scholarly journals Environmental Pollution and Non-Perinatal Faulty Hormonal Imprinting: A Critical Review

2018 ◽  
Vol 1 (1) ◽  
pp. 54-62
Author(s):  
Csaba G
Keyword(s):  
Hormone Receptors ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Critical Periods ◽  
Hormone Production ◽  
Hormonal Imprinting ◽  
Functional Changes ◽  
Dividing Cells ◽  
Synthetic Hormones ◽  
Survivors Of Childhood Cancer

The perinatal hormonal imprinting takes place perinatally, when the developing hormone receptors meet the hormones of the newborn and this suits the normal receptor-hormone connections for life. In this period the developmental window for imprinting is open and the receptors can be cheated by hormone-related exogeneous molecules, provoking faulty hormonal imprinting with lifelong consequences, as alteration of receptor binding capacity and hormone production, functional changes, altered sexual behavior, immunological alterations and inclination to or manifestation of diseases. However, there are other critical periods of life, when the window is open, as weaning, adolescence, regeneration in adults as well, as in continously dividing cells. The most sensitive non-perinatal critical period is the adolescence. In these periods hormone-like endocrine disruptors (e.g. bisphenol A, benzpyrene, pesticides and herbicides, soy isoflavones, medically used synthetic hormones etc) are provoking faulty hormonal imprinting with lifelong consequences. The hormonal imprinting is an epigenetic process, which is inherited to the progeny cells of the organism and to the offspring of the organism, by which it can chip in the evolution. The non-perinatal faulty hormonal imprinting is justified in animal experiments and seems to be likely in case of survivors of childhood cancer treatment. Similar to the faulty perinatal hormonal imprinting, the late (non-perinatal) faulty imprinting can participate in the provocation of later manifested diseases.

Bone Manifestation of Faulty Perinatal Hormonal Imprinting: A Review

2019 ◽  
Vol 15 (1) ◽  
pp. 4-9
Author(s):  
G. Csaba
Keyword(s):  
Animal Behavior ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Osteoporotic Fractures ◽  
Postnatal Period ◽  
Hormonal Imprinting ◽  
Adult Age ◽  
Pathological Development ◽  
Synthetic Hormones ◽  
Critical Developmental Period

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.

scholarly journals Hormonal imprinting in the central nervous system: causes and consequences

2013 ◽  
Vol 154 (4) ◽  
pp. 128-135 ◽  
Author(s):  
György Csaba
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Environmental Pollutants ◽  
Methylation Pattern ◽  
Critical Periods ◽  
Hormonal Imprinting ◽  
Modern Age ◽  
The Central Nervous System

The notion of the perinatal „hormonal imprinting” has been published at first in 1980 and since that time it spred expansively. The imprintig develops at the first encounter between the developing receptor and the target hormone – possibly by the alteration of the methylation pattern of DNA – and it is transmitted to the progeny generations of the cell. This is needed for the complete development of the receptor’s binding capacity. However, molecules similar to the target hormone (hormone-analogues, drugs, chemicals, environmental pollutants) can also bind to the developing receptor, causing faulty imprinting with life-long consequences. This can promote pathological conditions. Later it was cleared that in other critical periods such as puberty, imprinting also can be provoked, even in any age in differentiating cells. The central nervous system (brain) also can be mistakenly imprinted, which durably influences the dopaminergic, serotonergic and noradrenergic system and this can be manifested – in animal experiments – in alterations of the sexual and social behavior. In our modern age the faulty hormonal imprintig is inavoidable because of the mass of medicaments, chemicals, the presence of hormone-like materials (e.g. soya phytosteroids) in the food, and environmental pollutants. The author especially emphasizes the danger of oxytocin, as a perinatal imprinter, as it is used very broadly and can basically influence the emotional and social spheres and the appearance of certain diseases such as auitism, schizophrenia and parkinsonism. The danger of perinatal imprinters is growing, considering their effects on the human evolution. Orv. Hetil., 2013, 154, 128–135.

scholarly journals Hormonal Imprinting: The First Cellular-level Evidence of Epigenetic Inheritance and its Present State

2019 ◽  
Vol 20 (6) ◽  
pp. 409-418 ◽  
Author(s):  
György Csaba
Keyword(s):  
Endocrine Disruptors ◽  
Binding Capacity ◽  
Endocrine System ◽  
Epigenetic Inheritance ◽  
Perinatal Period ◽  
Normal Function ◽  
Cellular Level ◽  
Critical Periods ◽  
Hormonal Imprinting ◽  
Adult Age

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.

