Disease relevance of Benzo-Ginestryl

• Replacement therapy with 17 beta-estradiol-3-benzoate (10 micrograms/100 g body weight) subcutaneously daily for 7 d in GDX female rats resulted in a slight further increase in follistatin mRNA levels compared to GDX females [1].
• Expression of the endogenous gene in a rat hepatoma cell line is increased 5-fold and 2-fold in response to dexamethasone and 17 beta-estradiol-3-benzoate, respectively [2].
• These data suggest that considerably higher doses and serum concentrations of EB and/or P are required to elicit robust lordosis and PRO in ovx obese Zucker than in lean rats [3].
• The relationship between the amount and duration of administration of estradiol benzoate (EB) to newborn female rats and the induction of sterility was examined in 407 animals [4].
• Renal tubule lesions, uterine squamous metaplasia, vaginal keratinization and telangiectasia of pancreatic islets were also observed with EB [5].

Psychiatry related information on Benzo-Ginestryl

• In the minority of trials when EB-treated males approach a stimulus male, they occasionally receive a neck grip to which they display receptive postures as opposed to agonistic behaviors [6].
• Therefore, sensitivity to EB was enhanced both in response time and amount of LH released [7].
• Two experiments were conducted to evaluate the effect of estradiol benzoate (EB), progesterone (P), ovine prolactin (oPrl), or their combinations on temporal patterns of serum luteinizing hormone (LH) and Prl and on nesting behavior in adult ovariectomized female turkeys [8].
• On GD 16, animals were hysterectomized-ovariectomized and given estradiol benzoate (EB); they were then tested for maternal behavior 48 hr later [9].
• Time spent on the open arms and locomotor activity of OVX animals treated with estradiol benzoate (EB) did not differ from the vehicle-treated animals [10].

High impact information on Benzo-Ginestryl

• This dimorphism has an organizational nature: administration of estradiol-benzoate to quail embryos (a treatment that abolishes male sexual behavior) results in a dramatic decrease of the VT-immunoreactivity in all sexually dimorphic regions of the male quail brain [11].
• When the mice were injected with a variety of estrogenic compounds, 17 beta-estradiol-3-benzoate, which was the most potent stimulator of uterine cell proliferation among the estrogens tested, dramatically elevated the enzyme formation of the uterus in a dose- and time-dependent fashion [12].
• Prostatic S3 mRNA disappears after 8 days castration and is restored to intact levels by dihydrotestosterone (DHT) but not estradiol benzoate (EB) for 8 days [13].
• A pharmacological dose of estradiol-benzoate caused a significant increase in intestinal absorption of calcium, which was comparable to that of a pharmacological dose of calcitriol in both OVX and sham-operated rats [14].
• In wild-type males, DHT and hydroxyflutamide both induced increases in the number of spine synapses in the CA1 stratum radiatum, whereas EB had no effect [15].

Chemical compound and disease context of Benzo-Ginestryl

• When injected 48 h prior to testing, increasing doses of estradiol benzoate (EB) or testosterone propionate (TP) resulted in increasing levels of lordosis behaviour [16].
• Ovariectomized rats with unilateral cannulae aimed at the MPN were given 5microg 17beta-estradiol benzoate (EB), once every 4 days and tested for lordosis [17].
• Despite the induction by EB of a behaviorally-sufficient concentration of cytoplasmic progestin receptors, fewer males (3/10) than females (8/10) responded to EB (10 micrograms)-progesterone treatment with the expression of lordosis [18].
• Single injections of dihydrotestosterone propionate (DHTP), also injected 48 h prior to testing, inhibited lordosis behaviour in EB-primed female rats [16].
• Prenatal treatment with 3 micrograms DESDP caused delayed puberty, impaired ovarian function, reduced responsiveness of lordosis to EB and P in adulthood (defeminization), augmented mounting in the absence of hormones (masculinization), and reduced responsiveness of mounting to exogenous EB and P in adulthood (defeminization) [19].

