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György Csaba - One of the best experts on this subject based on the ideXlab platform.
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Possible contribution of trained immunity in faulty Hormonal Imprinting and DOHaD: Review and hypothesis.
Acta microbiologica et immunologica Hungarica, 2020Co-Authors: György CsabaAbstract:The faulty Hormonal Imprinting theory (published in 1980) and the DOHaD (Developmental Origin of Health and Disease theory (published in 1986) are twin-concepts: both justify the manifestation after long time (in adults) diseases which had been provoked in differentiating cells (e.g. during gestation). This was demonstrated using animal experiments as well, as comparative statistical methods (in human cases). However, there is no explanation for the tools of memorization (even after decades) of the early adversity and the tools of execution (manifestation) in adult age. It seems likely that immune memory is involved to the memorization of early adversity, up to the manifestation of the result (non-communicable diseases). Nevertheless, the relatively short timespan of adaptive immune memory makes this system insuitable for this function, however the newly recognized trained memory of the innate immune system seems to be theoretically suitable for the storage of the records and handling the sequalae, which is the epigenetic reprogramming in the time of provocation, without changes in base sequences (mutation). The flawed (damaged) program is manifested later, in adult age. Evidences are incomplete, so further animal experiments and human observations are needed for justifying the theory.
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Reprogramming of the Immune System by Stress and Faulty Hormonal Imprinting.
Clinical therapeutics, 2020Co-Authors: György CsabaAbstract:Abstract Purpose Hormonal Imprinting is taking place perinatally at the first encounter between the developing hormone receptors and their target hormones. However, in this crucial period when the developmental window for physiological Imprinting is open, other molecules, such as synthetic hormones and endocrine disruptors can bind to the receptors, leading to faulty Imprinting with life-long consequences, especially to the immune system. This review presents the factors of stress and faulty Hormonal Imprinting that lead to reprogramming of the immune system. Methods Relevant publications from Pubmed since 1990 were reviewed and synthesized. Findings The developing immune system is rather sensitive to Hormonal effects. Faulty Hormonal Imprinting is able to reprogram the original developmental program present in a given cell, with lifelong consequences, manifested in alteration of hormone binding by receptors, susceptibility to certain (non-infectious) diseases, and triggering of other diseases. As stress mobilizes the hypothalamic-pituitary-adrenal axis if it occurred during gestation or perinatally, it could lead to faulty Hormonal Imprinting in the immune system, manifested later as allergic and autoimmune diseases or weakness of normal immune defenses. Hormonal Imprinting is an epigenetic process and is carried to the offspring without alteration of DNA base sequences. This means that any form of early-life stress alone or in association with Hormonal Imprinting could be associated with the developmental origin of health and disease (DOHaD). As puberty is also a period of reprogramming, stress or faulty Imprinting can change the original (developmental) program, also with life-long consequences. Implications Considering the continuous differentiation of immune cells (from blast-cells) during the whole life, there is a possibility of late-Imprinting or stress-activated reprogramming in the immune system at any periods of life, with later pathogenetic consequences.
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Az egyedfejlődés kritikus fázisaiban történő gyógyszeres kezelések késői következményei. A hibás hormonális Imprinting koncepciójának kiterjesztése
Orvosi hetilap, 2020Co-Authors: György CsabaAbstract:Hormonal Imprinting is a physiological process, which is a part of the receptor-hormone complex development. It determines the binding capacity of the receptors across the lifespan. It takes place perinatally in the critical period of hormone receptor development, when the developmental window for Imprinting is open and permits the binding of hormone-like molecules (related or synthetic hormones, endocrine disruptors etc.) causing disturbances of the endocrine system, and the systems- influenced organs by it, for life. This is the faulty Hormonal Imprinting. However, studying the medical database, PubMed, a lot of data can be found on the harmful late (adult age) effects of medication in the critical period of development with non-Hormonal molecules, which are manifested later in functional alterations or diseases. This could mean that in the process of faulty Imprinting, the openness of the developmental window could be more important than the structural similarity of a molecule to hormones. As developmentally critical period for faulty Imprinting by hormone-like molecules is not exclusively the perinatal one (this is justified in the case of faulty Hormonal Imprinting), the pubertal period was also studied from this aspect and similarities to the impact of perinatal use have been found (this could be called "Pubertal Origin of Health and Disease = POHaD). While in the case of Hormonal faulty Imprinting, the mechanism seems to be clear (considering the role of receptors), the mechanism of drug-provoked Imprinting is presently uncleared (considering the variety of medications which cause late-manifested alterations). The medicaments-caused faulty Imprinting conception calls attention to the dangers of medication in the perinatal as well as the pubertal periods. Orv Hetil. 2020; 161(2): 43-49.
