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1
Karashima, Shigehiro, and Issey Osaka. "Rapidity and Precision of Steroid Hormone Measurement." Journal of Clinical Medicine 11, no. 4 (February 12, 2022): 956. http://dx.doi.org/10.3390/jcm11040956.
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Steroids are present in all animals and plants, from mammals to prokaryotes. In the medical field, steroids are commonly classified as glucocorticoids, mineralocorticoids, and gonadal steroid hormones. Monitoring of hormones is useful in clinical and research fields for the assessment of physiological changes associated with aging, disease risk, and the diagnostic and therapeutic effects of various diseases. Since the discovery and isolation of steroid hormones, measurement methods for steroid hormones in biological samples have advanced substantially. Although immunoassays (IAs) are widely used in daily practice, mass spectrometry (MS)-based methods have been reported to be more specific. Steroid hormone measurement based on MS is desirable in clinical practice; however, there are several drawbacks, including the purchase and maintenance costs of the MS instrument and the need for specialized training of technicians. In this review, we discuss IA- and MS-based methods currently in use and briefly present the history of steroid hormone measurement. In addition, we describe recent advances in IA- and MS-based methods and future applications and considerations.
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BLAND, Rosemary. "Steroid hormone receptor expression and action in bone." Clinical Science 98, no. 2 (January 31, 2000): 217–40. http://dx.doi.org/10.1042/cs0980217.
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The skeleton is a complex tissue, and hormonal control of bone remodelling is elaborate. The important role that steroid hormones play in bone cell development and in the maintenance of normal bone architecture is well established, but it is only relatively recently that it has become possible to describe their precise mechanism of action. This review focuses not only on the steroid hormones (oestrogens, corticosteroids, androgens and progesterone), but also on related hormones (vitamin D, thyroid hormone and the retinoids), all of which act via structurally homologous nuclear receptors that form part of the steroid/thyroid receptor superfamily. By examining the actions of all of these hormones in vivo and in vitro, this review gives a general overview of the current understanding of steroid hormone action in bone. In addition, a comprehensive review of steroid hormone receptor expression in bone cells is included. Finally, the role that future developments, such as steroid hormone receptor knockout mice, will play in our understanding of steroid hormone action in bone is considered.
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Shore, L. S., and M. Shemesh. "Naturally produced steroid hormones and their release into the environment." Pure and Applied Chemistry 75, no. 11-12 (January 1, 2003): 1859–71. http://dx.doi.org/10.1351/pac200375111859.
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Steroidal hormones produced by humans and animals are constantly excreted into the environment in their active forms. The primary steroid hormones are progesterone, estrone, estradiol, testosterone, and cortisol, all of which are lipophilic and poorly soluble in water. The steroids of major concern are estrone and estradiol-17β, since they exert their physiological effects at a lower concentration than other steroids and can be found in the environment in concentrations above their LOEL for fish and plants (10 ng/l). The steroid hormones can be readily measured in run-off, soil, and groundwater, but each steroid has its distinct pathway of transport. Since the major source of steroids in the environment appears to be cattle and chickens, the hormonal steroid input into the environment could be drastically reduced by well-established techniques such as buffer strips and composting.
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Szczepanska-Sadowska, Ewa, Katarzyna Czarzasta, Wiktor Bogacki-Rychlik, and Michał Kowara. "The Interaction of Vasopressin with Hormones of the Hypothalamo–Pituitary–Adrenal Axis: The Significance for Therapeutic Strategies in Cardiovascular and Metabolic Diseases." International Journal of Molecular Sciences 25, no. 13 (July 5, 2024): 7394. http://dx.doi.org/10.3390/ijms25137394.
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A large body of evidence indicates that vasopressin (AVP) and steroid hormones are frequently secreted together and closely cooperate in the regulation of blood pressure, metabolism, water–electrolyte balance, and behavior, thereby securing survival and the comfort of life. Vasopressin cooperates with hormones of the hypothalamo–pituitary–adrenal axis (HPA) at several levels through regulation of the release of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and multiple steroid hormones, as well as through interactions with steroids in the target organs. These interactions are facilitated by positive and negative feedback between specific components of the HPA. Altogether, AVP and the HPA cooperate closely as a coordinated functional AVP-HPA system. It has been shown that cooperation between AVP and steroid hormones may be affected by cellular stress combined with hypoxia, and by metabolic, cardiovascular, and respiratory disorders; neurogenic stress; and inflammation. Growing evidence indicates that central and peripheral interactions between AVP and steroid hormones are reprogrammed in cardiovascular and metabolic diseases and that these rearrangements exert either beneficial or harmful effects. The present review highlights specific mechanisms of the interactions between AVP and steroids at cellular and systemic levels and analyses the consequences of the inappropriate cooperation of various components of the AVP-HPA system for the pathogenesis of cardiovascular and metabolic diseases.
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Simoncini, T., and AR Genazzani. "Non-genomic actions of sex steroid hormones." European Journal of Endocrinology 148, no. 3 (March 1, 2003): 281–92. http://dx.doi.org/10.1530/eje.0.1480281.
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Steroid hormone receptors have been traditionally considered to act via the regulation of transcriptional processes, involving nuclear translocation and binding to specific response elements, and ultimately leading to regulation of gene expression. However, novel non-transcriptional mechanisms of signal transduction through steroid hormone receptors have been identified. These so-called 'non-genomic' effects do not depend on gene transcription or protein synthesis and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Several relevant biological actions of steroids have been associated with this kind of signaling. Ubiquitous regulatory cascades such as mitogen-activated protein kinases, the phosphatidylinositol 3-OH kinase and tyrosine kinases are modulated through non-transcriptional mechanisms by steroid hormones. Furthermore, steroid hormone receptor modulation of cell membrane-associated molecules such as ion channels and G-protein-coupled receptors has been shown. TIssues traditionally considered as 'non-targets' for classical steroid actions are instead found to be vividly regulated by non-genomic mechanisms. To this aim, the cardiovascular and the central nervous system provide excellent examples, where steroid hormones induce rapid vasodilatation and neuronal survival via non-genomic mechanisms, leading to relevant pathophysiological consequences. The evidence collected in the past Years indicates that target cells and organs are regulated by a complex interplay of genomic and non-genomic signaling mechanisms of steroid hormones, and the integrated action of these machineries has important functional roles in a variety of pathophysiological processes. The understanding of the molecular basis of the rapid effects of steroids is therefore important, and may in the future turn out to be of relevance for clinical purposes.
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He, Jinhan, Qiuqiong Cheng, and Wen Xie. "Minireview: Nuclear Receptor-Controlled Steroid Hormone Synthesis and Metabolism." Molecular Endocrinology 24, no. 1 (January 1, 2010): 11–21. http://dx.doi.org/10.1210/me.2009-0212.
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Abstract Steroid hormones are essential in normal physiology whereas disruptions in hormonal homeostasis represent an important etiological factor for many human diseases. Steroid hormones exert most of their functions through the binding and activation of nuclear hormone receptors (NRs or NHRs), a superfamily of DNA-binding and often ligand-dependent transcription factors. In recent years, accumulating evidence has suggested that NRs can also regulate the biosynthesis and metabolism of steroid hormones. This review will focus on the recent progress in our understanding of the regulatory role of NRs in hormonal homeostasis and the implications of this regulation in physiology and diseases.
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Marcinkowska, Ewa, and Antoni Wiedłocha. "Steroid signal transduction activated at the cell membrane: from plants to animals." Acta Biochimica Polonica 49, no. 3 (September 30, 2002): 735–45. http://dx.doi.org/10.18388/abp.2002_3782.
