 and 5.91 Gy respectively). No evidence of dominant lethal induction was found in the first experiment, but in the second there was a significant increase over controls in pre-implantation loss in all three series. Post-implantation lethality increased significantly (by 12 per cent) only after 12 weeks' exposure. With the 6- and 12-week exposures (especially the latter) luteal counts fell and fewer females became pregnant than in controls. This is attributed to oocyte killing by the alpha-particles. Histological and autoradiographic investigations showed a marked reduction in ovarian size and follicular numbers with fission-tracks clustered mainly over the medullary stroma. The pre-implantation loss may stem from lowered fertilization of oocytes because of their damage, so that the best measure of dominant lethality is that based on post-implantation death. Thus there is only slight evidence for the induction of genetic damage, which is in line with previous findings after chronic exposures of female mice.

Animals↗