Horm Metab Res. 2001 Oct;33(10):608-11.
Coadministration of melatonin and estradiol in rats: effects on oxidant status.
Gurdol F, Genc S, Oner-Iyidogan Y, Suzme R.
Department of Biochemistry, Istanbul Faculty of Medicine, Istanbul University, Turkey.
This study was designed to investigate the effects of melatonin and estradiol (E2) on lipid peroxidation and antioxidant defense enzymes in blood and liver tissue when administered in vivo. Wistar albino rats were divided into three experimental groups and treated with either estradiol (25 mg/kg bw, s.c.), melatonin (i. p.), or melatonin plus E2, whereas control animals had diluent injections only. Melatonin was given 10 mg/kg bw x 2 intraperitoneally 30 min before and 60 min after E2 treatment to the melatonin plus E2 group. Animals were sacrificed three hours after the estradiol injection, and their blood and liver tissues were prepared for biochemical analyses. Tissue malondialdehyde (MDA) levels and antioxidant enzyme activities--superoxide dismutase (SOD) and glutathione peroxidase (GPx)--were determined in the postmitochondrial fraction, and the results were compared. Estradiol injection caused significant increases in both MDA levels and GPx activity in liver. When melatonin was administered in combination with E2, the effect of estradiol on MDA levels was abolished. A significant decrement in SOD activity occurred in melatonin-treated animals. GPx activity in the blood of E2 plus melatonin-injected animals was significantly higher than those in control animals. Melatonin-treated animals exhibited relatively lower levels of SOD activity than those from the control and E2 plus melatonin groups. This indicates that estradiol could exert oxidant action resulting in an increment in tissue malondialdehyde levels. Enhanced activity of GPx in both liver and blood following melatonin injection may indicate the contribution of this neurohormone on the antioxidant defense.
Res Vet Sci. 2001 Aug;71(1):23-5.
Activin-A differentially regulates steroidogenesis by sheep granulosa cells.
Shidaifat F, Khamas W, Hailat N.
Department of Basic Veterinary Medical Sciences, Faculty of Veterinary Medicine, Jordan University of Science and Technology, Irbid, Jordan. falaust.edu.jo
Intra-ovarian factors, such as activin, are implicated in multiple aspects of follicular development in mammalian ovaries. This study was conducted to investigate a possible effect of activin-A on steroidogenesis in sheep granulosa cells in vitro. Sheep granulosa cells were obtained from medium antral follicles and cultured in a chemically defined RPMI -1640. Oestradiol and progesterone production, secreted by the cultured cells, was evaluated by enzyme-linked immunosorbent assay. In order to determine the dose effect of activin-A on steroidogenesis, granulosa cells were cultured in the presence of increasing concentrations of activin-A (0, 0.5, 5 and 50 ng ml(-1)) for 48 hours. The results revealed that activin-A exerts a differential effect on steroidogenesis in granulosa cells in such a way that it significantly (P < 0.05) suppressed progesterone production and enhanced oestradiol production. These results were confirmed by the time effect of activin-A on oestradiol and progesterone production in granulosa cells. In the absence of activin-A treatment, granulosa cells showed enhanced capacity to produce progesterone, but not oestradiol, as the time progressed from 12 to 48 hours. Treatment of sheep granulosa cells with 25 ng ml(-1)activin-A for 12, 24 and 48 hours significantly stimulated oestradiol production but inhibited progesterone production. These results suggest that activin-A is a local regulator of sheep folliculogenesis that might act to support differentiation in granulosa cells and suppress luteinisation. Copyright 2001 Harcourt Publishers Ltd.
Am J Physiol Heart Circ Physiol. 2001 Nov;281(5):H2204-10.
Chronic estradiol treatment attenuates stiffening, glycoxidation, and permeability in rat carotid arteries.
Mullick AE, Walsh BA, Reiser KM, Rutledge JC.
Division of Endocrinology, Clinical Nutrition, and Vascular Medicine, Department of Internal Medicine, University of California, Davis, California 95616, USA.
Aging-related changes in vascular stiffening and permeability are associated with cardiovascular disease. We examined the interaction of estradiol on the aging process in vascular tissue from rats by assessing the changes in endothelial layer permeability, arterial compliance, and glycoxidative damage levels. We isolated carotid arteries from ovariectomized (OVX) rats that underwent 1 yr of estrogen treatment with subcutaneous pellets and a subsequent 1 mo of cessation of treatment. Endothelial layer permeability and arterial compliance were determined using quantitative fluorescence microscopy. Endothelial layer permeability was reduced with estradiol treatment (estrogen groups, 2.58 +/- 0.21 ng dextran x min(-1) x cm(-2) vs. nonestrogen groups, 4.01 +/- 0.30 ng dextran x min(-1) x cm(-2); P < 0.05). Additionally, arteries from animals treated with estradiol had an increased compliance index (estrogen groups, 82.9 +/- 3.8 mm2. Torr vs. nonestrogen groups, 69.3 +/- 3.2 mm2. Torr; P < 0.05). Estradiol treatment also reduced levels of pentosidine, which is a specific marker of glycoxidative damage (estrogen groups, 0.11 +/- 0.03 pmol pentosidine/nmol collagen vs. nonestrogen groups, 0.20 +/- 0.03 pmol pentosidine/nmol collagen; P < 0.05). These results indicate that estradiol has multiple chronic vasculoprotective effects on the artery wall to maintain normal vascular wall function.