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Steroid hormones in plants and in animals are very important for physiological and developmental regulation. In animals steroid hormones are recognized by nuclear receptors, which transcriptionally regulate specific target genes following binding of the ligand. In addition, numerous rapid effects generated by steroids appear to be mediated by a mechanism not depending on the activation of nuclear receptors. Although the existence of separate membrane receptors was postulated many years ago and hundreds of reports supporting this hypothesis have been published, no animal membrane steroid receptor has been cloned to date. Meanwhile, a plant steroid receptor from Arabidopsis thaliana has been identified and cloned. It is a transmembrane protein which specifically recognizes plant steroids (brassinosteroids) at the cell surface and has a serine/threonine protein kinase activity. It seems that plants have no intracellular steroid receptors, since there are no genes homologous to the family of animal nuclear steroid receptors in the genome of A. thaliana. Since the reason of the rapid responses to steroid hormones in animal cells still remains obscure we show in this article two possible explanations of this phenomenon. Using 1,25-dihydroxyvitamin D(3) as an example of animal steroid hormone, we review results of our and of other groups concordant with the hypothesis of membrane steroid receptors. We also review the results of experiments performed with ovarian hormones, that led their authors to the hypothesis explaining rapid steroid actions without distinct membrane steroid receptors. Finally, examples of polypeptide growth factor that similarly to steroids exhibit a dual mode of action, activating not only cell surface receptors, but also intracellular targets, are discussed.
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Welch, Kma. "Migraine and ovarian steroid hormones." Cephalalgia 17, no. 20_suppl (December 1997): 12–16. http://dx.doi.org/10.1177/0333102497017s2005.
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This chapter reviews clinical and epidemiological data that support a role for ovarian steroid hormones in the migraine syndrome. Changes in the clinical presentation of migraine are discussed on the basis of current knowledge of biochemistry and pharmacology of ovarian steroids. Finally, special treatment considerations of ovarian hormone-sensitive migraine are discussed.
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Krause, Diana N., Sue P. Duckles, and Dale A. Pelligrino. "Influence of sex steroid hormones on cerebrovascular function." Journal of Applied Physiology 101, no. 4 (October 2006): 1252–61. http://dx.doi.org/10.1152/japplphysiol.01095.2005.
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The cerebral vasculature is a target tissue for sex steroid hormones. Estrogens, androgens, and progestins all influence the function and pathophysiology of the cerebral circulation. Estrogen decreases cerebral vascular tone and increases cerebral blood flow by enhancing endothelial-derived nitric oxide and prostacyclin pathways. Testosterone has opposite effects, increasing cerebral artery tone. Cerebrovascular inflammation is suppressed by estrogen but increased by testosterone and progesterone. Evidence suggests that sex steroids also modulate blood-brain barrier permeability. Estrogen has important protective effects on cerebral endothelial cells by increasing mitochondrial efficiency, decreasing free radical production, promoting cell survival, and stimulating angiogenesis. Although much has been learned regarding hormonal effects on brain blood vessels, most studies involve young, healthy animals. It is becoming apparent that hormonal effects may be modified by aging or disease states such as diabetes. Furthermore, effects of testosterone are complicated because this steroid is also converted to estrogen, systemically and possibly within the vessels themselves. Elucidating the impact of sex steroids on the cerebral vasculature is important for understanding male-female differences in stroke and conditions such as menstrual migraine and preeclampsia-related cerebral edema in pregnancy. Cerebrovascular effects of sex steroids also need to be considered in untangling current controversies regarding consequences of hormone replacement therapies and steroid abuse.
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Mukudai, Shigeyuki, Ken Ichi Matsuda, Takeshi Nishio, Yoichiro Sugiyama, Hideki Bando, Ryuichi Hirota, Hirofumi Sakaguchi, Yasuo Hisa, and Mitsuhiro Kawata. "Differential Responses to Steroid Hormones in Fibroblasts From the Vocal Fold, Trachea, and Esophagus." Endocrinology 156, no. 3 (March 1, 2015): 1000–1009. http://dx.doi.org/10.1210/en.2014-1605.
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Abstract There is accumulating evidence that fibroblasts are target cells for steroids such as sex hormones and corticoids. The characteristics of fibroblasts vary among tissues and organs. Our aim in this study is to examine differences in responses to steroid hormones among fibroblasts from different cervicothoracic regions. We compared the actions of steroid hormones on cultured fibroblasts from the vocal folds, which are considered to be the primary target of steroid hormones, and the trachea and esophagus in adult male rats. Expression of steroid hormone receptors (androgen receptor, estrogen receptor α, and glucocorticoid receptor) was identified by immunofluorescence histochemistry. Androgen receptor was much more frequently expressed in fibroblasts from the vocal fold than in those from the trachea and esophagus. Cell proliferation analysis showed that administration of testosterone, estradiol, or corticosterone suppressed growth of all 3 types of fibroblasts. However, mRNA expression for extracellular matrix–associated genes, including procollagen I and III and elastin, and hyaluronic acid synthase I was elevated only by addition of testosterone to fibroblasts from the vocal fold. These results indicate that each steroid hormone exerts region-specific effects on cervicothoracic fibroblasts with different properties through binding to specific receptors.
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Sandor, Luca F., Reka Ragacs, and David S. Gyori. "Local Effects of Steroid Hormones within the Bone Microenvironment." International Journal of Molecular Sciences 24, no. 24 (December 14, 2023): 17482. http://dx.doi.org/10.3390/ijms242417482.
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Steroid hormone production via the adrenal cortex, gonads, and placenta (so-called glandular steroidogenesis) is responsible for the endocrine control of the body’s homeostasis and is organized by a feedback regulatory mechanism based on the hypothalamus–pituitary–steroidogenic gland axis. On the other hand, recently discovered extraglandular steroidogenesis occurring locally in different tissues is instead linked to paracrine or autocrine signaling, and it is independent of the control by the hypothalamus and pituitary glands. Bone cells, such as bone-forming osteoblasts, osteoblast-derived osteocytes, and bone-resorbing osteoclasts, respond to steroid hormones produced by both glandular and extraglandular steroidogenesis. Recently, new techniques to identify steroid hormones, as well as synthetic steroids and steroidogenesis inhibitors, have been introduced, which greatly empowered steroid hormone research. Based on recent literature and new advances in the field, here we review the local role of steroid hormones in regulating bone homeostasis and skeletal lesion formation. The novel idea of extraglandular steroidogenesis occurring within the skeletal system raises the possibility of the development of new therapies for the treatment of bone diseases.
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Thompson, E. Brad. "Steroid Hormones: Membrane transporters of steroid hormones." Current Biology 5, no. 7 (July 1995): 730–32. http://dx.doi.org/10.1016/s0960-9822(95)00146-1.
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Fannon, Stacey A., Regina M. Vidaver, and Sherry A. Marts. "Historical Perspectives: An abridged history of sex steroid hormone receptor action." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1854–59. http://dx.doi.org/10.1152/jappl.2001.91.4.1854.
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The field of steroid hormone action is well established, although it is barely more than four decades old. Pivotal experiments in the late 1950s and 1960s showed that hormone-binding components exist within nuclei of target tissues and that steroid hormones act by regulating gene expression, rather than directly influencing enzymatic processes. The understanding that steroid hormone receptors interact with the general transcription machinery and alter chromatin structure came in the 1970s and 1980s, and details of this mechanism continue to be elucidated. In addition, the discovery of rapid cellular responses to steroid hormones has led to the identification of putative membrane-bound steroid receptors that act without affecting gene transcription. As noted in the recent Institute of Medicine report Exploring the Biological Contributions to Human Health: Does Sex Matter?, the effects of steroid hormones and defects in steroid hormone receptor action have a profound impact on human health and disease. Future research directives include the development of potent, selective steroid receptor modulators, the elucidation of nongenomic steroid hormone effects, and further exploration of hormone-genome interactions.
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Merrill, L., S. J. Chiavacci, R. T. Paitz, and T. J. Benson. "Quantification of 27 yolk steroid hormones in seven shrubland bird species: interspecific patterns of hormone deposition and links to life history, development, and predation risk." Canadian Journal of Zoology 97, no. 1 (January 2019): 1–12. http://dx.doi.org/10.1139/cjz-2017-0351.