scholarly journals A fejlődési rendellenesség fogalmának átértelmezése: a hibás perinatalis imprinting jelentősége

2015 ◽  
Vol 156 (28) ◽  
pp. 1120-1127
Author(s):  
György Csaba
Keyword(s):  
Binding Capacity ◽  
Animal Experiments ◽  
Perinatal Period ◽  
Environmental Pollutant ◽  
Intrauterine Development ◽  
Developmental Abnormalities ◽  
Hormonal Imprinting ◽  
Long Time ◽  
Definition Of ◽  
Hormone System

The classic definition of developmental abnormalities referred to malformations observed at birth. Later the functional teratogenicity was also recognized and accepted, which can be revealed in functional abnormalities caused by harms during the intrauterine development and can be manifested at any time of life. However, the ontogeny is not closed with the birth, because some systems or organs are developing for a long time after it, and can be influenced by different factors. From this aspect the perinatal period is especially important when the mutual adjustment of the receptor-hormone system is taking place and the hormonal imprinting develops. If this is faulty, it influences the hormone binding capacity of receptors that has consequences for life. The faulty hormonal imprinting is functionally teratogen; it provokes a fault up to the level of a malformation and aggravated with its heredity to the progenies. False imprinting is provoked (in animal experiments, proportioning to human doses) by drugs acting at receptor level, as oxytocin, steroid hormone analogues (pregnancy protectors, oral contraceptives, surfactants), vitamin A and D, environmental pollutant endocrine disruptors (benzpyrene, bisphenol A, pesticides, herbicides) and certain soybean components, etc. From this aspect these are functional teratogens, and their evasion in prevention as well as therapy seems to be vital. This means that the concept of developmental abnormality must be broadened, as developmental abnormalities: 1.) can originate not only in the intrauterine period, but also perinatally or even later, 2.) it can be manifested at any time of life, 3.) it can be present in a latent form which can be activated by inner or outer environmental factors, 4.) the faulty hormonal imprinting is a teratogen factor. Orv. Hetil., 2015, 156(28), 1120–1127.

The interrelationship between and the regulation of hepatic growth hormone receptors and circulating GH binding protein in the pig

1992 ◽  
Vol 126 (2) ◽  
pp. 155-161 ◽  
Author(s):  
Geoffrey R Ambler ◽  
Bernhard H Breier ◽  
Andrzej Surus ◽  
Hugh T Blair ◽  
Stuart N McCutcheon ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Receptor ◽  
Hormone Receptors ◽  
Binding Capacity ◽  
Binding Protein ◽  
Somatic Growth ◽  
Gh Receptor ◽  
Age Related ◽  
Igf I ◽  
Serum Gh

We evaluated the interrelationship between, and regulation of, the hepatic growth hormone receptor and serum GH binding protein (GH BP) in pigs treated with recombinant porcine growth hormone (rpGH). Infant and pubertal male pigs (N = 5 per group) received either rpGH 0.15 mg/kg daily or diluent intramuscularly for 12 days. Somatic growth, serum IGF-I and GH BP and [125I]bovine GH (bGH) binding to MgCl2-treated hepatic membrane homogenates were examined. Marked age-related increases were seen in serum GH BP (p<0.001) and [125I]bGH binding to hepatic membranes (p<0.001). GH BP was increased in rpGH treated animals (p = 0.03), from 13.8±1.2 (mean±1 x sem) (controls) to 17.8±2.0% in infants, and from 35.2±2.6 (controls) to 41.8±3.4% in pubertal animals. [125I]bGH binding to hepatic membranes was also increased by rpGH treatment (p<0.05), from 7.0±1.6 (controls) to 15.4±3.6% in infants and from 53.7±7.1 (controls) to 65.1±11.8% in pubertal animals. No significant interaction between age and treatment was seen. Overall, serum GH BP correlated significantly with [125I]bGH membrane capacity (r=0.82, p<0.001), with a correlation of r= 0.83 in the infant animals but no significant correlation in the pubertal animals considered alone (r=0.13). Serum IGF-I correlated significantly with serum GH BP (r=0.93, p<0.001) and [125]bGH membrane binding capacity (r = 0.91, p< 0.001). These observations suggest that serum GH BP levels reflect major changes of hepatic GH receptor status. In addition, the present study demonstrates that the hepatic GH receptor can be induced by GH in the infant pig, despite a developmentally low GH receptor population at this age, suggesting potential efficacy of GH at earlier ages than generally considered.

