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Results for “Estradiol Benzoate--side effects”

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At least 19 recordsLinked to original sources
PubMed1975

[Effects of estrogenic hormones on blood lipids].

The authors have followed the effects of application of the deposit estradiolbenzoat on the blood lipides level of women at the beginning of menopause and women with arteriosclerosis. They have registered a moderate drop of the concentration of cholesterol, beta-lipoproteins, and slight changes of the non-esterified fatty acids level. Women using contraceptive hormonal mixtures were found with higher level of cholesterol in the blood serum than those being watched. The application of a single dose of androgen did not have any substantial effects on the blood lipides level.

Adult↗
PubMed1976

Estrogenic effects of an antiestrogen, MER-25, on eating and body weight in rats.

Ethamoxytriphetol, MER-25, which acts as an estrogen antagonist on other estrogen-sensitive behaviors and in peripheral tissues, was found to be fully estrogenic with respect to eating behavior and body weight regulation. The MER-25 causes decreases in eating and weight gain that are not due to toxicity, as indicated by its failure to induce a learned aversion to saccharin and by its failure to alter spontaneous activity. Estradiol benzoate (EB) and MER-25 similarly affect eating and body weight in gonadectomized rats: Both cause a transient decrease in food intake and a permanent decrease in body weight relative to controls; the eating and body weight effects of both MER-25 and EB are attenuated by progesterone; and both MER-25 and EB affect females more than males. Because of its full estrogenicity, MER-25 fails to antagonize the effects of EB on eating and body weight while simultaneously antagonizing effects of EB on sexual behavior, the uterus, and the vagina. The results indicate that the systems mediating the effects of estrogens on eating and body weight differ biochemically from other behavioral and somatic estrogen-sensitive systems.

Animals↗
PubMed1976

Importance of progesterone in DNA synthesis of pregnancy-dependent mammary tumors in mice.

Hormone responsiveness of pregnancy-independent mammary tumors in SHN mice and pregnancy-dependent tumors in GR/A mice and in F1-hybrids between these strains was studied. Force-bred female mice with palpable mammary tumors were given subcutaneous injections of several hormones singly or in combination twice daily from 1 day before to 1 day after parturition. One group received a graft of three pituitary glands under the kidney capsule (3AP) during days 12-14 of pregnancy. One day after parturition, the in vivo incorporation of 3H-thymidine into DNA of normal and neoplastic mammary glands was determined as the index of DNA synthesis. Plasma prolactin in some groups of GR/A mice was assayed by radioimmunoassay. In GR/A mice, estradiol benzoate (EB: 0.5 mug X 2/day) or 3AP had no effect on either normal glands or tumors, despite an increase in plasma prolactin level. Progesterone (P:100 or 1,000 mug X 2/day) significantly increased DNA synthesis of both normal and neoplastic glands when compared to the controls, while the plasma prolactin level in this group was low. The administration of human placental lactogen (HPL: 100 mug X 2/day) stimulated DNA synthesis of normal glands only. P plus HPL promoted DNA synthesis of tumors more than P alone, but not P plus EB. While DNA synthesis of the tumors of SHN was never affected by these hormone treatments, the hormone responsiveness of tumors of F1-hybrids was almost the same as that of GR/A mice; the effect of P was prominent. Correlation of DNA synthesis between pregnancy-dependent mammary tumors and normal glands was significant only in groups treated with P alone or in combination with other hormones.

Animals↗
PubMed1977

Estrogen-induced sexual receptivity and localization of 3H-estradiol in brains of female mice: effects of 5 alpha-reduced androgens, progestins and cyproterone acetate.

Sexual receptivity induced in ovariectomized CD-1 mice with chronic daily administration of estradiol benzoate (E2 B) was blocked by concurrent administration of the 5 alpha-reduced androgen, dihydrotestosterone (DHT). Receptivity was restored in these females with progesterone-, but not with dihydroprogesterone-priming 6 hr prior to testing. Delaying the DHT injections until 12 hr after the E2 B injections greatly reduced its inhibitory properties. Receptivity in E2 B-primed females was also blocked by concurrent treatment with cyproterone acetate and 3 alpha-, but not 3 beta-adrostanediol. Pretreatment with DHT, or 3 alpha- or 3 beta-androstanediol failed to consistently affects 3H-estradiol accumulation in crude nuclear and supernatant fractions from brain and pituitary.

20-alpha-Dihydroprogesterone↗
PubMed1976

Facilitation of receptivity in estrogen-primed rats during successive mating tests with progestins and methysergide.