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Steroid hormones play critical organizational and activational roles during vertebrate development, impacting everything from sexual differentiation to metabolic activity. For oviparous species such as birds, these hormones are transferred from female to egg during follicle maturation, and differences in relative and absolute concentrations of the steroid hormones may reflect differences in life history, developmental, and ecological conditions. Prior work on yolk steroid hormones has focused on a handful of candidate hormones (e.g., testosterone, androstenedione, and corticosterone), but we used high-performance liquid chromatography with tandem mass spectroscopy (LC–MS–MS) to quantify 27 yolk steroids from the eggs of seven shrubland bird species (American Robin, Turdus migratorius Linnaeus, 1766; Brown-headed Cowbird, Molothrus ater (Boddaert, 1783); Brown Thrasher, Toxostoma rufum (Linnaeus, 1758); Eastern Towhee, Pipilo erythrophthalmus (Linnaeus, 1758); Field Sparrow, Spizella pusilla (A. Wilson, 1810); Gray Catbird, Dumetella carolinensis (Linnaeus, 1766); Northern Cardinal, Cardinalis cardinalis (Linnaeus, 1758)). In addition to comparing steroid profiles across species, we conducted exploratory analyses to determine how the hormones clustered using a principal component (PC) approach and if PCs were correlated with aspects of egg resources (relative egg size, proportion yolk), life-history traits (embryonic and nestling development speed), and nest-predation risk (daily survival rate (DSR)). We documented substantial interspecific variation in both absolute and proportional endocrine profiles. PCAs indicated that glucocorticoids generally clustered together (PC1), but other classes of steroids did not. PC2 and PC3 strongly covaried with egg resources, DSR, and development speed, suggesting that they reflect adaptive patterns of maternal hormone deposition.
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Shackleton, C. H. L. "Profiling steroid hormones and urinary steroids." Journal of Chromatography B: Biomedical Sciences and Applications 379 (June 1986): 91–156. http://dx.doi.org/10.1016/s0378-4347(00)80683-0.
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ROMEO, RUSSELL D., ELIZABETH M. WATERS, and BRUCE S. MCEWEN. "Steroid-induced hippocampal synaptic plasticity: sex differences and similarities." Neuron Glia Biology 1, no. 3 (August 2004): 219–29. http://dx.doi.org/10.1017/s1740925x05000086.
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Early in development, steroid hormones structurally organize various regions of the CNS. However, steroid hormones continue to affect the structure and function of the CNS throughout the life of the individual. In this review, we discuss sex differences and similarities in steroid-induced synaptic plasticity in the adult brain. Particular emphasis is placed on steroid-induced plasticity in the hippocampus, a brain region important in learning and memory. This topic is relevant to the growing evidence for the actions of sex hormones outside of the reproductive neuroendocrine axis. It also tells an important and emerging story about non-genomic and genomic actions of steroids at the cellular and molecular levels. Specifically, the effects of estrogen and progesterone as well as the androgens and glucocorticoids are discussed. The influence of steroids on hippocampal structure and function can differ vastly between the sexes. However, there are certain similarities that might aid in our understanding of how steroids affect CNS plasticity in general. Although future studies will undoubtedly lead us to a greater understanding of these phenomena, the data reviewed indicate that when studying synaptic plasticity, the sex and hormonal milieu of the individual might significantly influence the outcome and interpretation of the research.
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Nghiem, L. D., J. McCutcheon, A. I. Schäfer, and M. Elimelech. "The role of endocrine disrupters in water recycling: risk or mania?" Water Science and Technology 50, no. 2 (July 1, 2004): 215–20. http://dx.doi.org/10.2166/wst.2004.0128.
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The widespread occurrence of endocrine disrupting chemicals (EDCs), such as steroid hormones, in secondary wastewater effluents has become a major concern in the water recycling practice. This paper investigates the risk of steroid hormone breakthrough during nanofiltration membrane filtration in water recycling applications. The results indicate a dynamic equilibrium between adsorption and desorption of steroid hormone with regard to the membrane. This equilibrium can be pH dependent and there is a possibility for release of steroid hormones at high pH during membrane cleaning procedures or erratic pH variations. Increase in water recovery can severely increase the hormone breakthrough concentration. The results also indicate a possibility of accumulation of steroid hormones in the NF membrane, followed by subsequent release.
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Wade, S. E. "An Oral-Diffusion-Sink Device for Extended Sampling of Multiple Steroid Hormones from Saliva." Clinical Chemistry 38, no. 9 (September 1, 1992): 1878–82. http://dx.doi.org/10.1093/clinchem/38.9.1878.
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Abstract Performance of a new oral-diffusion-sink (ODS) device for sampling the steroid hormones cortisol, progesterone, estradiol, and testosterone from human saliva was tested in vitro. The tested device differed from an earlier ODS sampler by using a polymeric composition of beta-cyclodextrin rather than an antiserum to bind analytes diffusing into the device. The capacity of the cyclodextrin-driven device to accumulate the steroid hormones from a simple buffer, human saliva, and saliva fortified with high concentrations of glucocorticosteroids was evaluated. Further, the ability of this device to accurately register the average analyte concentration resulting from treatments simulating physiological episodic secretion events was tested. Each steroid showed a characteristic rate of uptake that was unaffected by saliva or high physiological concentrations of competing steroids, and ODS uptake resulting from temporally varied concentrations of the hormone in the medium accurately reflected the time-integrated average concentration. This ODS provides a potential noninvasive and unobtrusive means of sampling the tissue-available concentrations of multiple steroid hormones, with averaging over physiological secretion events.
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Polyakov, L. M., D. V. Sumenkova, R. A. Knyazev, and L. E. Panin. "The analysis of interaction between lipoproteins and steroid hormones." Biomeditsinskaya Khimiya 57, no. 3 (2011): 308–13. http://dx.doi.org/10.18097/pbmc20115703308.
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Using the methods of ultracentrifugation, gel-filtration and fluorescence quenching, we demonstrated, that plasma lipoproteins bind steroid hormones and can therefore play a role of their active transport form in an organism. High density lipoproteins have revealed the highest affinity to steroids for. It has been found, that protein component of lipoproteins takes part in the formation of lipoprotein-steroid complex. The apolipoprotein A-I, the main protein component of high density lipoproteins, is responsible for binding of steroid hormones. The calculated constants formation of the complexes of lipoproteins with steroid hormones testifies to specificity of linkage. The results obtained allow to considering real opportunity of transfer of steroid hormones into cell by a receptor-mediated endocytosis in structure of lipoproteins complexes.
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Abe, Ai, Masamitsu Maekawa, Toshihiro Sato, Yu Sato, Masaki Kumondai, Hayato Takahashi, Masafumi Kikuchi, Katsumi Higaki, Jiro Ogura, and Nariyasu Mano. "Metabolic Alteration Analysis of Steroid Hormones in Niemann–Pick Disease Type C Model Cell Using Liquid Chromatography/Tandem Mass Spectrometry." International Journal of Molecular Sciences 23, no. 8 (April 18, 2022): 4459. http://dx.doi.org/10.3390/ijms23084459.
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Niemann–Pick disease type C (NPC) is an autosomal recessive disease caused by a functional deficiency of cholesterol-transporting proteins in lysosomes, and exhibits various clinical symptoms. Since mitochondrial dysfunction in NPC has recently been reported, cholesterol catabolism to steroid hormones may consequently be impaired. In this study, we developed a comprehensive steroid hormone analysis method using liquid chromatography/tandem mass spectrometry (LC–MS/MS) and applied it to analyze changes in steroid hormone concentrations in NPC model cells. We investigated the analytical conditions for simultaneous LC–MS/MS analysis, which could be readily separated from each other and showed good reproducibility. The NPC phenotype was verified as an NPC model with mitochondrial abnormalities using filipin staining and organelle morphology observations. Steroid hormones in the cell suspension and cell culture medium were also analyzed. Steroid hormone analysis indicated that the levels of six steroid hormones were significantly decreased in the NPC model cell and culture medium compared to those in the wild-type cell and culture medium. These results indicate that some steroid hormones change during NPC pathophysiology and this change is accompanied by mitochondrial abnormalities.
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Cheng, Yu-Jung, Chieh-Hsin Lin, and Hsien-Yuan Lane. "From Menopause to Neurodegeneration—Molecular Basis and Potential Therapy." International Journal of Molecular Sciences 22, no. 16 (August 11, 2021): 8654. http://dx.doi.org/10.3390/ijms22168654.