Cytokine. 2001 Oct 7;16(1):22-30.
Testosterone and estrogen differently effect Th1 and Th2 cytokine release following trauma-haemorrhage.
Angele MK, Knoferl MW, Ayala A, Bland KI, Chaudry IH.
Center for Surgical Research, Department of Surgery, University of Alabama at Birmingham, 1670 University Blvd., Birmingham, AL 35294, USA.
The object of the study was to determine whether male and female sex steroids produce divergent effects on Th1 and Th2 cytokine release following trauma-haemorrhage. Recent studies indicate that androgens are responsible for the depressed splenocyte Th1 cytokine release in males following trauma-haemorrhage. In contrast, female mice maintain their Th1 cytokine release capacity following trauma-haemorrhage. Nonetheless, the effect of male and female sex steroids on Th1 and Th2 cytokine release following trauma-haemorrhage remains unknown. Male C3H/HeN mice were castrated and treated with pellets containing either vehicle, 5alpha-dihydrotestosterone (DHT), 17beta-estradiol (estradiol), or a combination of both steroid hormones, for 14 days prior to soft-tissue trauma (i.e. laparotomy) and haemorrhagic shock (35+/-5 mmHg for 90 min followed by adequate fluid resuscitation) or sham operation. Untreated male and female mice, as well as DHT treated female mice, served as control groups. Twenty-four hours later the animals were sacrificed, plasma obtained and splenocytes harvested. Plasma DHT and estradiol levels in treated animals were comparable with intact male and female mice, respectively. A significant depression of splenocyte Th1 cytokines, i.e. IL-2, IFN-gamma, was observed in DHT treated castrated animals, DHT treated females, and untreated males following trauma-haemorrhage, as opposed to maintained Th1 cytokine release in estradiol treated and estradiol/DHT treated castrated animals and females. The release of the anti-inflammatory cytokine IL-10 was markedly increased in DHT treated mice and males subjected to trauma-haemorrhage compared to shams, but de
Mol Hum Reprod. 2001 Nov;7(11):1085-91.
Comparative analysis of cyclin D1 and oestrogen receptor (alpha and beta) levels in human leiomyoma and adjacent myometrium.
Kovacs KA, Oszter A, Gocze PM, Kornyei JL, Szabo I.
Department of Obstetrics and Gynecology, Pecs University Medical School, Edesanyak u.13/15, Pecs, H-7624, Hungary. kovacskalmaahoo.com
The aim of these experiments was to investigate the expression of cyclin D1 and of oestradiol receptors as well as the level of [(3)H]oestradiol binding in leiomyoma and adjacent myometrium from human uteri at different menstrual phases and at an early stage of menopause. [(3)H]oestradiol binding was determined by saturation analysis, while the oestradiol receptor (ER) alpha and beta and cyclin D1 levels were determined by Western blot analysis of 16 samples of human leiomyomas and corresponding myometria at different hormonal stages. In leiomyomas during all phases of the menstrual cycle, ERalpha expression, high affinity oestradiol binding and cyclin D1 expression were all elevated in comparison with adjacent myometrium. ERbeta expression and low affinity oestradiol binding were enhanced in leiomyomas only during the proliferative phase. During menopause, ERbeta expression and low affinity binding were enhanced in leiomyomas, while the ERalpha expression was not significantly enhanced and cyclin D1 levels were similar to that in myometrium. Only the oestradiol binding exhibited any menstrual cycle-related changes. Our data suggest the involvement of cyclin D1 in the growth of leiomyomas during the menstrual cycle. In menopause, there appears to be a switch from ERalpha to ERbeta expression in leiomyomas, and the induction of cyclin D1 is decreased. The regression of tumour may ensue from these changes at menopause.
Methods Find Exp Clin Pharmacol. 2001 May;23(4):169-73.
Estrogen inhibits lipopolysaccharide-induced tumor necrosis factor-alpha release from murine macrophages.
Zhang X, Wang L, Zhang H, Guo D, Qiao Z, Qiao J.