Influence of imprinting with A and B chains of insulin on binding and functional changes in tetrahymena

1990 ◽  
Vol 10 (5) ◽  
pp. 431-436 ◽  
Author(s):  
G. Csaba ◽  
P. Kovács
Keyword(s):  
Binding Site ◽  
Binding Capacity ◽  
Combined Treatment ◽  
The Other ◽  
Hormone Binding ◽  
Functional Effect ◽  
Functional Changes ◽  
Positive Material ◽  
A Chain ◽  
The One

Insulin and its A and B chain increased the quantity of intracellular PAS-positive material (glycogen) in tetrahymena, whereas the combined A+B chains decreased it. Imprinting—previous interaction—with insulin, its A and B chains in themselves and with the A+B chain increased the hormone binding capacity of tetrahymena, but the functional effect of imprinting (storage or breakdown of glycogen) showed a different tendency with insulin and A+B chain on the one hand, and A chain and B chain on the other. Since the imprinting potential of a molecule promotes the induction of receptor formation, the fact remains that both component chains of insulin were able to act as potential imprinters, although the A chain was superior to the B chain in this respect throughout, and combined treatment with the A+B chain ultimately induced the formation of a similar binding site as insulin itself.

Effects of glucocorticosteroids on prolactin and growth hormone production and characterization of the intracellular hormone receptors in rat pituitary tumour cells

1980 ◽  
Vol 95 (3) ◽  
pp. 319-327 ◽  
Author(s):  
Oddvar Naess ◽  
Egil Haug ◽  
Kaare Gautvik
Keyword(s):  
Growth Hormone ◽  
Hormone Receptors ◽  
Pituitary Tumour ◽  
Tumour Cells ◽  
Scatchard Analysis ◽  
Hormone Production ◽  
Single Class ◽  
High Affinity ◽  
Rat Pituitary

Abstract. The effect of corticosterone and dexamethasone on the production of growth hormone and prolactin was studied in rat pituitary tumour cells (GH3-cells) in culture. Corticosterone and dexamethasone caused a dose-dependent stimulation of growth hormone synthesis, and the highest concentration (10−6 mol/l) increased growth hormone levels to 250% of controls. This concentration, however, decreased prolactin synthesis to 25% of the control values. The cytosol fractions from monolayer cultures as well as from tumours of GH3-cells were found to possess receptor molecules for glucocorticoid hormones, having a sedimentation constant close to 8 S in a salt-free buffer and 4 S in the presence of 0.5 mol/l KCL. Isoelectric point of the receptor was 5.8. Scatchard analysis showed one single class of binding sites with high affinity (Kd 2.1 ± 0.4 (sd × 10−9 mol/l). Studies on the steroid specificity revealed that dexamethasone had the highest affinity for the receptor. Corticosterone, cortisol and progesterone had also high affinity, whereas testosterone and oestradiol-17β had no significant affinity for the receptors. After in vivo administration of [3H]dexamethasone to GH3 tumour-bearing rats, radioactivity could be extracted from purified nuclei bound to 4 S macromolecules. The presence of receptors for glucocorticosteroid hormones in the GH3-cells, suggests that these hormones may alter growth hormone and prolactin production at the anterior pituitary level.

Gonadotrophin releasing hormone receptors and the response of pituitary gonadotrophs in culture

1983 ◽  
Vol 98 (3) ◽  
pp. 391-399 ◽  
Author(s):  
A. Bérault ◽  
M.-T. Jansem de Almeida Catanho ◽  
M. Théoleyre ◽  
M. Jutisz
Keyword(s):  
Hormone Receptors ◽  
Binding Capacity ◽  
High Capacity ◽  
Biological Response ◽  
Cell Number ◽  
Culture Period ◽  
Pituitary Cells ◽  
Cell Content ◽  
Releasing Hormone ◽  
Gonadotrophin Releasing Hormone

We have investigated the effect of the time of culture on cell number, cell content of LH, cell responsiveness to gonadotrophin releasing hormone (GnRH) and binding parameters of GnRH in rat anterior pituitary cells in culture. Although a decrease in the cell number was observed during the culture period, the cell content of LH remained unchanged. The receptor affinity (Ka) in acutely dispersed cells was 0·86 × 107l/mol for [3H]GnRH and 1·36 × 1010l/mol for a highly potent agonist, d-Ser(But)6]GnRH(1–9)nonapeptide-ethylamide (GnRH-A). The affinity and binding capacity (0·3 fmol/106 cells) for iodinated GnRH-A did not change significantly during the 6-day culture period. On the contrary, the values of Ka and binding capacity (257 fmol/106 cells) for tritiated GnRH decreased by about 50% betweeen days 1 and 6 of culture. Our results suggest that 125I-labelled GnRH-A binds mostly to high-affinity and low-capacity receptor sites, while [3H]GnRH, which must be used at a higher concentration, also binds to low-affinity, high-capacity binding sites and is therefore useless for the measurement of GnRH receptor binding affinity and binding capacity. Since the biological response of the cells to GnRH increased with the time of culture, it is concluded that although GnRH action is receptor-mediated, binding capacity and biological activity are not necessarily correlated.