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The impacts of menopause on neurodegenerative diseases, especially the changes in steroid hormones, have been well described in cell models, animal models, and humans. However, the therapeutic effects of hormone replacement therapy on postmenopausal women with neurodegenerative diseases remain controversial. The steroid hormones, steroid hormone receptors, and downstream signal pathways in the brain change with aging and contribute to disease progression. Estrogen and progesterone are two steroid hormones which decline in circulation and the brain during menopause. Insulin-like growth factor 1 (IGF-1), which plays an import role in neuroprotection, is rapidly decreased in serum after menopause. Here, we summarize the actions of estrogen, progesterone, and IGF-1 and their signaling pathways in the brain. Since the incidence of Alzheimer’s disease (AD) is higher in women than in men, the associations of steroid hormone changes and AD are emphasized. The signaling pathways and cellular mechanisms for how steroid hormones and IGF-1 provide neuroprotection are also addressed. Finally, the molecular mechanisms of potential estrogen modulation on N-methyl-d-aspartic acid receptors (NMDARs) are also addressed. We provide the viewpoint of why hormone therapy has inconclusive results based on signaling pathways considering their complex response to aging and hormone treatments. Nonetheless, while diagnosable AD may not be treatable by hormone therapy, its preceding stage of mild cognitive impairment may very well be treatable by hormone therapy.
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Konstandi, Maria, Jie Cheng, and Frank J. Gonzalez. "Sex steroid hormones regulate constitutive expression of Cyp2e1 in female mouse liver." American Journal of Physiology-Endocrinology and Metabolism 304, no. 10 (May 15, 2013): E1118—E1128. http://dx.doi.org/10.1152/ajpendo.00585.2012.
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CYP2E1 is of paramount toxicological significance because it metabolically activates a large number of low-molecular-weight toxicants and carcinogens. In this context, factors that interfere with Cyp2e1 regulation may critically affect xenobiotic toxicity and carcinogenicity. The aim of this study was to investigate the role of female steroid hormones in the regulation of CYP2E1, as estrogens and progesterone are the bases of contraceptives and hormonal replacement therapy in menopausal women. Interestingly, a fluctuation in the hepatic expression pattern of Cyp2e1 was revealed in the different phases of the estrous cycle of female mice, with higher Cyp2e1 expression at estrus (E) and lower at methestrus (ME), highly correlated with that in plasma gonadal hormone levels. Depletion of sex steroids by ovariectomy repressed Cyp2e1 expression to levels similar to those detected in males and cyclic females at ME. Hormonal supplementation brought Cyp2e1 expression back to levels detected at E. The role of progesterone appeared to be more prominent than that of 17β-estradiol. Progesterone-induced Cyp2e1 upregulation could be attributed to inactivation of the insulin/PI3K/Akt/FOXO1 signaling pathway. Tamoxifen, an anti-estrogen, repressed Cyp2e1 expression potentially via activation of the PI3K/Akt/FOXO1 and GH/STAT5b-linked pathways. The sex steroid hormone-related changes in hepatic Cyp2e1 expression were highly correlated with those observed in Hnf-1α, β-catenin, and Srebp-1c. In conclusion, female steroid hormones are clearly involved in the regulation of CYP2E1, thus affecting the metabolism of a plethora of toxicants and carcinogenic agents, conditions that may trigger several pathologies or exacerbate the outcomes of various pathophysiological states.
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Ishihara, Yasuhiro, Takuya Takemoto, Atsuhiko Ishida, and Takeshi Yamazaki. "Protective Actions of 17β-Estradiol and Progesterone on Oxidative Neuronal Injury Induced by Organometallic Compounds." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/343706.
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Steroid hormones synthesized in and secreted from peripheral endocrine glands pass through the blood-brain barrier and play a role in the central nervous system. In addition, the brain possesses an inherent endocrine system and synthesizes steroid hormones known as neurosteroids. Increasing evidence shows that neuroactive steroids protect the central nervous system from various harmful stimuli. Reports show that the neuroprotective actions of steroid hormones attenuate oxidative stress. In this review, we summarize the antioxidative effects of neuroactive steroids, especially 17β-estradiol and progesterone, on neuronal injury in the central nervous system under various pathological conditions, and then describe our recent findings concerning the neuroprotective actions of 17β-estradiol and progesterone on oxidative neuronal injury induced by organometallic compounds, tributyltin, and methylmercury.
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Taylor, David R., Lea Ghataore, Lewis Couchman, Royce P. Vincent, Ben Whitelaw, Dylan Lewis, Salvador Diaz-Cano, et al. "A 13-Steroid Serum Panel Based on LC-MS/MS: Use in Detection of Adrenocortical Carcinoma." Clinical Chemistry 63, no. 12 (December 1, 2017): 1836–46. http://dx.doi.org/10.1373/clinchem.2017.277624.
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Abstract BACKGROUND Adrenocortical carcinoma (ACC) is a rare malignancy, with an annual incidence of 1 or 2 cases per million. Biochemical diagnosis is challenging because up to two-thirds of the carcinomas are biochemically silent, resulting from de facto enzyme deficiencies in steroid hormone biosynthesis. Urine steroid profiling by GC-MS is an effective diagnostic test for ACC because of its capacity to detect and quantify the increased metabolites of steroid pathway synthetic intermediates. Corresponding serum assays for most steroid pathway intermediates are usually unavailable because of low demand or lack of immunoassay specificity. Serum steroid analysis by LC-MS/MS is increasingly replacing immunoassay, in particular for steroids most subject to cross-reaction. METHODS We developed an LC-MS/MS method for the measurement of serum androstenedione, corticosterone, cortisol, cortisone, 11-deoxycorticosterone, 11-deoxycortisol, 21-deoxycortisol, dehydroepiandrosterone sulfate, pregnenolone, 17-hydroxypregnenolone, progesterone, 17-hydroxyprogesterone, and testosterone. Assay value in discriminating ACC from other adrenal lesions (phaeochromocytoma/paraganglioma, cortisol-producing adenoma, and lesions demonstrating no hormonal excess) was then investigated. RESULTS In ACC cases, between 4 and 7 steroids were increased (median = 6), and in the non-ACC groups, up to 2 steroids were increased. 11-Deoxycortisol was markedly increased in all cases of ACC. All steroids except testosterone in males and corticosterone and cortisone in both sexes were of use in discriminating ACC from non-ACC adrenal lesions. CONCLUSIONS Serum steroid paneling by LC-MS/MS is useful for diagnosing ACC by combining the measurement of steroid hormones and their precursors in a single analysis.
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Wierman, Margaret E. "Sex steroid effects at target tissues: mechanisms of action." Advances in Physiology Education 31, no. 1 (January 2007): 26–33. http://dx.doi.org/10.1152/advan.00086.2006.
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Our understanding of the mechanisms of sex hormone action has changed dramatically over the last 10 years. Estrogens, progestins, and androgens are the steroid hormones that modulate reproductive function. Recent data have shown that many other tissues are targets of sex hormones in addition to classical reproductive organs. This review outlines new advances in our understanding of the spectrum of steroid hormone ligands, newly recognized target tissues, structure-function relationships of steroid receptors, and, finally, their genomic and nongenomic actions. Sex-based specific effects are often related to the different steroid hormone mileu in men compared with women. Understanding the mechanisms of sex steroid action gives insight into the differences in normal physiology and disease states.
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Saloniemi, Taija, Heli Jokela, Leena Strauss, Pirjo Pakarinen, and Matti Poutanen. "The diversity of sex steroid action: novel functions of hydroxysteroid (17β) dehydrogenases as revealed by genetically modified mouse models." Journal of Endocrinology 212, no. 1 (November 1, 2011): 27–40. http://dx.doi.org/10.1530/joe-11-0315.
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Disturbed action of sex steroid hormones, i.e. androgens and estrogens, is involved in the pathogenesis of various severe diseases in humans. Interestingly, recent studies have provided data further supporting the hypothesis that the circulating hormone concentrations do not explain all physiological and pathological processes observed in hormone-dependent tissues, while the intratissue sex steroid concentrations are determined by the expression of steroid metabolising enzymes in the neighbouring cells (paracrine action) and/or by target cells themselves (intracrine action). This local sex steroid production is also a valuable treatment option for developing novel therapies against hormonal diseases. Hydroxysteroid (17β) dehydrogenases (HSD17Bs) compose a family of 14 enzymes that catalyse the conversion between the low-active 17-keto steroids and the highly active 17β-hydroxy steroids. The enzymes frequently expressed in sex steroid target tissues are, thus, potential drug targets in order to lower the local sex steroid concentrations. The present review summarises the recent data obtained for the role of HSD17B1, HSD17B2, HSD17B7 and HSD17B12 enzymes in various metabolic pathways and their physiological and pathophysiological roles as revealed by the recently generated genetically modified mouse models. Our data, together with that provided by others, show that, in addition to having a role in sex steroid metabolism, several of these HSD17B enzymes possess key roles in other metabolic processes: for example, HD17B7 is essential for cholesterol biosynthesis and HSD17B12 is involved in elongation of fatty acids. Additional studiesin vitroandin vivoare to be carried out in order to fully define the metabolic role of the HSD17B enzymes and to evaluate their value as drug targets.