Laboratory of Molecular Biology, Shanxi Medical University, Taiyuan, P.R. China. zdqiaublic.ty.sx.cn
During their reproductive years, female have a lower risk for atherosclerosis as compared with age-matched males, although the mechanisms behind this are not clearly understood. Cytokines, including TNF-alpha play an important role in the pathogenesis of atherosclerosis. We therefore evaluated whether or not there was any difference between 17 beta-estradiol and testosterone in modulating TNF-alpha release from murine bone marrow-derived macrophages (BMM) in vitro. Cells were incubated with or without physiological concentrations (10(-10)-10(-8) M) of 17 beta-estradiol or testosterone for 48 h, followed by an additional 6 h in the absence or presence of lipopolysaccharide (LPS; 10 micrograms/ml). The amount of TNF-alpha released into the culture medium was determined with radioimmunoassay. We found that 17 beta-estradiol or testosterone alone did not affect TNF-alpha release from BMM as compared to untreated controls. Preincubation with 17 beta-estradiol significantly inhibited LPS-induced TNF-alpha release by 18.15% (p < 0.05). 25.28% (p < 0.05) and 40.83% (p < 0.01) for 10(-10), 10(-9) and 10(-8) M of 17 beta-estradiol, respectively, as compared to LPS alone. In contrast, testosterone tested for 3 concentrations did not significantly effect TNF-alpha release induced by LPS. The results indicate that 17 beta-estradiol, but not testosterone, inhibits TNF-alpha release from LPS-stimulated macrophages, which may be one of the mechanisms by which estrogen protects against atherosclerosis.
J Auton Pharmacol. 2001 Apr;21(2):95-9.
Vascular inhibitory actions of 17beta-oestradiol in rat portal vein.
Leong S, Docherty JR.
Department of Physiology, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin 2, Ireland.
1. We have examined the effects of 17beta-oestradiol on spontaneous spikes and contractions to noradrenaline in rat portal vein. 2. The 17beta-oestradiol (10 microM) significantly reduced the maximum height of spontaneous spike contractions and significantly reduced the maximum contraction to noradrenaline (10 microM) in portal vein from both male and female rats. 3. The protein synthesis inhibitor cycloheximide (10 microM) did not significantly affect the inhibitory actions of 17beta-oestradiol (10 microM) against spontaneous spike contractions and contractions to noradrenaline. 4. In summary, 17beta-oestradiol diminishes spontaneous spike contractions and the contractile response to noradrenaline in rat portal vein, by a non-genomic action.
Epidemiology. 2001 Nov;12(6):676-81.
Ovarian function in late reproductive years in relation to lifetime experiences of abuse.
Allsworth JE, Zierler S, Krieger N, Harlow BL.
Department of Community Health, Brown University School of Medicine, Providence, RI, USA.
The objective of this study was to investigate the relation between violence victimization and levels of ovarian hormones during women's late reproductive years, as measured by serum levels of follicle-stimulating hormone and estradiol, which respectively rise and fall with onset of menopause. In March 1999, 732 women 36-45 years of age from the Harvard Study of Moods and Cycles cohort completed a survey of lifetime experiences of physical and sexual harm. Follicle-stimulating hormone and estradiol levels were measured during the menstrual period after entry into the cohort. Associations for violence and follicle-stimulating hormone and estradiol levels were estimated using crude and adjusted risk differences. Overall, women who experienced abuse during childhood or adolescence relative to never-abused women had a slight positive association of violence with high follicle-stimulating hormone. However, a positive association with high follicle-stimulating hormone was not observed among women whose first abuse occurred during adulthood. Age stratification indicated modification of the association between violence and low estradiol. Women 36-40 years of age had no evidence of a positive association between violence before adulthood and low estradiol, whereas first violence in adulthood was associated with an 11% increase in the estimate of risk difference [95% confidence limits (CL) = -0.14, 0.36]. Among women 41-45 years, there was a 17-23% increase in the estimate of risk difference for low estradiol, regardless of life stage at first experience of abuse (before adulthood, 95% CL = 0.06, 0.28; during adulthood, 95% CL = 0.01, 0.46). This investigation supports the credibility of a hypothesis that physical and sexual abuse may lea
J Biol Chem. 2001 Dec 28;276(52):49435-42. Epub 2001 Oct 26.
Effect of estradiol on histone acetylation dynamics in human breast cancer cells.
Sun JM, Chen HY, Davie JR.
Manitoba Institute of Cell Biology, Winnipeg, Manitoba R3E 0V9, Canada.
Histone acetylation plays an important role in remodeling chromatin structure, facilitating nuclear processes such as transcription. We investigated the effect of estradiol on global histone acetylation in hormone-responsive human breast cancer cells. Pulse-chase experiments and immunoblot analyses of dynamically acetylated histones show that estradiol rapidly increases histone acetylation in estrogen receptor (ER)-positive, hormone-dependent T5, but not in ER-negative, hormone-independent MDA MB 231 breast cancer cells. The effect of estradiol on the rates of histone acetylation and deacetylation in T5 cells was determined. We found that estradiol increased the level of acetylated histones by reducing the rate of histone deacetylation, whereas the rate of histone acetylation was not altered. Enzymatic assays and immunoblot analyses of cell fractions showed that estradiol did not affect the level, subnuclear distribution, or activity of class I and II histone deacetylases. However, estradiol did alter the intranuclear distribution of ER and histone acetyltransferases, with both becoming tightly bound in the nucleus and associated with the nuclear matrix. We propose that, following the association of ER with nuclear matrix sites, ER alters the balance of histone acetyltransferases and histone deacetylases at these sites and the dynamics of acetylation of histones associated with transcriptionally active and competent chromatin.
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