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Lifelong Impact of Perinatal Endocrine Disruptor Exposures (Faulty Hormonal Imprinting)
The International Journal of Plant Animal and Environmental Sciences, 2019Co-Authors: György CsabaAbstract:Perinatal Hormonal Imprinting is taking place when the developing hormone receptors meet the target hormone at first occasion. This is needed for the normal function of receptor-hormone complex and valid for life. However, when the developmental window is open, related molecules, as endocrine disruptors also can be bound, causing life-long distortion (faulty Hormonal Imprinting) which could be manifested as diseases in any period of life (adult age), even it is transgenerationally inherited by an epigenetic route. The nervous system, sexuality and immune system are touched first of all however, some alteration can be observed in the whole human organism. At present most of the well-known endocrine disruptors are man-made steroid hormone-like molecules, utilized in the industry, agrotechnics and medical treatments. The effect of endocrine disruptor molecules seems to be noxious in any period of life however, most deleterious perinatally, causing late manifested faulty Imprinting. Nevertheless, faulty Imprinting can be provoked also later, at weaning, at adolescence and in continously differentiating cells in the whole life, with less decisive however important consequences. The recognition of faulty Hormonal Imprinting changed our picture on teratogenesis, as a mass of functional teratogens appeared in the form of endocrine disruptors, and the period of teratogenicity has been prolonged over birth.The industrial, communal or agrotechnical endocrine disruptors are very difficultly avoided however, medical disruptors (hormones, lipid-soluble vitamins etc) must be observed and omitted in the critical periods. The hereditary transmission of faulty Hormonal Imprinting seems to be dangerous for the future of mankind, although positive effects by the adaptation of endocrine system to the present and future circumstances can be imagined.
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Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State.
Current genomics, 2019Co-Authors: György CsabaAbstract:Hormonal Imprinting takes place perinatally at the first encounter between the developing hormone receptor and its target hormone. This process is needed for the normal function of the receptor-hormone pair and its effect is life-long. However, in this critical period, when the developmental window is open, related molecules (members of the same hormone family, synthetic hormones and hormone-like molecules, endocrine disruptors) also can be bound by the receptor, causing life-long faulty Imprinting. In this case, the receptors' binding capacity changes and alterations are caused at adult age in the sexual and behavioral sphere, in the brain and bones, inclination to diseases and manifestation of diseases, etc. Hereby, faulty Hormonal Imprinting is the basis of metabolic and immunological Imprinting as well as the developmental origin of health and disease (DOHaD). Although the perinatal period is the most critical for faulty Imprinting, there are other critical periods as weaning and adolescence, when the original Imprinting can be modified or new Imprintings develop. Hormonal Imprinting is an epigenetic process, without changing the base sequence of DNA, it is inherited in the cell line of the imprinted cells and also transgenerationally (up to 1000 generations in unicellulars and up to the 3rd generation in mammals are justified). Considering the enormously growing number and amount of faulty imprinters (endocrine disruptors) and the hereditary character of faulty Imprinting, this latter is threatening the whole human endocrine system.
Péter Kovács - One of the best experts on this subject based on the ideXlab platform.
