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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen stimulation of the uterus produces a spectrum of biochemical responses that are customarily linked together. This report is an overview of a series of studies by our laboratory investigating the role of different ligand structures in eliciting hormonal responses. Diethylstilbestrol (DES) and certain structural analogs, indenestrol A (IA), indenestrol B (IB), and pseudo-DES, were used as probes to segregate various genomic responses previously considered interrelated, most notably the events of specific protein synthesis and DNA synthesis. These compounds have weak uterotrophic activity; however, they interact with high affinity specifically with mouse uterine estrogen receptors (ERs). All of them produce stoichiometrically similar amounts of ER complex in the nucleus. Indenestrol A and IB possess a single chiral carbon atom and exist as a mixture of enantiomers (ENTs). Competitive binding assays of pure ENTs and cytosolic ERs demonstrated a stereochemical chiral preference for the IA isomer but not IB. This preference was also evident from nuclear ER occupancy experiments. Biologic activity of the IA ENTs also demonstrated differences as seen by receptor binding. Ornithine decarboxylase (ODC) activity was stimulated 600% by DES and partially by IA (rac). All of the ODC activity produced by IA (rac) was due to the IA(C3)-S ENT. Uterine DNA synthesis was measured after treatment with the IA compounds. Indenestrol A (rac) increased DNA synthesis to 40% of the level seen with DES. The weak ENTs showed no activity and the active ENTs were weaker than the IA racemic. These compounds should be useful probes for studying the individual responses involved in estrogen-induced uterine growth.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1991 May
PMID:Estrogen receptor stereochemistry: ligand binding and hormonal responsiveness. 187 66

Rat uterine luminal epithelial cells (LEC) responded differently when exposed to an injection of 1.0 microgram estradiol-17 beta (E2) compared to a continuous infusion of E2 at the rate of 1.0 microgram/24 hours. After injection or beginning infusion, LEC mean nuclear area significantly decreased by 4 h, then increased thereafter. After injection, nuclear area distributions were determined at each time point. The percentage of large nuclei (greater than 40 mu 2) decreased by 4h postinjection and remained a relatively small proportion of the population, while the percentage of nuclei of 20-30 mu 2 areas increased throughout the experiment. During infusion, the percentage of large nuclei decreased by 4h after pump implantation, then increased. Only infusion induced sustained, increased uterine protein content, DNA synthesis and ornithine decarboxylase activity. This study suggests that E2 treatment modality induces differences in nuclear size in target cells as well as in biochemical parameters.
Steroids 1985 Jun
PMID:Rat luminal cell nuclear area changes correlated with uterine growth responses induced by a low dose infusion or injection of estradiol-17 beta. 383 30

A single injection of 0.5 micrograms estradiol-17 beta (E2) plus 0.5 micrograms estriol (E3) stimulated a different pattern in 22-24 day-old rat uterine ornithine decarboxylase (ODC) and S-adenosyl methionine decarboxylase (SAMDC) activities than was induced by either a single injection of 0.5 micrograms E2 or multiple injections of 0.5 micrograms E3. Differences included alterations in enzyme activity peak timing as well as activity duration. Every 3 hour injections of 0.05 micrograms E2 induced maximum uterine ODC activity at 4, 24, 32, and 40 hours, intermediate activity at 48, 64, and 72 hours as well as a small peak by 56 hours. When 0.05 micrograms E2 plus 0.05 micrograms E3 were injected simultaneously every 3 hours, the ODC activity pattern was similar except that activity fell to intermediate levels by 40 hours. It is suggested that E3 alterations of E2 induced uterine enzyme activities (when monitored at frequent intervals) could be physiological alterations in uterine growth responses due to E2-E3 hormone interactions. However, there appeared to be no differences between E2 or E2 plus E3 induction of DNA synthesis and luminal epithelial cell height and cross-sectional area or ODC and SAMDC activities when measured at 24, 48, or 72 hours.
Steroids 1984 Apr
PMID:Rat uterine polyamine biosynthetic decarboxylase activities following multiple injections of estradiol-17 beta and/or estriol. 652 52

To examine estrogen-stimulated uterine growth we have monitored changes in uterine DNA synthesis, ornithine decarboxylase (ODC) activity and protein content as well as luminal epithelial (LE) cell mitotic index and ultrastructural changes. We have utilized this model to examine castrate mature rat uterine growth as a function of time between 18 and 40 hours following a single injection of 25.0 ug of estradiol-17B. LE cell mitotic index and protein content increases were maximally elevated as early as 18 hours postinjection while uterine ODC activity was maximal at 28 hours; uterine DNA synthesis increases continued throughout the experiment. In addition, the infusion of either 1 or 2 ug E2 plus progesterone over a 24 hour period, stimulated elevated ODC activity under both treatment regimens and LE cell mitotic index which was inversely related to E2 dose.
Steroids 1984 Jun
PMID:Uterine growth responses of the mature castrate rat to estradiol-17B. 653 44

Following a single intraperitoneal injection of 0.5 microgram estradiol-17 beta (E2) into immature female rats uterine ornithine decarboxylase (ODC) activity increased to a peak at 4 hours postinjection. It decreased to intermediate levels by 6 hours and remained elevated until returning to control levels by 18 hours. When either 0.5 microgram estriol (E3) or 0.05 microgram E2 was injected, activity increased to a 4 hour ODC peak then decreased to control levels by 10 hours. The decrease to intermediate levels of ODC activity after dosing with 0.5 microgram E2 occurred at the same time activity decreased to control levels following treatment with either 0.05 microgram E2 or 0.5 micrograms E3. S-Adenosyl methionine decarboxylase (SAMDC) activity had increased by 4 hours following an injection of 0.5 microgram E2 and remained elevated until 16 hours then decreased to control levels. An injection of 0.05 microgram E3 stimulated only a 4 hour peak after which time SAMDC decreased to control levels by 14 hours. After an injection of 5.0 microgram E2 SAMDC activity had increased by 4 hours and remained elevated for the remainder of the experiment (16 hours). Decreases in ODC activity following 4 and 10 hours may reflect a decrease in nuclear estrogen receptor levels. The ODC activity seen here following 0.5 microgram E2 injection is similar in timing to that seen in other proliferating systems and may be due to a common mechanism.
Steroids 1983 Dec
PMID:Polyamine biosynthetic decarboxylase activities following estradiol-17 beta or estriol stimulation of the immature rat uterus. 668 Sep 31

Steroids alter the transport function of the intestine. This study was undertaken to assess the effect of glucocorticosteroids on lipid uptake in rats fed either a saturated (SFA) or a polyunsaturated fatty acid (PUFA) diet. Sprague-Dawley rats underwent transection or 50% resection of the small intestine. The steroids had no effect on the uptake of lipids. However, resection decreased the jejunal uptake of palmitic acid in animals fed SFA and increased the jejunal uptake of palmitic and linoleic acids in those fed PUFA. In animals undergoing intestinal resection, fed SFA, and given control vehicle, there was a reduction in jejunal proglucagon mRNA expression as compared to those fed chow or PUFA. Ornithine decarboxylase (ODC) mRNA expression in the jejunum of resected animals was reduced. In summary, dietary lipids modify the uptake of lipids in resected animals and ODC and proglucagon may be involved in this adaptive response.
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PMID:Dietary lipids alter the effect of steroids on the uptake of lipids following intestinal resection in rats. 1218 29