Effect of synthetic progestins on the uptake of labelled testosterone and estradiol-17beta by the accessory genital organs of male rats

The effect of pretreatment with norethindrone (NE) or 17-hydroxyprogesterone caproate (17-OHPC) on the uptake of tritiated testosterone and estradiol-17beta by the accessory sex organs of castrated and intact rats was investigated. A selective in vivo increase in the incorporation of tritiated testosterone and estradiol-17beta was observed at 48 hours after castration. The uptake of testosterone was greatest in the epididymis, while the maximum incorporation of estradiol-17beta was by the vas deferens. Pretreatment with NE or 17-OHPC decreased the incorporation of testosterone by all the accessory organs of castrated rats. NE decreased the incorporation of tritiated estradiol-17beta in the epididymis and seminal vesicles only, while 17-OHPC decreased the uptake in all accessory organs.     

Effect of estradiol-17 beta on preprolactin messenger ribonucleic acid activity in the rat pituitary gland

Rat pituitary RNA was translated in the wheat germ system. Preprolactin messenger RNA activity was estimated by adsorption of cell-free products to solid phase antiprolactin. When male rats were injected for 4 days with estradiol-17beta, pituitary preprolactin mRNA activity was increased 2.5- to 3.0-fold over controls. This increase was evident when either total RNA, poly(adenylic acid) RNA, or polysomal RNA was translated in the cell-free system. In male rats receiving daily injections of estradiol-17beta, preprolactin mRNA activity was increased to an apparent maximum of 300% of controls after 7 days of treatment. Our data also indicate that estradiol increases preprolactin mRNA activity per microgram of RNA as well as the pituitary content of RNA. After estradiol treatment was discontinued, preprolactin mRNA activity declined to 50% of the maximum stimulation after approximately 2 days. In ovariectomized retired breeder female rats, a 5-fold increase in preprolactin activity over ovariectomized controls was obtained. In other studies, a 2-fold increase in preprolactin mRNA activity was obtained in male rats 24 h after a single injection of pimozide, a dopamine blocking drug.     

Role of estradiol-17 beta and progesterone in regulating constriction of ovine uterine arteries

Fistulas between the abdominal aorta and renal vein are exceedingly rare. Diagnostic delays are not unusual. Correction can be extremely difficult because of anatomical distortion and size of the arterialized veins. A young woman with such a fistula following a gunshot wound is presented. Four years following injury, the fistula was repaired successfully during intentional arrest of the circulation for 7 minutes. This was accomplished with deep hypothermia and cardiopulmonary bypass. No serious problems occurred during the operation. The patient tolerated the procedure well and has been relieved of her symptoms completely. Most patients with traumatic or spontaneous arteriovenous fistulas can be managed safely and effectively by conventional operative techniques. In selected situations, the risk of total circulatory arrest and deep hypothermia may be less than the risk of uncontrollable bleeding inherent in conventional techniques. Suggested indications for use of total circulatory arrest in vascular surgery are (1) inability to achieve vascular control by more conventional means, (2) massive distention of regional veins as occurrs in well established fistulas of the trunk, (3) one or more prior corrective attempts with use of conventional techniques, and (4) anticipated anatomical distortion and/or multiple abnormal vascular communications. This technique is a valuable approach to the correction of otherwise inoperable cardiovascular lesions.     

Influence of light dark cycles on estradiol-17 beta induced luteinizing hormone patterns of the prepuberal gilt

Two groups of Yorkshire gilts (110 d of age) were maintained in two light regimens. Both light regimens consisted of 14 h of light and 10 h of darkness, but were 180 degrees out of phase. Gilts in Group 1 received light from 1200 to 0200 and gilts in Group 2 from 2400 to 1400. At approximately 140 d of age each group was divided into four subgroups of eight gilts each (1A, 1B, 1C, 1D or 2A, 2B, 2C, 2D). All gilts were blood sampled at 2-h intervals for 5 d commencing on d 142. The four subgroups received a single injection of estradiol (15 micrograms/kg body weight) on d 143 at either 2400 (A), 0600 (B), 1200 (C), or 1800 (D). For pigs in Groups 1A and 1D, the injection of estradiol coincided with the animals' "subjective day" and the injections given to Groups 1B and 1C with their "subjective night." When estradiol-17 beta (E2) was administered to the gilts during their subjective day the LH profile showed one peak, whereas when E2 was administered during dark hours the profile exhibited two peaks (P < .0001). In Group 2 for which the light cycle was reversed, the well-defined spikes of LH were found to coincide with the injections of estradiol administered during the dark hours. Smaller biphasic peaks of LH occurred when injections of estradiol coincided with the light hours.(ABSTRACT TRUNCATED AT 250 WORDS)     

Studies of binding of testosterone-estradiol binding globulin for estradiol-17beta (author''s transl)