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A hormonális Imprinting humán patológiai hatásainak modellezése állatkísérletekben = Model experiments of the human pathological effects of Hormonal Imprinting
2007Co-Authors: György Csaba, Péter Kovács, Karabélyos C, Barbara Knippel, Ágnes Inczefiné Gonda, Kornélia TekesAbstract:A Hormonalis Imprinting a kozponti idegrendszerre is hat, akar perinatalisan, akar kesőbbi erzekenysegi időpontban tortenik meg. Endorfin Imprinting csokkenti az agyi szerotonin szintet, ami befolyasolja az agresszivitast es szexualis magatartast es extrem modon megnoveli a nocistatin szintet, ami a fajdalomtűresre lehet hatassal. Perinatalis szerotonin Imprinting csokkenti a striatum szerotonin szintjet es noveli himekben a szexualis aktivitast. Az immunsejtekben (feherversejtek es hizosejtek) szamos hormon van jelen. Az allatok neme befolyasolja a hormon tartalmat. Ujszulottkori endorfin Imprinting utan a nőstenyek hizosejtjei kevesebb endorfint, szerotonint es EGF-et tartlmaztak. A kesői terhessegi korban bekovetkező endorfin Imprinting immunsejt szerotonin es hisztaminra valo hatasa transzgeneraciosan is kovethető az F2 generacioig. Kozvetett Imprinting is lehetseges, amennyiben stressz (elvalasztasi vagy felnőtt korban) vagy alkohol fogyasztas (terhesseg vagy szoptatas alatt) maradandoan befolyasolja az immunsejtek hormon tartalmat. Egyes hormonok (szerotonin, hisztamin)a sejtmagban is jelen vannak. HDC-gen kiutott egerekben az immunsejtek szerotonin tartalma megnőtt, de a sejtmagbol hianyzott. A kiserletek eredmenyeiből egy, az immunrendszerben jelen levő endokrin halozatra is lehet kovetkeztetni. | Perinatal as well as later (at weaning or at adult age) Hormonal Imprinting influences also the central nervous system. Endorphin Imprinting reduces the serotonin level of the brain, which influences the animals? aggressivity and sexual behavior and extremly elevates the nocistatin level which affects pain tolerance. Perinatal serotonin Imprinting reduces the serotonin level of striatum and increases males? sexual activity. Immune cells (white blood cells and mast cells) contain numerous hormones. There are differences in the hormone contents of males and females. After neonatal endorphin Imprinting females? mast cells contain less endorphin, serotonin and EGF. The effects of endorphin Imprinting in late pregnancy on the serotonin and histamine concentration can be followed up to the second filial generation.There is also a possibility of indirect Imprinting when stress (at weaning or in adult age) or alcohol consumption (during pregnancy or lactation) durably influence the hormone content of immune cells. Certain hormones (histamine and serotonin) are present also in the nucleus of mast cells. In HDC-KO mice the serotonin content of immune cells increases, however it was absent in the nucleus. Considering the results, an endocrine network inside the immune system can be surmized.
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Prolonged effect of an H1-receptor blocker antihistamine on the histamine content of white blood cells and mast cells.
Cell biochemistry and function, 2004Co-Authors: György Csaba, Péter Kovács, Éva PállingerAbstract:Hormonal Imprinting usually takes place perinatally at the first encounter between the developing receptor and its target hormone, determining the future binding capacity of the receptor for life. Molecules similar to a hormone can cause faulty Imprinting also with life-long consequences. Hormone production of the imprinted cell is also durably influenced. In cytogenic organs Imprinting can also be provoked in adulthood. At present the effect of a single terfenadine treatment in adult rats on the histamine content of peritoneal cells (lymphocytes, mast cells and the monocyte-macrophage-granulocyte group), white blood cells (lymphocytes, granulocytes, monocytes) and thymic lymphocytes was studied 3 weeks after treatment to clarify the effect of prolonged treatment with an antihistamine in adulthood. The cells were studied by flow cytometric analysis. Peritoneal mast cells contained significantly more and thymic lymphocytes significantly less histamine than controls. In the other cells the differences were not significant. The results support earlier observations on the effect of antihistamines on mast cell histamine release (inhibition) and call attention to the fact that this effect is durable (Hormonal Imprinting provoked in adults).
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Single treatment (Hormonal Imprinting) of newborn rats with serotonin increases the serotonin content of cells in adults.
Cell biology international, 2002Co-Authors: György Csaba, Péter Kovács, Éva PállingerAbstract:Abstract Hormonal Imprinting takes place perinatally at the first encounter between the hormone and its target receptor, causing the finishment of the maturation of receptor–signal transduction system. In the presence of an excess of the target hormone or related molecules faulty Imprinting develops with life-long consequences. In earlier experiments single neonatal treatment with minute dose of IL-6 caused also prolonged stimulation of IL-6 production. In the present experiment newborn female and male rats were treated with 20 μg serotonin (Hormonal Imprinting) and were studied for serotonin content of different cell types in adult age. Serotonin content was measured by flow cytometry and its localization was determined by confocal microscopy. Serotonin content was detected in white blood cells (lymphocytes, monocytes and granulocytes); in lymphocytes, monocytes (macrophages), granulocytes and mast cells of peritoneal fluid and thymic lymphocytes. Serotonin was present in all cell types of control animals studied. Serotonin content extremely elevated in the white blood cells and also increased in the peritoneal cells of neonatally treated female animals. There was no elevation in thymic lymphocytes. The mean values of male animals remained at the control level. The experiments call attention to the life-long effect of the perinatal Hormonal Imprinting manifested presently in the elevation of serotonin content and point to the gender differences of serotonin Imprinting. Considering the role of serotonin in mood and psychiatric diseases, the observations could have some clinical importance.