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Groothuis, Ton G. G., and Hubert Schwabl. "Hormone-mediated maternal effects in birds: mechanisms matter but what do we know of them?" Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1497 (November 28, 2007): 1647–61. http://dx.doi.org/10.1098/rstb.2007.0007.
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Over the past decade, birds have proven to be excellent models to study hormone-mediated maternal effects in an evolutionary framework. Almost all these studies focus on the function of maternal steroid hormones for offspring development, but lack of knowledge about the underlying mechanisms hampers further progress. We discuss several hypotheses concerning these mechanisms, point out their relevance for ecological and evolutionary interpretations, and review the relevant data. We first examine whether maternal hormones can accumulate in the egg independently of changes in hormone concentrations in the maternal circulation. This is important for Darwinian selection and female physiological trade-offs, and possible mechanisms for hormone accumulation in the egg, which may differ among hormones, are reviewed. Although independent regulation of plasma and yolk concentrations of hormones is conceivable, the data are as yet inconclusive for ovarian hormones. Next, we discuss embryonic utilization of maternal steroids, since enzyme and receptor systems in the embryo may have coevolved with maternal effect mechanisms in the mother. We consider dose–response relationships and action pathways of androgens and argue that these considerations may help to explain the apparent lack of interference of maternal steroids with sexual differentiation. Finally, we discuss mechanisms underlying the pleiotropic actions of maternal steroids, since linked effects may influence the coevolution of parent and offspring traits, owing to their role in the mediation of physiological trade-offs. Possible mechanisms here are interactions with other hormonal systems in the embryo. We urge endocrinologists to embark on suggested mechanistic studies and behavioural ecologists to adjust their interpretations to accommodate the current knowledge of mechanisms.
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Problems of endocrinology, Editorial team of. "Nikolai Petrovich Goncharov (To his 60th birthday)." Problems of Endocrinology 41, no. 2 (April 15, 1995): 47. http://dx.doi.org/10.14341/probl11379.
Full textAbstract:
60 years have passed since the birth of the famous scientist biochemist-endocrinologist, head of the laboratory of biochemical endocrinology and hormonal analysis of the Endocrinology Research Center of the Russian Academy of Medical Sciences, doctor of medical sciences, professor Nikolai Petrovich Goncharov. He is a pioneer in the study of the synthesis and metabolism of steroid hormones in primates; he developed and implemented an adequate experimental model within the framework of the WHO Human Reproduction program to evaluate the pharmacokinetics, mechanism of action, efficacy and safety of both new steroid preparations and regulators of endocrine secretion of steroid hormones. A significant section of the research of N.P. Goncharov is devoted to a comparative study of the endocrine system of primates, the endocrine support of the stress response, the formation of the function of the endocrine glands in various periods of postnatal ontogenesis, and the role of steroid hormones in the pathogenesis of human leukemia. He is an author of about 200 scientific papers on various problems of hormone biochemistry and endocrinology.
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Gasser, Benedikt Andreas, Johann Kurz, Bernhard Dick, and Markus Georg Mohaupt. "Are Steroid Hormones Dysregulated in Autistic Girls?" Diseases 8, no. 1 (March 14, 2020): 6. http://dx.doi.org/10.3390/diseases8010006.
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Evidence of altered cholesterol and steroid hormones in autism is increasing. However, as boys are more often affected, evidence mainly relates to autistic males, whereas evidence for affected autistic girls is sparse. Therefore, a comprehensive gas chromatography mass spectrometry-based steroid hormone metabolite analysis was conducted from autistic girls. Results show increased levels of several steroid hormones, especially in the class of androgens in autistic girls such as testosterone or androstenediol. The increase of the majority of steroid hormones in autistic girls is probably best explained multifactorially by a higher substrate provision in line with the previously developed cholesterol hypothesis of autism.
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Panin, L. Ye, O. M. Khoshchenko, and I. F. Usynin. "Role of apolipoprotein A-I in the anabolic effect of steroid hormones." Problems of Endocrinology 48, no. 6 (December 15, 2002): 45–48. http://dx.doi.org/10.14341/probl11727.
Full textAbstract:
As early shown, a portion of steroid hormones binds to blood lipoproteins, primarily to high-density lipoproteins (HDL) [Panin et al. 1988]. Steroid hormones together with HDL are captured by resident macrophages of the liver where in secondary lysosomes HDL are degraded to form apoA-I and steroid hormones restore a ∆4, 3-keto group with the participation of 5-α and 5β- reductases to give rise to tetrahydro compounds. In this study, an attempt was undertaken to show a role of a complex of some steroid hormones with apo A-I in realization of the anabolic action of these steroid hormones by using the cultured hepatocytes and concurrently cultured hepatocytes and Kupffer’s cells isolated from the liver of male Wistar rats weighing 180-200 g.
Steroid hormones having an anabolic action, such as androsterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate and tetrahydrocortisol as ingredients of a complex with apolipoprotein A-I (apoA-I), increased the rate of protein biosynthesis and dehydroepiandrosterone sulfate and tetrahydrocortisol also did the rate of DNA synthesis in the cultured hepatocytes. All the hormones had a restored ∆4,3-keto group in the A ring structure. Restoration of this group of steroid hormones and formation of their complex with apoA-I are associated with the action of resident macrophages (Kupffer’s cells). That is the reason that addition of HDL (a source of apoA-I) and cortisol (a source of the restored form - tetrahydrocortisol) to the coculture of hepatocytes and macrophages, by concurrently stimulating the latter by lipopolysaccharide led to a significant increase in the rate of protein and DNA biosynthesis. The findings show an important role of a ∆4,3-keto group of the A ring of steroid hormones and their complex with apo A-I in realizing the anabolic action of steroids.
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Batth, Rituraj, Clément Nicolle, Ilenuta Simina Cuciurean, and Henrik Toft Simonsen. "Biosynthesis and Industrial Production of Androsteroids." Plants 9, no. 9 (September 3, 2020): 1144. http://dx.doi.org/10.3390/plants9091144.
Full textAbstract:
Steroids are a group of organic compounds that include sex hormones, adrenal cortical hormones, sterols, and phytosterols. In mammals, steroid biosynthesis starts from cholesterol via multiple steps to the final steroid and occurs in the gonads, adrenal glands, and placenta. This highly regulated pathway involves several cytochrome P450, as well as different dehydrogenases and reductases. Steroids in mammals have also been associated with drug production. Steroid pharmaceuticals such as testosterone and progesterone represent the second largest category of marketed medical products. There heterologous production through microbial transformation of phytosterols has gained interest in the last couple of decades. Phytosterols being the plants sterols serve as inexpensive substrates for the production of steroid derivatives. Various genes and biochemical pathways involved in phytosterol degradation have been identified in many Rhodococcus and Mycobacterium species. Apart from an early investigation in mammals, presence of steroids such as androsteroids and progesterone has also been demonstrated in plants. Their main role is linked with growth, development, and reproduction. Even though plants share some chemical features with mammals, the biosynthesis is different, with the first C22 hydroxylation as an example. This is performed by CYP11A1 in mammals and CYP90B1 in plants. Moreover, the entire plant steroid biosynthesis is not fully elucidated. Knowing this pathway could provide new processes for the industrial biotechnological production of steroid hormones in plants.
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Baker, ME. "Albumin, steroid hormones and the origin of vertebrates." Journal of Endocrinology 175, no. 1 (October 1, 2002): 121–27. http://dx.doi.org/10.1677/joe.0.1750121.