The in vitro incorporation of [3H]thymidine has been examined in thin slices of sheep skin. Most of the radioactivity (88%) was incorporated into the bulb cells of the wool follicles, and the technique is therefore suitable for the study of some aspects of wool follicle DNA synthesis. The effect of mimosine and a number of related 4(1H)-pyridones on [3H]thymidine incorporation into sheep skin slices was examined. Mimosine was shown to inhibit the incorporation at a concentration of 0-2 mM. At this concentration, the incorporation of [3H]uridine or [14C]leucine was not affected. The inhibition of [3H]thymidine incorporation was time dependent, 2 h of incubation being required for maximal inhibition of DNA synthesis, and was readily reversible by removal of mimosine from the incubation medium. The 3-hydroxyl-4-oxo function of the pyridone ring appears to be directly involved in DNA synthesis inhibition. The amino acid side chain is not a toxophoric centre, but changes in its polarity have been shown to affect the inhibitory activity. The results suggest that the primary action of mimosine on the inhibition of wool biosynthesis in vivo is the inhibition of follicle bulb cell DNA synthesis and consequently of cell division.     

Effect of estradiol-17 beta on basal and hCG stimulated progesterone secretion by porcine luteal cells isolated in various stages of the luteal phase

T cells of mice display V beta-specific reactivity for a spectrum of mouse mammary tumor virus (Mtv) antigens; confrontation with these antigens during ontogeny causes substantial "holes" in the T cell repertoire. Since endogenous Mtv antigens are rare in other species, the question arises whether V beta-specific recognition of Mtv antigens is unique to mice. To examine this question, rat T cells were allowed to differentiate from stem cells in severe combined immunodeficiency (SCID) mice. These rat-->mouse xenochimeras were prepared under a variety of conditions. The results show that rat T cells are strongly reactive to mouse Mtv antigens, both in terms of tolerogenicity and immunogenicity. In fact, the V beta specificity of rat and mouse T cells for Mtv antigens is almost indistinguishable.     

Time-course of the uterine response to estradiol-17beta in ovariectomized ewes: expression of angiogenic factors

Uterine expression of angiogenic factors (vascular endothelial growth factor [VEGF] and basic fibroblast growth factor [bFGF]) was evaluated in ovariectomized ewes at 0, 2, 4, 8, 24, 48, or 72 h after estradiol (E2) treatment. Endometrial VEGF mRNA increased more than 5-fold from 0 to 4 h, remained elevated at 8 h, and then declined through 72 h after E2 treatment. In contrast, endometrial bFGF mRNA remained constant from 0 to 4 h, increased 2.2-fold from 4 to 8 h, remained elevated at 24 h, and then declined through 72 h. Immunostaining for VEGF was present in myometrial and endometrial microvessels (arterioles, venules, and/or capillaries) and also in myometrial smooth muscle; the pattern of VEGF immunostaining followed that of mRNA expression, being elevated at 4 and 8 h after E2 treatment. Immunostaining for bFGF was present exclusively in uterine glands; the pattern of bFGF immunostaining also followed that of its mRNA, being elevated at 8 and 24 h after E2. On the basis of these observations, we suggest that VEGF and bFGF are probably important factors responsible for the dramatic uterine microvascular response that occurs 8 to 24 h after E2 treatment in ovariectomized ewes.     

Interaction between estradiol-17b and growth hormone in control of food intake in weanling rats.

Discusses previous studies indicating that estradiol reduces the food intake of adult female rats, while prepubertal females are refractory to its appetite-depressing action unless they have been hypophysectomized. In an experiment with 30 ovariectomized and hypophysectomized Sprague-Dawley female rats, treatment of weanlings with pituitary growth hormone restored the refractoriness of the neural feeding system to estradiol. It is suggested that growth hormone masks ventromedial hypothalamic restraint of food intake. Because estradiol affects eating by acting on the ventromedial hypothalamus, it is ineffective in young animals, which are highly responsive to growth hormone. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Adenosine triphosphate-dependent transport of estradiol-17beta(beta-D-glucuronide) in membrane vesicles by MDR1 expressed in insect cells

