The aim of this study was to compare serum 17?-estradiol (breast cancer biomarker) levels and its relationship with some breast cancer risk factors in athlete and non-athlete postmenopausal women. 19 postmenopausal body building athletes aged 53.57±7.87 years and 21 postmenopausal non-athletes aged 56.61±5.17 years in Urmia province participated in this study. 17?-estradiol concentrations were measured by electrochemiluminescence. All participants completed a questionnaire witch included details of age, menarche age, menopause age, pregnant age, null parity, family history, alcohol consumption and smoking. Body fat percentage and body mass were measured by body logic/body fat and lyzer (Omron Model). Variables were compared by independent t test and the relationship among variables by Pierson correlation coefficient. Athlete women had lower serum estradiol concentration, BMI and ratio of waist to hip than non-athlete women. But this difference was not significant (P<0.05) and only body fat percentage significantly differed (P=0.044). There was no relationship among weight, age, body fat percentage, ratio of waist to hip, BMI and serum concentration of estradiol in subjects. Senescence, early menses, late onset of menopause, pregnancy, alcohol consumption and smoking risk factors were lower in athlete women than non-athlete women. This study showed that although low body fat percentage and estradiol exposure, late menarche and early menopause in athlete women can indicate low breast cancer risk, an insignificant difference in serum estradiol between athlete and non-athlete women can be the result of athlete women's irregular intensity and duration of exercises

Relation between sexual maturity and levels of two main steroid hormones in gonads, 17- estradiol (E2) and testosterone (T) were studied by using histological and adioimmunoassay in female kutum Rutilus frisii kutum during spawning season of the southern Caspian Sea. The study was carried out from February to May 2008 using 105 migrated fish specimens catched from the River sefid-rood by various tools of catching
including (Gillnet, Cast net, Seine net and Sheyl or Kulham). The results revealed that changes in plasma levels of gonadal steroids, (E2) and (T) were closely correlated with ovarian development and increased in Gonadosomatic index (GSI) (P

Female sex hormones have a pro-inflammatory effect, which may help to minimize inflammation. Estrogen's immunoregulatory properties play a significant role in the bi-directional neuroendocrine-immune activity in females. As a result, sex hormones can play a role in men's high mortality rate from coronavirus-2019 (COVID-19). It is aimed to clarify the role of 17-estradiol (E2) in the battle against COVID-19.

Until April 2021, a study on PubMed was performed. COVID-19, 17-estradiol (E2), immunoregulatory properties, pregnancy, menopausal symptoms, hormonal therapy,
ER/ expression on immune cells, and mortality were some of the concepts used in the search.

Regulation of pro-inflammatory immune processes against COVID-19 appears to be associated with increased immune function (pro-inflammatory), anti-inflammatory regulation, and antiviral defense. Women with a severe coronavirus infection had higher serum IgG antibody levels than men, and their IgG production was faster in the early stages of infection. 17-estradiol (E2) levels of blood will increase by 100-fold during pregnancy. COVID-19 in pregnant women had a 15-fold lower mortality rate than other women. While menopause replacement therapy (MRT) for pre/post-menopausal women and its effectiveness in reducing COVID-19 infection is debatable.

MRT may be considered as a viable treatment option for pre/post-menopause women with coronavirus, referring to the fact that sex hormones reduce inflammatory responses and modulate
ACE2 expression. The task's difficulty and achieving the desired outcome seem to be challenging.

One-eighth of women will develop breast cancer in their lifetime, resulting in approximately annual one million women worldwide with breast cancer. Approximately 70% of breast cancers are positive for estrogen receptor alpha (ER-). The presence of ER- receptor is associated with better prognosis and usually indicates that the anti-estrogen drugs such as tamoxifen can be useful in the treatment. Nevertheless, a significant number of ER--positive breast cancers does not respond to tamoxifen. Causes of resistance to tamoxifen and how to sensitize to tamoxifenis not yet known. Preliminary studies indicate that garlic and its derivatives such as allicin, have anti-cancer effects. This study aims to investigate the inhibitory effect of allicin on tamoxifen-sensitive MCF-7 cells. To investigate this theory, the effect of allicin on tamoxifen-sensitive cells (MCF-7), and -resistant cells (Sk-Br-3) in the presence and absence of tamoxifen and 17- estradiol were studied. The cell viability was assessed using MTT assay at 24, 48 and 72 hours. The study revealed that allicin in MCF-7 cells enhances the effectiveness of tamoxifen in the presence and absence of 17-b estradiol. Allicin as an adjunct to tamoxifen can sensitize breast cancer cells to tamoxifen.