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Albumin, the major serum protein, binds a wide variety of lipophilic compounds including steroids, other lipophilic hormones and various phytochemicals and xenobiotics that bind to receptors for steroids and other lipophilic hormones. Despite albumin's low affinity (K(d) approximately 10(-4) M to 10(-6) M) for these lipophilic compounds, the high concentration of albumin in serum makes this protein a major carrier of steroids and lipophilic hormones and a regulator of their access to receptors. Albumin also functions as a sink for xenobiotics, diminishing the binding of xenobiotics to hormone receptors and other cellular proteins. This protects animals from endocrine disruption by xenobiotics. We propose that these properties of albumin were important in protochordates and primitive vertebrates, such as jawless fish, about 600 to 530 million years ago, just before and during the Cambrian period. It is at that time that the ancestral receptors of adrenal and sex steroids - androgens, estrogens, glucocorticoids, mineralocorticoids, and progestins - arose in multicellular animals. Albumin regulated access of steroids to their receptors, as well as protecting animals from endocrine disruptors, such as phytochemicals, fungal chemicals and phenolics, and other chemicals formed at hydrothermal vents by geochemical processes. Thus, animals in which albumin expression was high had a selective advantage in regulating the steroid response and avoiding endocrine disruption by xenobiotics.
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Wilson, Jean D. "The role of 5a-reduction in steroid hormone physiology." Reproduction, Fertility and Development 13, no. 8 (2001): 673. http://dx.doi.org/10.1071/rd01074.
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A role for 5α-reduction in androgen physiology was first established with the recognition that dihydrotestosterone, the 5α-reduced metabolite of testosterone, is formed in many androgen target tissues, binds to the androgen receptor with greater affinity than testosterone, and plays an essential role in virilization of the urogenital sinus and urogenital tubercle during male development. Two 5α-reductases perform this reaction, and both isoenzymes utilize NADPH as cofactor and have broad specificity for steroids containing a Δ4, 3-keto configuration. 5α-Reduction, which is essentially irreversible, flattens the steroid molecule because of altered relation of the A and B rings, and stabilizes the hormone–receptor complex. Studies involving in vitro reporter gene assays and intact mice in which both isoenzymes are disrupted, indicate that the fundamental effect of dihydrotestosterone formation is to amplify hormonal signals that can be mediated by testosterone at higher concentrations. 5α-Reduction also plays a role in the action of other steroid hormones, including the plant growth hormone, brassinolide, the boar pheromones, androstanol and androstenol, progesterone (in some species), and, possibly, aldosterone and cortisol. The fact that the reaction is important in plants and animals implies a fundamental role in steroid hormone action.
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Villablanca, Amparo C., Muthuvel Jayachandran, and Carole Banka. "Atherosclerosis and sex hormones: current concepts." Clinical Science 119, no. 12 (September 1, 2010): 493–513. http://dx.doi.org/10.1042/cs20100248.
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CVD (cardiovascular disease) is the leading cause of death for women. Considerable progress has been made in both our understanding of the complexities governing menopausal hormone therapy and our understanding of the cellular and molecular mechanisms underlying hormone and hormone receptor function. Understanding the interplay of atherosclerosis and sex steroid hormones and their cognate receptors at the level of the vessel wall has important ramifications for clinical practice. In the present review, we discuss the epidemiology of CVD in men and women, the clinical impact of sex hormones on CVD, and summarize our current understanding of the pathogenesis of atherosclerosis with a focus on gender differences in CVD, its clinical presentation and course, and pathobiology. The critical animal and human data that pertain to the role of oestrogens, androgens and progestins on the vessel wall is also reviewed, with particular attention to the actions of sex hormones on each of the three key cell types involved in atherogenesis: the endothelium, smooth muscle cells and macrophages. Where relevant, the systemic (metabolic) effects of sex hormones that influence atherogenesis, such as those involving vascular reactivity, inflammation and lipoprotein metabolism, are discussed. In addition, four key current concepts in the field are explored: (i) total hormone exposure time and coronary heart disease risk; (ii) the importance of tissue specificity of sex steroid hormones, critical timing and the stage of atherosclerosis in hormone action; (iii) biomarkers for atherosclerosis with regard to hormone therapy; and (iv) the complex role of sex steroids in inflammation. Future studies in this field will contribute to guiding clinical treatment recommendations for women and help define research priorities.
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N. Smirnova, Irina, Elena V. Fedulova, Maxim M. Nazarov, and Оlga P. Cherkasova. "Structurally Sensitive Changes in Absorption THz Spectra of Corticosteroids." Siberian Journal of Physics 5, no. 4 (December 1, 2010): 162–67. http://dx.doi.org/10.54362/1818-7919-2010-5-4-162-167.
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The series of steroid hormones, such as progesterone, 17α-hydroxyprogesterone, cortisol and other was measured by terahertz time-domain spectroscopy (THz TDS). It was obtained that THz absorption spectra of steroid hormones have characteristic lines of absorption in the frequency range 0.1-3.0 THz. We investigate the relation between the position of side functional groups and THz spectral response. Besides pellets of polycrystalline pure substances, steroids solution in methanol was analyzed. The given method can be applied for express diagnostics of different classes of steroid
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Alonso-Diez, Ángela, Sara Cáceres, Laura Peña, Belén Crespo, and Juan Carlos Illera. "Anti-Angiogenic Treatments Interact with Steroid Secretion in Inflammatory Breast Cancer Triple Negative Cell Lines." Cancers 13, no. 15 (July 21, 2021): 3668. http://dx.doi.org/10.3390/cancers13153668.
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Human inflammatory breast cancer (IBC) is a highly angiogenic disease for which antiangiogenic therapy has demonstrated only a modest response, and the reason for this remains unknown. Thus, the purpose of this study was to determine the influence of different antiangiogenic therapies on in vitro and in vivo steroid hormone and angiogenic growth factor production using canine and human inflammatory breast carcinoma cell lines as well as the possible involvement of sex steroid hormones in angiogenesis. IPC-366 and SUM149 cell lines and xenotransplanted mice were treated with different concentrations of VEGF, SU5416, bevacizumab and celecoxib. Steroid hormone (progesterone, dehydroepiandrostenedione, androstenedione, testosterone, dihydrotestosterone, estrone sulphate and 17β-oestradiol), angiogenic growth factors (VEGF-A, VEGF-C and VEGF-D) and IL-8 determinations in culture media, tumour homogenate and serum samples were assayed by EIA. In vitro, progesterone- and 17β-oestradiol-induced VEGF production promoting cell proliferation and androgens are involved in the formation of vascular-like structures. In vivo, intratumoural testosterone concentrations were augmented and possibly associated with decreased metastatic rates, whereas elevated E1SO4 concentrations could promote tumour progression after antiangiogenic therapies. In conclusion, sex steroid hormones could regulate the production of angiogenic factors. The intratumoural measurement of sex steroids and growth factors may be useful to develop preventive and individualized therapeutic strategies.
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Hammond, Geoffrey L. "Plasma steroid-binding proteins: primary gatekeepers of steroid hormone action." Journal of Endocrinology 230, no. 1 (July 2016): R13—R25. http://dx.doi.org/10.1530/joe-16-0070.
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Biologically active steroids are transported in the blood by albumin, sex hormone-binding globulin (SHBG), and corticosteroid-binding globulin (CBG). These plasma proteins also regulate the non-protein-bound or ‘free’ fractions of circulating steroid hormones that are considered to be biologically active; as such, they can be viewed as the ‘primary gatekeepers of steroid action’. Albumin binds steroids with limited specificity and low affinity, but its high concentration in blood buffers major fluctuations in steroid concentrations and their free fractions. By contrast, SHBG and CBG play much more dynamic roles in controlling steroid access to target tissues and cells. They bind steroids with high (~nM) affinity and specificity, with SHBG binding androgens and estrogens and CBG binding glucocorticoids and progesterone. Both are glycoproteins that are structurally unrelated, and they function in different ways that extend beyond their transportation or buffering functions in the blood. Plasma SHBG and CBG production by the liver varies during development and different physiological or pathophysiological conditions, and abnormalities in the plasma levels of SHBG and CBG or their abilities to bind steroids are associated with a variety of pathologies. Understanding how the unique structures of SHBG and CBG determine their specialized functions, how changes in their plasma levels are controlled, and how they function outside the blood circulation provides insight into how they control the freedom of steroids to act in health and disease.