MDR1, an ABC transporter that confers multidrug resistance in tumor cells, is constitutively expressed in normal liver canalicular membrane. Human MDR1-expressing multidrug-resistant cells display increased resistance to estradiol-17beta(beta-D-glucuronide) (E217G). MDR1 substrates/modulators inhibit adenosine triphosphate (ATP)-dependent transport of E217G in the rat canalicular membrane and protect against E217G-mediated cholestasis in isolated perfused rat liver. The present studies were designed to determine if E217G is a substrate for MDR1 using a baculovirus expression system and if other estrogen glucuronides interact with MDR1. ATP-dependent transport of E217G (10 micromol/L) was linear for up to 2 minutes and yielded a rate of 45.6 pmol/min/mg protein in membrane vesicles from Sf9 cells infected with MDR1-baculovirus. This transport was saturable (Km = 62 micromol/L) and occurred into an osmotically sensitive space. ATP-dependent transport of E217G (10 micromol/L) was inhibited 63% by 10 micromol/L daunomycin, but not by 100 micromol/L S-(2,4-dinitrophenyl)glutathione (GS-DNP) (a substrate for canalicular multispecific organic anion transporter [cMOAT]). Glucuronide conjugates of the estrogen D-ring (100 micromol/L), estriol-17beta(beta-D-glucuronide) (E317G) and estriol-16(beta-D-glucuronide) (E316G), inhibited MDR1-mediated E217G transport by 58% and 35%, respectively. In contrast, noncholestatic glucuronides, estradiol-3-(beta-D-glucuronide) (E23G) or estradiol-3-sulfate-17beta(beta-D-glucuronide) (E23SO417G), had no effect. E217G neither stimulated MDR1 ATPase activity nor inhibited verapamil-stimulated ATPase activity. Infusion of 1.5 micromol/L doxorubicin or 1 micromol/L taxol protected against cholestasis induced by E316G and E317G in isolated perfused rat liver. These studies identify E217G, and probably E316G and E317G, as endogenous substrates for MDR1.     

Plasma concentrations of unconjugated estrone, estradiol-17beta and estriol, and HCS throughout pregnancy in diabetics and gestational diabetics

Plasma unconjugated estrone (E1), estradiol-17beta (E2) and estriol (E3), and HCS were measured in the same plasma samples collected throughout pregnancy in 19 gestational diabetics (GD) and 21 diabetics (D). When compared to the results obtained in 22 normal subjects, plasma levels of E1 and E2 were significantly elevated in D in the second half of gestation. The results were intermediate although closer to the normals, in GD. E3 values were not different from the normals in both D and GD. HCS values were lower than normal in early pregnancy in both D and GD. In late pregnancy HCS levels were not different from normal in either D or GD, although some individual values were much above the upper limit in some diabetic patients. The hormonal ratios in D and GD parallel those in normals, although E3/E2 and HCS/E2 were lower in D. These results are discussed with respect to the different behaviour of E2 and E3, taking into account the difference in their respective biosynthetic pathways. Besides a possible quantitative modification of the placental function in D, the results could tentatively be explained by a qualitative change in the fetal estrogen precursors to placental aromatization, in favour of the 16 non-hydroxylated compound. However, maternal modifications in precursor production or in estrogen metabolism can be an alternative hypothesis. Finally, the present work does not support the hypothetical estrogen deficiency in diabetic pregnancy. Estrogen treatment appears to have no objective justification.     

Effect of prolactin on metabolism of human spermatozoa

The effect of prolactin on adenyl cyclase, rate of fructose utilization, and glucose oxidation by human spermatozoa was studied. Prolactin stimulated all of these processes at a concentration generally available in seminal plasma. These results suggest that prolactin plays an important role in the energy metabolism of human spermatozoa.     

Forebrain sites of estradiol-17!b action on sexual behavior and aggression in female Syrian hamsters.

The effects of intracranial implants of estradiol in the ventromedial hypothalamus (VMH), the anterior hypothalamus (AH), or the medial amygdala (AMG) on aggression, sexual behavior, and serum estradiol were examined in female Syrian hamsters. Estradiol implants in the VMH, followed by systemic progesterone, stimulated sexual behavior and inhibited aggression. Estradiol implants in other intracranial sites activated sexual behavior but did not reliably inhibit aggression. Intracranially implanted and systemically treated animals had equivalent peripheral estradiol concentrations at sacrifice. Results suggest that (1) the VMH is an important neural site for estradiol actions on sexual and aggressive behavior, (2) the caudal AH and AMG may also be sites of estradiol action on sexual behavior, and (3) intracranial implants may only be effective given systemic estradiol exposure or the concurrent stimulation of multiple brain areas. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effect of dietary trans fatty acids on cholinesterase and monoamine oxidase activities in different organs of rats

The effect of trans fatty acids and essential fatty acid deficiency upon the activities of cholinesterase and monoamine oxidase in livers, hearts, brains and lungs of rats was studied. This study was performed using three groups of male albino rats. Two out of these three groups were fed essential fatty acid low diets containing 10% hydrogenated coconut oil (HCNO) or margarine stock (MS, partially hydrogenated soybean oil) while the third group was fed an adequate supply of essential fatty acids through a diet containing 10% corn oil (CO). In the group of rats fed HCNO the activities of cholinesterase and monoamine oxidase in their livers, hearts, brains and lungs were not significantly different from those of the control group fed CO. In the group of rats fed MS, the activity of cholinesterase was significantly decreased in the livers, hearts and brains, but not affected in the lungs, while the activity of monoamine oxidase was significantly decreased in the livers and hearts but not affected in the brains and lungs as compared to the control group fed CO. The levels of serum total lipids, total cholesterol and triglycerides were elevated in both groups of rats fed HCNO or MS than in the group fed CO, but this elevation was more highly significant in the group fed MS than in the group fed HCNO.