Main function of corpus luteum is progesterone synthesis that is significantly accompanied with an increase in levels of mRNA encoding of steroidogenic enzymes known as luteal markers. This study was designed to evaluate effects of lithium chloride on the release of steroid hormones and steroidogenic enzymes in gonadotropin-stimulated rats. Immature 23 days old Wistar rats were divided into 10 groups; each group comprised of 8 rats, and induced with single injection of pregnant mare’s serum gonadotrophin (PMSG) and followed by single injection of human chorionic gonadotropin (hCG). Then, rats were given lithium chloride (LiCl) or saline at 12 hours post-hCG injection. Ovaries were collected in 4-hour interval from 8-24 hour post-hCG injection. Expression pattern of steroidogenic acute regulatory protein (StAR), side-chain cleavage cytochrome P450 (P450scc) and 3?-hydroxysteroid dehydrogenase (3?-HSD) genes were determined by semi-quantitative RT-PCR. In addition, serum levels of progesterone and 17?-estradiol were measured by ELISA. Our results showed that hCG stimulation of progesterone was markedly diminished and transcript levels of key steroidogenic enzymes were altered in the hormone-stimulated rats following LiCl treatment. These results suggest that critical steps in the function of corpus luteum are disrupted by lithium. It is concluded that LiCl is an effective factor for suppressing of steroid genes expression. Key words: Luteal steroidogenesis, Lithium chloride, Corpus luteum, Progesterone, Estradiol. Introduction orpus luteum (CL) is a steroidogenic gland that plays a central role in the maintenance of pregnancy. This function is carried out largely by progesterone which is the main steroid synthesized by this transient endocrine gland” (1). The CL produces high levels of key proteins involved in the processing of cholesterol to progesterone. The rate-limiting step in steroid hormone production, the translocation of cholesterol from the outer to the inner mitochondrial membrane, is mediated by steroidogenic acute regulatory protein (StAR) (2). Once cholesterol is present in the inner mitochondrial membrane, transformation of cholesterol into steroid hormones begins. This step involves the several proteins, including side-chain cleavage cytochrome P450 (P450scc) and one of the six isoforms.

Paragigantocellularis lateralis (LPGi) nucleus plays a key role in the processing of pain information related to the descending pain modulation. Also, 17β-estradiol is involved in the pain modulation. The aim of the present study was to investigate the role of estrogen receptors of LPGi nucleus in the 17β-estradiol-induced pain modulation in the ovariectomized rats.
In this study, the female Wistar rats (180-250 gr) were used. In order to study the role of the NMDA receptors in the 17β-estradiol-induced pain modulation in the ovariectomized rats, primarily, rats were bilaterally ovariectomized and immediately cannulation of LPGi nucleus was performed. First, drugs were injected and 15 minutes later 50 μl of 5% formalin was injected into the rat's hind paw; and then, formalin-induced paw jerking behavior was recorded for 60 min.
Our results indicated that intra-LPGi injection of 17β-estradiol significantly attenuated paw jerking behavior in the both phases of formalin test. Intra-LPGi injection of estrogen receptor antagonist (ICI 182,780), had no effect on the paw jerking behavior. Pre-treatment of LPGi nucleus by ICI 182,780 counteracted the anti-nociceptive effect of 17β-estradiol both in the acute and in the chronic phases of formalin-induced paw jerking behaviour.
Based on the results of this study, it can be concluded that the intra-LPGi 17β-estradiol produces modest analgesia on the formalin-induced inflammatory pain in the ovariectomized rats, which is probably mediated via the esterogen receptors of this nucleus.

In this study, the effects of genistein and 17β-estradiol (E2) was investigated on some semen seminal plasma biochemical and enzymes in male gibel carp, during the spermiation phase. Mature male gibel carp (with ~ 30 to 40 g body weight (BW)) received intramuscular injections of one of two genistein doses (5 μg/g BW; G5, or 50 μg/g BW; G50), (10 μg/g BW 17β-estradiol, E2), 10 μg/g BW corn oil DMSO .Then, milt were collected in order to measure seminal plasma ionic, nonionic compounds and enzymes. The results of this study showed, there were significant differences in seminal plasma ionic, nonionic compounds and enzymes among the treated groups (p