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Gao, Bei, Yixin Zhu, Weishou Shen, Peter Stärkel, and Bernd Schnabl. "Correlation between Serum Steroid Hormones and Gut Microbiota in Patients with Alcohol-Associated Liver Disease." Metabolites 12, no. 11 (November 13, 2022): 1107. http://dx.doi.org/10.3390/metabo12111107.
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Alcohol-associated liver disease is a major public health concern globally. Alterations of steroid hormones and gut microbiota were both found in patients with alcohol-associated liver disease. However, their correlation has not been well characterized in these patients. In this study, we measured the level of 30 steroid hormones in serum and fecal samples collected from non-alcoholic controls, patients with alcohol use disorder, and patients with alcohol-associated hepatitis. The profile of serum and fecal steroid hormones was quite different in patients with alcohol-associated hepatitis from that in patients with alcohol use disorder and control subjects. Stronger alterations were observed in male patients than in females. Correlations were found not only between serum steroids and gut bacteria but also between serum steroids and gut fungi. These correlations need to be taken into consideration during the development of treatment strategies for alcohol-associated liver disease.
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Levin, Ellis R. "Rapid signaling by steroid receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 5 (November 2008): R1425—R1430. http://dx.doi.org/10.1152/ajpregu.90605.2008.
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Steroid receptors transcribe genes that lead to important biological processes, including normal organ development and function, tissue differentiation, and promotion of oncogenic transformation. These actions mainly result from nuclear steroid receptor action. However, for 50 years, it has been known that rapid effects of steroid hormones occur and could result from rapid signal transduction. Examples of these effects include stress responses to secreted glucocorticoids, rapid actions of thyroid hormones in the heart, and acute uterine/vaginal responses to injected estrogen. These types of responses have increasingly been attributed to rapid signaling by steroid hormones, upon engaging binding proteins most often at the cell surface of target organs. It is clear that rapid signal transduction serves an integrated role to modify existing proteins, altering their structure and activity, and to modulate gene transcription, often through collaboration with the nuclear pool of steroid receptors. The biological outcomes of steroid hormone actions thus reflect input from various cellular pools, cocoordinating the necessary events that are restrained in temporal and kinetic fashion. Here I describe the current understanding of rapid steroid signaling that is now appreciated to extend to virtually all members of this family of hormones and their receptors.
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Borsellino, Giovanni, Arturo Buonaguidi, Mario Baroni, Gaetano Elli, Augusta Sonato, Silvano Poma, Stefania Rescalli, and Roberto Mondina. "Plasma Steroid Transport in Subjects with Tumors of Hormonal Target Organs: A Review." Tumori Journal 78, no. 3 (June 1992): 155–58. http://dx.doi.org/10.1177/030089169207800302.
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Tumors derived from a hormonal target organ are assumed to be stimulated by the same hormone that stimulates the normal target tissue. In spite of attempts to acquire direct indications of a correlation between hormones and cancer, none have been definitive because studies of total and free hormone levels have given contradictory results. For this reason, attention has shifted to the study of plasma binding and transport of hormones, that is, of the proteins responsible for modulation of the hormone effect and thus of hormone bioavailability. The data reviewed indicate that in-depth study of the transport and binding system of sex steroids would give new information about the endocrine characteristics of cancer patients.
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ATANASOFF, Alexander, Anton RUSENOV, Dimitrinka ZAPRYANOVA, Lazarin LAZAROV, Cigdem URKU, and Galin NIKOLOV. "Estradiol and testosterone hormones as a method for sex determination of Siberian sturgeon (Acipenser baerii) from Zhrebchevo Dam Lake, Bulgaria." Danubian Animal Genetic Resources 8, no. 2 (August 15, 2023): 73–80. http://dx.doi.org/10.59913/dagr.2023.12359.
Full textAbstract:
Determination of the gender in sturgeon is very important in fish farmers, as sex is one of the main factors that determine aim of cultivating them. One of the method for maturation monitoring of sturgeons is steroid hormone analysis. On this base the current study used estradiol and testosterone hormones to determine the gender of 2-3-year-old Siberian sturgeon (Acipenser baerii) cultivated in sturgeon broodstock farm located in the Zhrebchevo Dam lake, Bulgaria. The serum concentrations of circulating reproductive hormones found in the both sex were similar to the hormonal profiles in previously reports. The results were confirmed also by histological examination, which showed pre-vitellogenic stage (Stage I) in female and maturity (Stage V) at the male individuals. The findings indicate the force of current steroid hormones as a method for sex determination. In conclusion, analysis of circulating reproductive hormones may be a useful method in early determining the sex of Siberian sturgeon.
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Coates, John M., Mark Gurnell, and Zoltan Sarnyai. "From molecule to market: steroid hormones and financial risk-taking." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1538 (January 27, 2010): 331–43. http://dx.doi.org/10.1098/rstb.2009.0193.
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Little is known about the role of the endocrine system in financial decision-making. Here, we survey research on steroid hormones and their cognitive effects, and examine potential links to trader performance in the financial markets. Preliminary findings suggest that cortisol codes for risk and testosterone for reward. A key finding of this endocrine research is the different cognitive effects of acute versus chronic exposure to hormones: acutely elevated steroids may optimize performance on a range of tasks; but chronically elevated steroids may promote irrational risk-reward choices. We present a hypothesis suggesting that the irrational exuberance and pessimism observed during market bubbles and crashes may be mediated by steroid hormones. If hormones can exaggerate market moves, then perhaps the age and sex composition among traders and asset managers may affect the level of instability witnessed in the financial markets.
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Walker, William H., and Paul S. Cooke. "Functions of Steroid Hormones in the Male Reproductive Tract as Revealed by Mouse Models." International Journal of Molecular Sciences 24, no. 3 (February 1, 2023): 2748. http://dx.doi.org/10.3390/ijms24032748.
Full textAbstract:
Steroid hormones are capable of diffusing through cell membranes to bind with intracellular receptors to regulate numerous physiological processes. Three classes of steroid hormones, namely androgens, estrogens and glucocorticoids, contribute to the development of the reproductive system and the maintenance of fertility. During the past 30 years, mouse models have been produced in which the expression of genes encoding steroid hormone receptors has been enhanced, partially compromised or eliminated. These mouse models have revealed many of the physiological processes regulated by androgens, estrogens and to a more limited extent glucocorticoids in the testis and male accessory organs. In this review, advances provided by mouse models that have facilitated a better understanding of the molecular regulation of testis and reproductive tract processes by steroid hormones are discussed.
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Mariotti, Angelo. "Sex Steroid Hormones and Cell Dynamics in the Periodontium." Critical Reviews in Oral Biology & Medicine 5, no. 1 (January 1994): 27–53. http://dx.doi.org/10.1177/10454411940050010201.
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The biological changes that occur in tissues of the periodontium during puberty, the menstrual cycle, pregnancy, menopause, and oral contraceptive use have heightened interest in the relationship between sex steroid hormones and periodontal health. These clinical observations coupled with tissue specificity of hormone localization, identification of hormone receptors, as well as the metabolism of hormones have strongly suggested that periodontal tissues are targets for androgens, estrogens, and progestins. The etiologies of periodontal endocrinopathies are diverse; nonetheless, periodontal pathologies may be a consequence of the actions and interactions of sex steroid hormones on specific cells found in the periodontium.
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Honma, Naoko, Yoko Matsuda, and Tetuo Mikami. "Carcinogenesis of Triple-Negative Breast Cancer and Sex Steroid Hormones." Cancers 13, no. 11 (May 25, 2021): 2588. http://dx.doi.org/10.3390/cancers13112588.
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Triple-negative breast cancer (TNBC) lacks an effective treatment target and is usually associated with a poor clinical outcome; however, hormone unresponsiveness, which is the most important biological characteristic of TNBC, only means the lack of nuclear estrogenic signaling through the classical estrogen receptor (ER), ER-α. Several sex steroid receptors other than ER-α: androgen receptor (AR), second ER, ER-β, and non-nuclear receptors represented by G-protein-coupled estrogen receptor (GPER), are frequently expressed in TNBC and their biological and clinical importance has been suggested by a large number of studies. Despite the structural similarity between each sex steroid hormone (androgens and estrogens) or each receptor (AR and ER-β), and similarity in the signaling mechanisms of these hormones, most studies or reviews focused on one of these receptors, and rarely reviewed them in a comprehensive way. Considering the coexistence of these hormones and their receptors in TNBC in a clinical setting, a comprehensive viewpoint would be important to correctly understand the association between the carcinogenic mechanism or pathobiology of TNBC and sex steroid hormones. In this review, the carcinogenic or pathobiological role of sex steroid hormones in TNBC is considered, focusing on the common and divergent features of the action of these hormones.