The role of hormonal and experiential variables in mediating the gradual increase of receptivity occurring during weekly tests was evaluated in adult ovariectomized females. Hormone treatment consisted of estradiol benzoate (EB) injection followed by progesterone (P), 20alpha-hydroxyprogesterone (20alpha-OHP), methysergide maleate (Me), or oil during weekly mating tests. The experiential conditions were vaginal stimulation, mounts only, or no interaction with males. There was a gradual increase in receptivity in all groups even en the one receiving oil. Progressive facilitation occurred even when no interaction with the male was permitted. Interchanging the synergists on the sixth and seventh tests was not detrimental to the display of receptivity attained with synergists given previously. Thus, we concluded that successive injections of EB rather than synergists or experience mediate this increase in receptivity.

Animals↗
PubMed1976

Studies on the puberty-controlling function of the mediocortical amygdala in the immature female rat.

The puberty-controlling function of the mediocortical amygdala in immature female rats was investigated by lesioning this region at different ages and by studying the effects on the onset of spontaneous and experimentally-induced precocious puberty. At 21 days of age, bilateral lesions in the anterior mediocortical amygdala (AMCA) caused precocious puberty and enhanced the puberty-accelerating effect of bilateral lesions produced simultaneously in the medial preoptic area (MPA). Similar lesions, ineffective on day 26, delayed the onset of puberty when produced on day 32 in otherwise untreated rats. Lesions in the posterior mediocortical amygdala (PMCA) at 26 or 32 days of age postponed puberty in untreated rats and inhibited the advancement of their 1st pubertal ovulation that resulted from damage to the ventromedial-arcuate region (VAH) or daily administration of 0.05 mug estradiol benzoate (EB) per 100 g b.w. The results confirm earlier findings of different gonadotropin-controlling activities of the AMCA and PMCA in immature female rats and suggest maturational changes in the function of both areas. The gonadotropin-inhibiting action exerted by the AMCA at 3 weeks of age is lost when puberty approaches; a gonadotropin-stimulating activity seems to develop in both the AMCA and PMCA.

Age Factors↗
PubMed1976

Immobilization does not inhibit the post-coital ovulatory surge of luteinizing hormone in the rabbit.

Heparinized blood samples were obtained through an indwelling catheter in the central ear artery from sexually mature female New Zealand white rabbits after copulation. Immediately after 1 or 2 matings the female was transferred to a restraining cage; blood samples were taken at intervals while the animal was completely immobilized for 3-5 h or was only immobilized for blood withdrawal. Ovulation was detected by the presence of corpora lutea at laparotomy the following day. Plasma was analyzed for LH by established radioimmunoassay procedures. Immobilization did not inhibit ovulation or the pre-ovulatory surge of LH in either group. These data suggest that immobilization cannot inhibit the reflex release of LH in the female rabbit.

Animals↗
PubMed1976

Plasma norepinephrine during the rat estrous cycle and after progesterone treatment to the ovariectomized estrogen-primed rat.

In four-day cycling rats studied during the estrous cycle, the levels of circulating norepinephrine (NE) showed a sharp rise concomitant with the LH surge in the afternoon of proestrus. Following the peak, plasma NE fell rapidly to the minimum value by the morning of estrus. The administration of progesterone to ovariectomized estrogen-primed rats resulted in a surge in plasma NE levels 4 h after progesterone treatment. The maximal levels attained were 3-fold greater than baseline values, falling rapidly to reach basal values 8 h after the administration of progesterone. The amine levels remained unaffected 12-20 h later. The LH values attained a maximum 8 h after the injection of progesterone. In rats treated with estradiol benzoate (EB) followed by 0.1 ml of oil instead of progesterone, neither the NE nor the LH peak were observed. These findings are discussed with respect to the significance of increased amounts of plasma NE related to the LH surge.

Animals↗
PubMed1976

[Mechanism of LH release with synthetic LH-RH (author's transl)].