The phytoestrogen, genistein and β-sitosterol, naturally occurring compounds found in soy products and pulp and paper mill effluent, respectively, could act as endocrine disrupting compounds (EDC) in the environment. The aim of this study was to evaluate the effects of β-sitosterol and genistein on the early life stages of Kutum (Rutilus kutum), specifically developing post-fertilized embryos. In this experimental study, Kutum’s fertilized egg exposed to 3 different levels of genistein and β-sitosterol (10, 50, 500ng.l-1, respectively) up to 7 days post-fertilization (dpf). At the end of the research period, newly hatched larvae were sampled and testosterone (T), 17β-estradiol (E2), Aromatase and ethoxyresorufin-O-deethylase (EROD) were measured according to standard protocols. One-way analysis of variance (ANOVA), Duncan multiple range test and SPSS 17 software were used for data analyses.
Findings: A high level of genistein lead to increased 17β-estradiol, testosterone concentration and aromatase activity. Also, β-sitosterol treated embryos (500ng.l-1) showed a high level of testosterone and EROD as compared to the control group. While other treatment had no significant effect. It seems that β-sitosterol and genistein could effect on the endocrine system of Kutum embryos by altering steroid biosynthesis and disturb enzyme activity. So it could lead to change the population structure and reduce reproduction performance of Kutum in the long period

Degeneration of dopaminergic neurons in the substantia nigra of the brain stem is the main pathological aspect of Parkinson’s disease (PD). 17 β-estradiol (E2) has neuroprotective effects on substantia nigra, however, the underlined mechanism is not well-known. In this study, we evaluated the neuroprotective effects of E2 in the ovariectomized 6-hydroxydopamine- (6-OHDA) rat model of PD. In this experimental study, all animals were ovariectomized to avoid any further bias in E2 levels and then these ovariectomized rats were randomly assigned into three experimental groups (10 rats in each group): ovariectomized control group (OCG), ovariectomized degeneration group receiving 25 μg of 6-OHDA into the left corpus striatum (ODG), and ovariectomized E2 pretreatment group pretreated with 0.1 mgkg-1of 17 β-estradiol for three days prior to the destruction of corpus striatum with 6-OHDA (OE2PTG). The apomorphine behavioral test and Nissl staining were performed in all experimental groups. The expressions of Sequestosome-1 (P62), Unc- 51 like autophagy activating kinase (Ulk1), and microtubule-associated proteins 1A/1B light chain 3B (Lc3) genes were evaluated using reverse transcription- polymerase chain reaction (RT-PCR). E2 administration reduced the damages to the dopaminergic neurons of the substantia nigra. The motor behavior, the number of rotations, and histological tests in the treatment group showed the cell survival improvement in comparison with the control groups indicating that E2 can inhibit the neurodegeneration. P62 and Lc3 were expressed in all experimental groups while Ulk1 was not expressed in ODG group. Moreover, Ulk1 was expressed after the treatment with E2 in OE2PTG group. E2 prevents neurodegeneration in dopaminergic neurons of the midbrain by over-expression of Ulk1 gene and augmenting the induction of autophagy.

Steroids promote the myelination and regeneration in the peripheral nervous system. Whereas, little is known about the inducing effects by which the hormones exert their effects on Schwann cells differentiation. This could be revealed by the expression of Schwann cell markers in adipose-derived stem cells (ADSCs). The purpose of this study was to present the effects of progesterone and 17 β-estradiol on the Schwann cell markers in rat ADSCs. The mesenchymal stem cell markers (CD73, and CD90) were assayed by flow cytometry. Rat ADSCs were sequentially treated with β-mercaptoethanol, and all-trans-retinoic acid, followed by a mixture of basic fibrobroblast growth factor, platelet-derived growth factor, forskolin and heregulin. In experimental groups, forskolin and heregulin were substituted by progesterone and 17 β-estradiol. After induction, the expression of Schwann cell markers P0, and S-100 and the cellular immunocytochemical staining positive rate of anti-S100 and anti-glial fibrillary acidic protein (GFAP) antibodies were compared in the experimental and control groups. Progesterone and 17 β-estradiol triggered P0 and S-100 genes expression and induced a cellular immunocytochemical staining positive rate of S-100 and GFAP in rats ADSCs. Progesterone induced these changes stronger than 17 β-estradiol. Thus, progesterone may induce rat ADSCs toward Schwann-like cells by expression of Schwann cell markers and is more potent than 17 β-estradiol in the expression of these markers.