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Mitsushima, Dai, Kenkichi Takase, Toshiya Funabashi, and Fukuko Kimura. "Gonadal Steroid Hormones Maintain the Stress-Induced Acetylcholine Release in the Hippocampus: Simultaneous Measurements of the Extracellular Acetylcholine and Serum Corticosterone Levels in the Same Subjects." Endocrinology 149, no. 2 (October 25, 2007): 802–11. http://dx.doi.org/10.1210/en.2007-0827.
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To examine the role of gonadal steroid hormones in the stress responses of acetylcholine (ACh) levels in the hippocampus and serum corticosterone levels, we observed these parameters simultaneously in intact, gonadectomized, or gonadectomized steroid-primed rats. In both sexes of rats, neither gonadectomy nor the replacement of gonadal steroid hormone affected the baseline levels of ACh. However, gonadectomy severely attenuated the stress response of ACh, whereas the replacement of corresponding gonadal hormone successfully restored the response to intact levels. The gonadal hormones affected the serum corticosterone levels in a different manner; the testosterone replacement in orchidectomized rats suppressed the baseline and the stress response of corticosterone levels, whereas the 17β-estradiol replacement in ovariectomized rats increased the levels. We further found that letrozole or flutamide administration in intact male rats attenuated the stress response of ACh. In addition, flutamide treatment increased the baseline levels of corticosterone, whereas letrozole treatment attenuated the stress response of corticosterone. Moreover, we found a low positive correlation between the ACh levels and corticosterone levels, depending on the presence of gonadal steroid hormone. We conclude that: 1) gonadal steroid hormones maintain the stress response of ACh levels in the hippocampus, 2) the gonadal steroid hormone independently regulates the stress response of ACh in the hippocampus and serum corticosterone, and 3) the sex-specific action of gonadal hormone on the cholinergic stress response may suggest a neonatal sexual differentiation of the septohippocampal cholinergic system in rats.
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McNerney, Kyle P., and Ana Maria Arbeláez. "Steroid Use in the NICU: Treatment and Tapering." NeoReviews 24, no. 4 (April 1, 2023): e207-e216. http://dx.doi.org/10.1542/neo.24-4-e207.
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Abstract The adrenal gland cortex produces life-sustaining steroid hormones that are critical for the development and survival of the fetus and neonate. Antenatal and postnatal administration of steroids has critical therapeutic effects in preterm infants. However, prolonged postnatal steroid therapy for more than 1 to 2 weeks is associated with iatrogenic adrenal insufficiency and should prompt consideration of a steroid taper and stress dose precautions. In this review, we will describe fetal adrenal development and steroidogenesis, the effect of antenatal exogenous steroids, the therapeutic role of postnatal steroids, evaluation and treatment of adrenal insufficiency, and the role of steroid tapers after prolonged steroid treatment.
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Freeman, M. R., A. Dobritsa, P. Gaines, W. A. Segraves, and J. R. Carlson. "The dare gene: steroid hormone production, olfactory behavior, and neural degeneration in Drosophila." Development 126, no. 20 (October 15, 1999): 4591–602. http://dx.doi.org/10.1242/dev.126.20.4591.
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Steroid hormones mediate a wide variety of developmental and physiological events in insects, yet little is known about the genetics of insect steroid hormone biosynthesis. Here we describe the Drosophila dare gene, which encodes adrenodoxin reductase (AR). In mammals, AR plays a key role in the synthesis of all steroid hormones. Null mutants of dare undergo developmental arrest during the second larval instar or at the second larval molt, and dare mutants of intermediate severity are delayed in pupariation. These defects are rescued to a high degree by feeding mutant larvae the insect steroid hormone 20-hydroxyecdysone. These data, together with the abundant expression of dare in the two principal steroid biosynthetic tissues, the ring gland and the ovary, argue strongly for a role of dare in steroid hormone production. dare is the first Drosophila gene shown to encode a defined component of the steroid hormone biosynthetic cascade and therefore provides a new tool for the analysis of steroid hormone function. We have explored its role in the adult nervous system and found two striking phenotypes not previously described in mutants affected in steroid hormone signaling. First, we show that mild reductions of dare expression cause abnormal behavioral responses to olfactory stimuli, indicating a requirement for dare in sensory behavior. Then we show that dare mutations of intermediate strength result in rapid, widespread degeneration of the adult nervous system.
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Pott, Janne, Yoon Ju Bae, Katrin Horn, Andrej Teren, Andreas Kühnapfel, Holger Kirsten, Uta Ceglarek, et al. "Genetic Association Study of Eight Steroid Hormones and Implications for Sexual Dimorphism of Coronary Artery Disease." Journal of Clinical Endocrinology & Metabolism 104, no. 11 (June 6, 2019): 5008–23. http://dx.doi.org/10.1210/jc.2019-00757.
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Abstract Context Steroid hormones are important regulators of physiological processes in humans and are under genetic control. A link to coronary artery disease (CAD) is supposed. Objective Our main objective was to identify genetic loci influencing steroid hormone levels. As a secondary aim, we searched for causal effects of steroid hormones on CAD. Design We conducted genome-wide meta-association studies for eight steroid hormones: cortisol, dehydroepiandrosterone sulfate (DHEAS), estradiol, and testosterone in two independent cohorts (LIFE-Adult, LIFE-Heart, maximum n = 7667), and progesterone, 17-hydroxyprogesterone, androstenedione, and aldosterone in LIFE-Heart only (maximum n = 2070). All genome-wide significant loci were tested for sex interactions. Furthermore, we tested whether previously reported CAD single-nucleotide polymorphisms were associated with our steroid hormone panel and investigated causal links between hormone levels and CAD status using Mendelian randomization (MR) approaches. Results We discovered 15 novel associated loci for 17-hydroxyprogesterone, progesterone, DHEAS, cortisol, androstenedione, and estradiol. Five of these loci relate to genes directly involved in steroid metabolism, that is, CYP21A1, CYP11B1, CYP17A1, STS, and HSD17B12, almost completing the set of steroidogenic enzymes with genetic associations. Sexual dimorphisms were found for seven of the novel loci. Other loci correspond, for example, to the WNT4/β-catenin pathway. MR revealed that cortisol, androstenedione, 17-hydroxyprogesterone, and DHEA-S had causal effects on CAD. We also observed enrichment of cortisol and testosterone associations among known CAD hits. Conclusion Our study greatly improves insight into genetic regulation of steroid hormones and their dependency on sex. These results could serve as a basis for analyzing sexual dimorphism in other complex diseases.
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He, Zihong, Tuomo Rankinen, Arthur Leon, James Skinner, André Tchernof, and Claude Bouchard. "Plasma Steroids are Not Associated with Resting and Exercise Blood Pressure." International Journal of Sports Medicine 39, no. 13 (October 5, 2018): 967–71. http://dx.doi.org/10.1055/a-0660-0121.
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AbstractWe investigated the associations between steroid hormones and resting and exercise blood pressure in the sedentary state and in response to an exercise program controlling for sex, body mass, ethnicity, age, oral contraceptives, hormone therapy, smoking and alcohol intake in subjects from the HERITAGE Family Study. In the sedentary state, 267 men (28% Blacks) and 301 women (37% Blacks) were available, and 241 men and 254 women completed the exercise program. Fourteen steroid hormones and sex hormone-binding globulin concentrations were assayed in a fasted state. Statistical significance was set at a Bonferroni adjusted p<0.0001. After controlling for the various covariates, only testosterone came close to a significant correlation with exercise systolic blood pressure at 50 W (r=−0.21, P=0.0006) in men. No other correlations with resting and exercise blood pressure traits were found at baseline. There were significant changes in blood pressure in response to the exercise program, but none of the correlations with baseline plasma steroids reached statistical significance. Plasma steroids do not correlate with resting and exercise blood pressure in sedentary adults and do not associate with blood pressure changes in response to a 20-week endurance exercise program.