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Insulin uptake, localization and production in previously insulin treated and untreated Tetrahymena. Data on the mechanism of Hormonal Imprinting.
Cell biochemistry and function, 2000Co-Authors: György Csaba, Péter KovácsAbstract:Confocal microscopic experiments demonstrate the presence of insulin in Tetrahymena, observed also in earlier experiments. However, there is a broad spectrum of insulin-containing cells from the immunocytochemically insulin-free, to the strongly antibody-reactive ones. During 1 h of insulin treatment (Imprinting) the cells gradually bind and take up insulin, and the process is slow. One minute after the start of treatment there is not difference in the number of insulin antibody-reactive cells and amount of insulin. After 5 or 10 min the cells bind and contain more insulin and after 1 h most of the cells are densely packed with the insulin antibody-reactive material. Insulin Imprinting accelerates binding and uptake alike: 48 h after Imprinting and 1 min after the start of the second treatment, more insulin is present on the surface and inside the cells, than after 10 min in the first-time treated cells. Theoretically, this effect of Hormonal Imprinting helps to maintain the species by facilitating molecular recognition and binding as well as uptake of useful molecules. The experiments also support previous observations on the parallel receptor-evoking (strengthening) and hormone-producing effect of Hormonal Imprinting.
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Human Chorionic Gonadotropin (HCG)-like Hormones (FSH, LH, TSH) in Tetrahymena. A Confocal Microscopic Analysis
Acta Protozoologica, 2000Co-Authors: György Csaba, Péter KovácsAbstract:Summary. The unicellular ciliate, Tetrahymena contains molecules which immunologically and functionally resemble to human hormones. Up to now, of the pituitary glycoprotein hormones only the presence of adrenocorticotropic hormone (ACTH) was demonstrated. In the present experiment we observed the presence of molecules immunologically similar to human chorionic gonadotropin (HCG). This hormone-li ke material is localized diffusely in the cell, and in higher amount in the cortical region, in the cilia and in the oral field. After one hour treatment (Hormonal Imprinting) with luteinizing hormone (LH), follicle stimulating hormone, mixture of these two hormones, HCG, or thyrotropic hor mone (TSH), more fluorescence intensity (given by the hormone) can be observed. Twenty four hours or four days after these treatments the a mount of hormone-like materials seems to be higher, than in the untreated cells or immediately after treatment. The diffuse localization disappears in the body of the cell after LH or FSH treatment and the hormone concentrates peripheral, in the cortex and especially in (or on) the cilia. The largest amount of hormone-like material seems to be present after LH+FSH or TSH treatment. These results mean that in Tetrahymena enhanced production of the appropriate hormone could be induced by hormone treatment (Imprinting), which is maintained in the progeny ge nerations. The experiments support that Hormonal Imprinting of receptor and hormone production can run parallel.
Ágnes Inczefi-gonda - One of the best experts on this subject based on the ideXlab platform.
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Impact of single neonatal serotonin treatment (Hormonal Imprinting) on the brain serotonin content and sexual behavior of adult rats.
Life sciences, 2003Co-Authors: György Csaba, Ágnes Inczefi-gonda, M. Hantos, Cs. Karabélyos, Barbara Knippel, Kornélia TekesAbstract:Hormonal Imprinting takes place perinatally at the first encounter between the developing receptor and its target hormone. As a consequence of Imprinting the receptor accomplishes its maturation and reaches the binding capacity characteristic to the adult age. In the excess of target hormone or presence of molecules similar to the target hormone, which are able to bind to the unmatured receptors, faulty Imprinting develops with life-long consequences. At present, serotonin was given to neonatal rats and their sexual activity, brain serotonin level and steroid receptor's binding capacity was measured in adult age. Brain serotonin level was significantly reduced in male's striatum and parallel with this, male's sexual activity significantly increased. In other regions of the male brain (prefrontal cortex, hypothalamus, hippocampus) there was a statistically non-significant tendency for a decrease in serotonin level. No significant differences were detected in female brain values, and there was only slight change in female's sexual activity. There was also no change in the binding capacity of thymic glucocorticoid and uterine estrogen receptors. The experiments call attention to the possibility of perinatal Imprinting by a neurotransmitter causing changes in brain neurotransmitter level for life, which is manifested in altered sexual activity.