scholarly journals Early Developmental Trajectories of Functional Connectivity Along the Visual Pathways in Rhesus Monkeys

2018 ◽  
Vol 29 (8) ◽  
pp. 3514-3526 ◽  
Author(s):  
Z Kovacs-Balint ◽  
E Feczko ◽  
M Pincus ◽  
E Earl ◽  
O Miranda-Dominguez ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Social Interactions ◽  
Social Engagement ◽  
Rhesus Monkeys ◽  
Developmental Trajectories ◽  
Visual Pathways ◽  
Neural Pathways ◽  
Critical Periods ◽  
Functional Changes ◽  
Monkey Model

Abstract Early social interactions shape the development of social behavior, although the critical periods or the underlying neurodevelopmental processes are not completely understood. Here, we studied the developmental changes in neural pathways underlying visual social engagement in the translational rhesus monkey model. Changes in functional connectivity (FC) along the ventral object and motion pathways and the dorsal attention/visuo-spatial pathways were studied longitudinally using resting-state functional MRI in infant rhesus monkeys, from birth through early weaning (3 months), given the socioemotional changes experienced during this period. Our results revealed that (1) maturation along the visual pathways proceeds in a caudo-rostral progression with primary visual areas (V1–V3) showing strong FC as early as 2 weeks of age, whereas higher-order visual and attentional areas (e.g., MT–AST, LIP–FEF) show weak FC; (2) functional changes were pathway-specific (e.g., robust FC increases detected in the most anterior aspect of the object pathway (TE–AMY), but FC remained weak in the other pathways (e.g., AST–AMY)); (3) FC matures similarly in both right and left hemispheres. Our findings suggest that visual pathways in infant macaques undergo selective remodeling during the first 3 months of life, likely regulated by early social interactions and supporting the transition to independence from the mother.

scholarly journals ASSESSMENT OF BIOLOGY ACTIVITY OF THE PEELING SUBSTANCES BY THE PHYSICOCHEMICAL APPROACHES ON THE SPIROSTOMUM AMBIGUUM CELL MODEL

2021 ◽  
pp. 82-86
Author(s):  
USPENSKAYA E. V. ◽  
PLETENEVA T. V. ◽  
PHAM MY HANH ◽  
KAZIMOVA I. V.
Keyword(s):  
Activation Energy ◽  
Cell Death ◽  
Cell Model ◽  
Equilibrium Constants ◽  
Animal Experiments ◽  
Acid Solutions ◽  
Arrhenius Kinetics ◽  
Functional Changes ◽  
Dead State ◽  
Spirostomum Ambiguum

Objective: To evaluate the biological activity of chemical peeling substances based on enzymatic and Arrhenius kinetics using Spirostomum ambiguum as an alternative approach to animal experiments. Methods: The Spirotox method was used to analyze the mechanism of «xenobiotic-cell» interaction, similar to the Michaelis-Menten enzymatic kinetics. The Hill-Langmuir equation was used to determine the degree of cooperativity in the binding of xenobiotics to cellular receptors. Using the Arrhenius kinetics, the observed activation energy obsEa of cell death in the model solutions of glycolic and carbolic acids was determed, which will allow predicting the toxicity parameters of any peeling substances. Results: The relationship Spirostomum ambiguum lifetime tL-lgC concentration of peeling compound solution made it possible to characterize the moment of cellular transition from the intermediate state C•Ln to the dead state DC, characterized by irreversible structural and functional changes in the cell/death. The values were 5.3 mmol•l-1 for glycolic acid solutions and 2.8 mmol•l-1 for carbolic acid solutions. Equilibrium constants Keq of complexation, the rate of infusoria death fm, and the degree of ligand cooperativity n were calculated. The activation energy °bsEa of cell death was determined in Arrhenius coordinates, which were 210±0.39 kJ·mol-1 and 108±0.09 kJ·mol-1 for glycolic and carbolic acids respectively. The correlation between the values ​​of activation energy and DL50 of mammals (rats) was discovered. Conclusion: The obtained kinetic parameters made it possible, without animals and humans testing, to characterize the mechanisms of interaction of peeling substances with the living cell.

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