Biological context of Benzo-Ginestryl

• Scatchard analysis showed that ovariectomy and thyroidectomy decreased the number of PRL binding sites in the liver as compared to those in intact controls or in ovariectomized-thyroidectomized rats treated with EB and T4 [20].
• On the other hand, the increase of EB exposure (Ei5, EI) resulted in a gradual and significant delay in the onset of first estrus and in a high number of estrous phases, as frequently observed during reproductive decline [21].
• A greater proportion of females displayed ovulation and/or luteinization following coitus than those given EB only [22].
• Almost all of the animals receiving 10 daily injections of 10 micrograms EB from Day 1 showed persistent diestrus until at least 100 days of age [4].
• Both aspects of reproductive behavior can be activated in a dose-dependent manner by injections of estradiol benzoate (EB) [23].

Anatomical context of Benzo-Ginestryl

• 125I-radiolabeled ovine prolactin (oPRL) binding activity was measured in microsomal membranes of liver tissue from intact, ovariectomized, ovariectomized-thyroidectomized, and ovariectomized-thyroidectomized rats injected with thyroxine (T4) or estradiol benzoate (EB) [20].
• In this study, 2 days of estradiol-benzoate treatment produced significant and comparable increases in synaptophysin, syntaxin, and spinophilin immunoreactivity (IR) in the CA1 region of the dorsal hippocampus of ovariectomized female rats [24].
• EB treatment to hypophysectomized females led to similar enzymatic changes as in ovariectomized females in all areas except the basomedial hypothalamus [25].
• The EB-stimulated growth of the oviduct was blocked by tamoxifen, which had no effects when administered alone [26].
• Histopathologically, proliferative lesions of the thyroid were only observed in the SDM treatment group and of the pituitary in the SDM or EB treatment groups [5].

Associations of Benzo-Ginestryl with other chemical compounds

• RESULTS: Both WT and D5KO females can display receptivity after treatment with EB and P, but APO was only able to facilitate receptivity in EB-primed WT, not in D5KO, mice [27].
• Male golden hamsters were castrated and received a unilateral intrahypothalamic implant of either testosterone propionate (TP) or estradiol benzoate (EB) [28].
• Eb replacement increased liver and thyroid D1 activity, but in the kidney, only the highest estradiol dose promoted a significant D1 increase [29].
• Male guinea pigs injected with 10 micrograms EB have a progestin binder in cytosol from HPS and cerebral cortex that is similar to that in females on the basis of apparent dissociation constant and steroid specificity [18].
• After receiving testosterone propionate, male ferrets with either extensive or partial lesions of the mPOA/AH showed significant deficits in neck gripping and mounting performance in tests with either female or male stimulus animals which were sexually receptive after gonadectomy and EB treatment [30].

Gene context of Benzo-Ginestryl

• The obtained results show that both EB and P increase CAT activity, whereas EB decreases GSH-Px, GST and GR activities [31].
• The PRL response to EB treatment was increased (P < 0.005) in old ovariectomized transgenic mice [32].
• On days 8 and 9 after ovariectomy, mice were injected (sc) with oil or primed with 0.5 micrograms estradiol benzoate (EB) in oil, 24 h later treated with 10 micrograms EB/100 g BW, and a day later bled for the determination of FSH, LH, PRL, and hGH levels by RIAs [32].
• Administration of EB to old and to young Ovx rats produced increases in both basal and TRH-stimulated secretions of PRL, but did not affect the difference in plasma PRL patterns between old and young animals [33].
• Twenty hours after the last administration of EB, rats were injected with TRH (10 micrograms/kg) through the catheter [33].

Analytical, diagnostic and therapeutic context of Benzo-Ginestryl

• Two months after ovariectomy the negative feedback effects of a single injection of 20 mug estradiol benzoate (EB) on plasma LH were measured in these three preparations [34].
• The combined EB/PFF treatment resulted in a decreased pituitary response in terms of FSH and LH compared to that of the EB-treated control group [35].
• In males castrated at different ages from birth to 8 months, the proportion showing an immobilization response was less for males castrated at 6 months than observed in males castrated at birth or 2 months of age, and the duration of response to EB was shorter for males castrated at 4 months of age or later [36].
• In the rats that were given 5 daily injections of 10 micrograms EB Day 1 through Day 5, or a single injection of 100 micrograms EB on Day 3, the incidence of the PD pattern was high at 41-60 days of age, but later the PD-type was replaced by the PE pattern of vaginal smears [4].
• Adult male Wistar rats were studied 21 days after orchiectomy (Tex), and adult females were studied 21 days after ovariectomy (Ovx), and after estradiol benzoate (Eb) replacement [29].

References