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Effect of a single treatment (Imprinting) with genistein or combined treatment with genistein+benzpyrene on the binding capacity of glucocorticoid and estrogen receptors of adult rats.
Human & experimental toxicology, 2002Co-Authors: György Csaba, Ágnes Inczefi-gondaAbstract:Hormonal Imprinting takes place perinatally at the first encounter between the hormone and its target receptor. This is needed for the normal finishment of the maturation of the receptor–signal tra...
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Effect of neonatal treatment with mifepristone or tamoxifen on the binding capacity of the thymic glucocorticoid or uterine estrogen receptor of adult rats: data on the mechanism of Hormonal Imprinting.
Life sciences, 2000Co-Authors: György Csaba, Ágnes Inczefi-gondaAbstract:Abstract For studying the mechanism of perinatal Hormonal Imprinting newborn rats were treated with a single injection of the antihormones, mifepristone (RU486) or tamoxifen (100 μg each). Glucocorticoid receptors of thymi of 6 weeks old male and female, and uterine estrogen receptors of 2 months old female rats were studied for dexamethasone or estradiol binding, respectively. Tamoxifen caused faulty Imprinting both in the thymic and uterine receptors, increasing affinity and density of males, and decreasing females' glucocorticoid receptors as well, as decreasing the density of uterine estradiol receptors. Neonatal mifepristone treatment was indifferent to the thymus, and decreasing to density of uterine estrogen receptors. Males' body weight significantly decreased 6 weeks after tamoxifen treatment. The results suggest that Imprinting can not be provoked by a molecule (hormone antagonist) which can bind to the receptor without any postreceptorial events (mifepristone/glucocorticoid receptor), in the presence of some postreceptorial effects the reaction takes place, however the strongest reaction can be observed by the hormone analogue (tamoxifen) with postreceptorial (agonist) effect, not considering that the receptor is the direct target of the molecule or a cross-reaction is present.
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The effect of perinatal Hormonal Imprinting with 13-cis-retinoic acid (isotretinoin) on the thymic glucocorticoid receptors of female and testosterone level of male adult rats.
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 1999Co-Authors: György Csaba, Annamária Gaál, Ágnes Inczefi-gondaAbstract:In earlier experiments, the long-term effect of perinatal treatment (Hormonal Imprinting) with all-trans-retinol and all-trans-retinoic acid on the thymic glucocorticoid and uterine estrogen receptors was studied and was found effective. In the present experiments, the Imprinting effect of four retinoids (13-cis-retinaldehyde, 13-cis-retinoic acid, 9-cis-retinaldehyde and 9-cis-retinoic acid) was investigated, using receptor kinetic analysis and sexual hormone (testosterone and progesterone) level determinations. Exclusively 13-cis-retinoic acid (isotretinoin) had an effect, significantly decreasing glucocorticoid receptor affinity and increasing serum testosterone level. Relationships with RAR-RXR receptor binding and teratogenicity is discussed.
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Fetal digoxin treatment enhances the binding capacity of thymic glucocorticoid receptors in adult female rats.
General pharmacology, 1998Co-Authors: György Csaba, Ágnes Inczefi-gondaAbstract:Abstract 1. Hormonal Imprinting is provoked in the perinatal critical period in the presence of the appropriate hormone or molecules similar to it. As a consequence of Hormonal Imprinting, the developing receptor finishes its maturation normally (in the presence of the adequate hormone) or abnormally (under the effect of foreign molecules that are able to bind to the receptor). 2. Digoxin—which has a steroid character—caused faulty Imprinting by treatments at the 15th, 17th and 20th days of pregnancy. In the adult (3-month-old) animals, the density of thymic glucocorticoid receptors was significantly elevated, whereas the density of uterine estrogen receptors was not, without any change in receptor affinity. 3. The experiments call attention to the steroid receptor Imprinting effect of fetal digoxin treatment that must be considered in regard to this treatment at this period and later in regard steroid treatments.
G. Csaba - One of the best experts on this subject based on the ideXlab platform.
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Bone Manifestation of Faulty Perinatal Hormonal Imprinting: A Review.