The purpose of this study is to examine the effect of LH-RH on LH release in the baboon. Fifteen female baboons having the normal menstrual cycle were used for this study. On hundred mug of synthetic LH-RH was injected subcutaneously in both the early follicular phase and the early luteal phase. For control purposes, 1 ml of saline was injected subcutaneously in the luteal phase. Blood samples were collected by femoral vein puncture with light anesthesia under prearranged schedule and were assayed for LH-RH, LH, estrogen and progestin. The plasma level of LH-RH reached a maximum within 4 minutes after s.c. injection of 100 mug LH-RH, decreased sharply at first, and then slowly later. Fast and slow disappearance components (t1/2 = 4.7 min., 37.1 min. respectively) were observed. In the baboon given LH-RH during the luteal phase, peaks in plasma levels of LH were observed within 30 minutes and within 90 to 150 minutes after injection. A lesser pituitary response to LH-RH for LH release occurred during the follicular phase. The first peak of LH was well-correlated with the peak of plasma LH-RH but the later elevations of LH (observed within 90 to 150 minutes after LH-RH injection) were not necessarily related to the plasma level of immunoassayable LH-RH. Elevation of plasma levels of estrogen and progestin was observed wtihin 45 minutes after LH-RH injection. In saline control, the plasma level of LH was not elevated; however, plasma levels of estrogen and progestin were increased within 45 minutes after saline injection. Later elevation of plasma LH observed between 90 and 150 minutes after LH-RH injection may be due to administered LH-RH in cooperation with elevated levels of plasma estrogen and progestin. To pursue this problem, injections of estrogen and/or progesterone were performed during the early follicular phase. Injection of 600 mug of estrodiol benzoate (EB) for 3 days caused an elevation of plasma level of LH and enhanced pituitary LH responsiveness to LH-RH for LH release; however, injection of 100 mug EB for 3 days showed less effect on LH release. Injection of 10 mg of progesterone for 3 days also caused an elevation of plasma level of LH and enhanced the pituitary responsiveness to LH-RH release. Injection of both 600 mug EB and 10 mg progesterone for 3 days did not elevate plasma level of LH and showed no significant effect of LH-RH on LH release as compared to control. These results suggest that elevated levels of circulating estrogen and progestin may determine LH release and exposure of the pituitary to LH-RH is necessary for LH release. In dose and time schedule used in this study, it is inferred that estrogen and progesterone may exert their direct effect to hypothalamus on endogenous LH-RH secretion and also may exert their effect on pituitary gonadotrophs to change the sensitivity to LH-RH, i.e. these steroid hormones may be major factors in the control of gonadotropin release in the baboon.

Animals↗
PubMed1975

The effect of ovarian steroid feedback upon radioimmunoreactive luteinizing hormone releasing hormone in the hypothalamus.

A radioimmunoassay (RIA) method for luteinizing hormone (LH) releasing hormone (RH) utilizing rabbit antiserum against synthetic (Glu1)-LH-RH coupled with human serum albumin at the N-terminus, is described. This assay system for LH-RH also cross-reacted with several LH-RH analogues or fragments, but not with pituitary trophic hormones. The assay was performed on the hypothalamic extracts of adult ovariectomized rats and female immature rats which had been treated with estradiol. The FSH and LH levels in the pituitary gland and serum of the same animals were determined by RIA. The radioimmunoreactive LH-RH content of the stalk median eminence markedly increased seven days after ovariectomy. The serum levels and the pituitary contents of FSH and LH of the same rats were also significantly augmented. In immature rats, the hypothalamic content of LH-RH, as measured by RIA, was significantly increased one hour after the injection of estradiol. The FSH and LH levels in the pituitary showed a significant rise after 7 hours.

Animals↗
PubMed1977

The role of follicle-stimulating hormone (FSH), in combination with luteinizing hormone (LH), in oestrogen-induced ovulation during the oestrous cycle in the rat.

Studies were undertaken to determine the role played by FSH in oestrogen-induced ovulation in 4-day cyclic female rats. About one half of the experimental animals receiving 10 microng oestradiol benzoate (OeB) subcutaneously, on the morning of dioestrus I, displayed luteinization or/and ovulation, when sacrificed on the morning of expected pro-oestrus. Pento-barbitone administered on dioestrus II at 18.00 did not prevent this action of OeB. A simultaneous LH and FSH surge was observed in the serum of half of the OeB-treated females killed by decapitation of dioestrus II at 17.30. The LH surge was decreased in OeB-treated females bled by cardiac puncture under pentobarbitone anaesthesia at dioestrus II at 17.30. This bleeding procedure almost completely suppressed the luteinizing effects of OeB. It was concluded that i) OeB caused a synergistic release of LH and FSH ii) bleeding by cardiac puncture as such may constitute a source of inhibition of OeB-induced luteinization.

Animals↗
PubMed1977

Sexual behaviour of neonatally castrated rats injected during infancy with oestrogen and dihydrotestosterone.

Male rats were castrated on the day of birth (day 1) and injected with either testosterone, dihydrotestosterone, a synthetic oestrogen (RU 2858 + dihydrotestosterone, or oil from days 1 to 5. The aromatizable androgen, testosterone, and RU 2858 suppressed both cyclic gonadotrophin secretion, indicated by the absence of corpora lutea from implanted ovarian grafts, and the behavioural response to oestradiol benzoate + progesterone injections in adulthood. The 5alpha-reduced androgen, dihydrotestosterone alone did not affect gonadotrophin secretion or female receptive behaviour, but like testosterone, it increased penis development in response to testosterone propionate, and this was positively correlated with copulatory efficiency, i.e. the ratio of intromission to mount frequencies. Nevertheless, ejaculation only occurred among animals that had received testosterone or RU 2858 + dihydrotestosterone. The results support the concept that during the preinatal period, neural conversion of androgens to oestrogens is important both for the suppression of female gonadotrophin secretion and behaviour patterns as well as for the organization of male behaviour patterns. The 5alpha-reduction of unsaturated C19-steriods to dihydrotestosterone in peripheral tissues is also required to complete the development of the male genital tract.

Animals↗