Current pediatric reviews, 2019Co-Authors: G. CsabaAbstract:Hormonal Imprinting takes place at the first encounter between the developing receptor and its target hormone and the encounter determines the receptor's binding capacity for life. In the critical period of development, when the window for Imprinting is open, the receptor can be misdirected by related hormones, synthetic hormones, and industrial or communal endocrine disruptors which cause faulty Hormonal Imprinting with life-long consequences. Considering these facts, the Hormonal Imprinting is a functional teratogen provoking alterations in the perinatal (early postnatal) period. One single encounter with a low dose of the imprinter in the critical developmental period is enough for the formation of faulty Imprinting, which is manifested later, in adult age. This has been justified in the immune system, in sexuality, in animal behavior and brain neurotransmitters etc. by animal experiments and human observations. This review points to the faulty Hormonal Imprinting in the case of bones (skeleton), by single or repeated treatments. The Imprinting is an epigenetic alteration which is inherited to the progeny generations. From clinical aspect, the faulty Imprinting can have a role in the pathological development of the bones as well, as in the risk of osteoporotic fractures, etc.
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Lifelong impact of breastmilk-transmitted hormones and endocrine disruptors.
2019Co-Authors: G. CsabaAbstract:BACKGROUND: Endocrine disruptors are hormone-like -usually lipid-soluble- natural or man-made molecules, which can be bound by human hormone receptors, simulating, stimulating or inhibiting the action of physiological hormones. They are harmful in adults however, more harmful perinatally, when faulty Hormonal Imprinting is provoked by them, with lifelong consequences (functional teratogenicity). By this effect alterations in hormone binding, hormone synthesis, sexual behavior, immune response, bone development, inclination to, or manifestation of diseases, etc in adult age, occur. REVIEW: Breastmilk is the main transporter of endocrine disruptors to the infant, as the mentioned molecules are concentrated in it. The perinatal faulty Hormonal Imprinting is epigenetically inherited to the progeny generations however, it is not known in man how many generations will be touched (experiments on unicellulars show at least 1000 generations, in rats two generations). CONCLUSION: Acknowledging the advances of breastfeeding in general, its disruptortransmissing faulty Imprinting-effect must be known in our chemically „infected” environment, in the light of developmental origin of health and disease (DOHaD).
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effect of a single neonatal oxytocin treatment Hormonal Imprinting on the biogenic amine level of the adult rat brain could oxytocin induced labor cause pervasive developmental diseases
Reproductive Sciences, 2013Co-Authors: F Hashemi, Kornélia Tekes, Rudolf Laufer, P Szegi, Laszlo Tothfalusi, G. CsabaAbstract:Perinatal single-hormone treatment causes Hormonal Imprinting with lifelong consequences in receptor-binding capacity, hormone production as well as in social and sexual behavior. In the present experiments, newborn rats were treated with a single dose of oxytocin, and the levels of biogenic amines and their metabolites were studied in 8 different brain regions and in the sera when the male and female animals were 4 months old. Both dopaminergic and serotonergic neurotransmission was found to be significantly influenced. The levels of 3,4-dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindole acetic acid metabolites decreased in the hypothalamus and striatum. Dopamine, serotonin, norepinephrine, and 5-hydroxytryptophol levels were hardly altered, and there was no difference in the epinephrine levels. The results show that dopamine and serotonin metabolism of hypothalamus and striatum are deeply and lifelong influenced by a single neonatal oxytocin treatment Oxytocin Imprinting resulted in decreased dopamine turnover in the hypothalamus and decreased serotonin turnover in the hypothalamus, medulla oblongata, and striatum of females. As the disturbance of brain dopamine and serotonin system has an important role in the development of pervasive developmental diseases (eg, autism) and neuropsychiatric disorders (eg, schizophrenia), the growing number of oxytocin-induced labor as a causal factor, cannot be omitted.
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a Hormonalis Imprinting human patologiai hatasainak modellezese allatkiserletekben model experiments of the human pathological effects of Hormonal Imprinting
2007Co-Authors: G. Csaba, P. Kovács, Barbara Knippel, Ágnes Inczefiné Gonda, C Karabelyos, Kornélia TekesAbstract:A Hormonalis Imprinting a kozponti idegrendszerre is hat, akar perinatalisan, akar kesőbbi erzekenysegi időpontban tortenik meg. Endorfin Imprinting csokkenti az agyi szerotonin szintet, ami befolyasolja az agresszivitast es szexualis magatartast es extrem modon megnoveli a nocistatin szintet, ami a fajdalomtűresre lehet hatassal. Perinatalis szerotonin Imprinting csokkenti a striatum szerotonin szintjet es noveli himekben a szexualis aktivitast. Az immunsejtekben (feherversejtek es hizosejtek) szamos hormon van jelen. Az allatok neme befolyasolja a hormon tartalmat. Ujszulottkori endorfin Imprinting utan a nőstenyek hizosejtjei kevesebb endorfint, szerotonint es EGF-et tartlmaztak. A kesői terhessegi korban bekovetkező endorfin Imprinting immunsejt szerotonin es hisztaminra valo hatasa transzgeneraciosan is kovethető az F2 generacioig. Kozvetett Imprinting is lehetseges, amennyiben stressz (elvalasztasi vagy felnőtt korban) vagy alkohol fogyasztas (terhesseg vagy szoptatas alatt) maradandoan befolyasolja az immunsejtek hormon tartalmat. Egyes hormonok (szerotonin, hisztamin)a sejtmagban is jelen vannak. HDC-gen kiutott egerekben az immunsejtek szerotonin tartalma megnőtt, de a sejtmagbol hianyzott. A kiserletek eredmenyeiből egy, az immunrendszerben jelen levő endokrin halozatra is lehet kovetkeztetni. | Perinatal as well as later (at weaning or at adult age) Hormonal Imprinting influences also the central nervous system. Endorphin Imprinting reduces the serotonin level of the brain, which influences the animals? aggressivity and sexual behavior and extremly elevates the nocistatin level which affects pain tolerance. Perinatal serotonin Imprinting reduces the serotonin level of striatum and increases males? sexual activity. Immune cells (white blood cells and mast cells) contain numerous hormones. There are differences in the hormone contents of males and females. After neonatal endorphin Imprinting females? mast cells contain less endorphin, serotonin and EGF. The effects of endorphin Imprinting in late pregnancy on the serotonin and histamine concentration can be followed up to the second filial generation.There is also a possibility of indirect Imprinting when stress (at weaning or in adult age) or alcohol consumption (during pregnancy or lactation) durably influence the hormone content of immune cells. Certain hormones (histamine and serotonin) are present also in the nucleus of mast cells. In HDC-KO mice the serotonin content of immune cells increases, however it was absent in the nucleus. Considering the results, an endocrine network inside the immune system can be surmized.
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effect of neonatal β endorphin Imprinting on sexual behavior and brain serotonin level in adult rats
Life Sciences, 2003Co-Authors: G. Csaba, M. Hantos, Cs. Karabélyos, Barbara Knippel, Laszlo Tothfalusi, Agnes Inczefigonda, Kornélia TekesAbstract:Abstract A single dose (3 μg) β-endorphin was administered to newborn female and male rats (Hormonal Imprinting). In adult age (at 5 months) sexual behavior, steroid hormone binding capacity and brain serotonin content was studied. Females' sexual activity (lordosis quotient) significantly decreased and more animals protested against mounting (ratio of kicking and crying 21/24 vs. 8/24; p
Éva Pállinger - One of the best experts on this subject based on the ideXlab platform.
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Verification of epigenetic inheritance in a unicellular model system: multigenerational effects of Hormonal Imprinting
Cell biology international, 2012Co-Authors: László Kőhidai, Éva Pállinger, Eszter Lajkó, György CsabaAbstract:The unicellular Tetrahymena has receptors for hormones of higher vertebrates, produces these hormones, and their signal pathways are similar. The first encounter with a hormone in higher dose provokes the phenomenon of Hormonal Imprinting, by which the reaction of the cell is quantitatively modified. This modification is transmitted to the progeny generations. The duration of the single imprinter effect of two representative signal molecules, insulin and 5-HT (5-hydroxytryptamine), in two concentrations (10 26 and 10 215 M) were studied. The effects of Imprinting were followed in 5 physiological indices: (i) insulin binding, (ii) 5-HT synthesis, (iii) swimming behaviour, (iv) cell growth and (v) chemotaxis in progeny generations 500 and 1000. The result of each index was different from the non-imprinted control functions, growth rate, swimming behaviour and chemotactic activity to insulin being enhanced, while others, e.g. synthesis and chemotactic responsiveness of 5-HT and the binding of insulin were reduced. This means that a function-specific heritable epigenetic change during Imprinting occurs, and generally a single encounter with a femtomolar hormone concentration is enough for provoking durable and heritable Imprinting in Tetrahymena. The experiments demonstrate the possibility of epigenetic effects at a unicellular level and call attention to the possibility that the character of unicellular organisms has changed through to the present day due to an enormous amount of non-physiological imprinter substances in their environment. The results – together with results obtained earlier in mammals – point to the validity of epigenetic Imprinting effects throughout the animal world.
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Prolonged effect of an H1-receptor blocker antihistamine on the histamine content of white blood cells and mast cells.
Cell biochemistry and function, 2004Co-Authors: György Csaba, Péter Kovács, Éva PállingerAbstract:Hormonal Imprinting usually takes place perinatally at the first encounter between the developing receptor and its target hormone, determining the future binding capacity of the receptor for life. Molecules similar to a hormone can cause faulty Imprinting also with life-long consequences. Hormone production of the imprinted cell is also durably influenced. In cytogenic organs Imprinting can also be provoked in adulthood. At present the effect of a single terfenadine treatment in adult rats on the histamine content of peritoneal cells (lymphocytes, mast cells and the monocyte-macrophage-granulocyte group), white blood cells (lymphocytes, granulocytes, monocytes) and thymic lymphocytes was studied 3 weeks after treatment to clarify the effect of prolonged treatment with an antihistamine in adulthood. The cells were studied by flow cytometric analysis. Peritoneal mast cells contained significantly more and thymic lymphocytes significantly less histamine than controls. In the other cells the differences were not significant. The results support earlier observations on the effect of antihistamines on mast cell histamine release (inhibition) and call attention to the fact that this effect is durable (Hormonal Imprinting provoked in adults).
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Prolonged impact of pubertal serotonin treatment (Hormonal Imprinting) on the later serotonin content of white blood cells.
Life sciences, 2002Co-Authors: György Csaba, Éva PállingerAbstract:The first encounter between the developing receptor and its target hormone establishes the Hormonal Imprinting which is needed for the normal function of the cell. In the presence of foreign-however able to bind-molecules, faulty Imprinting develops with lifelong consequences. Hormonal Imprinting influences not only the receptors, but also the later hormone production of cells. The critical time of Hormonal Imprinting is the perinatal period, however it can be executed sometimes (in continuously differentiating cells) also at puberty. As in earlier experiments single neonatal serotonin treatment caused a life-long alteration of white blood serotonin content in female rats, the early (10-19 day) and late (8 weeks) effect of single pubertal serotonin treatment was studied presently, by using flow cytometry. In contrast to the earlier (neonatal) results, pubertal treatment caused a radical reduction of serotonin content in male's lymphocytes, monocytes, granulocytes and mast cells, independent on the time of study. The effect in females was rather increasing, however uncertain. The experiments call attention to the possible different effects of neonatal and pubertal Hormonal Imprinting and to the imprintability of blood cells in adolescence.
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Single treatment (Hormonal Imprinting) of newborn rats with serotonin increases the serotonin content of cells in adults.
Cell biology international, 2002Co-Authors: György Csaba, Péter Kovács, Éva PállingerAbstract:Abstract Hormonal Imprinting takes place perinatally at the first encounter between the hormone and its target receptor, causing the finishment of the maturation of receptor–signal transduction system. In the presence of an excess of the target hormone or related molecules faulty Imprinting develops with life-long consequences. In earlier experiments single neonatal treatment with minute dose of IL-6 caused also prolonged stimulation of IL-6 production. In the present experiment newborn female and male rats were treated with 20 μg serotonin (Hormonal Imprinting) and were studied for serotonin content of different cell types in adult age. Serotonin content was measured by flow cytometry and its localization was determined by confocal microscopy. Serotonin content was detected in white blood cells (lymphocytes, monocytes and granulocytes); in lymphocytes, monocytes (macrophages), granulocytes and mast cells of peritoneal fluid and thymic lymphocytes. Serotonin was present in all cell types of control animals studied. Serotonin content extremely elevated in the white blood cells and also increased in the peritoneal cells of neonatally treated female animals. There was no elevation in thymic lymphocytes. The mean values of male animals remained at the control level. The experiments call attention to the life-long effect of the perinatal Hormonal Imprinting manifested presently in the elevation of serotonin content and point to the gender differences of serotonin Imprinting. Considering the role of serotonin in mood and psychiatric diseases, the observations could have some clinical importance.